RESUMEN
This article is a review of the findings of experimental and clinical studies of a new method of treatment of pulmonary hypertension - pulmonary artery denervation with the help of radiofrequency ablation, cryodenervation and ultrasonic impact. Pulmonary artery denervation results in decreased neurogenic tonic sympathetic and, probably, increased parasympathetic effects on pulmonary vessels. On models of experimental monocrotaline-induced pulmonary hypertension in various-species animals, it was determined that pulmonary artery denervation is followed by decreased activity of local pulmonary renin-angiotensin system, slowed processes of remodeling of pulmonary vessels, hypertrophy and fibrosis of the right ventricle, with inhibition of progression of pulmonary hypertension by means of suppression of extracellular signal-regulated kinase 1/2 (ERK 1/2) which regulates differentiation, proliferation and migration of smooth muscle cells. However, the problem of the pattern of pulmonary microcirculation changes (pre- and postcapillary resistance, capillary filtration coefficient) after pulmonary artery denervation warrants further study. The findings of clinical studies in patients with pulmonary hypertension suggest that pulmonary artery denervation inducing a decrease of pressure therein, as well as pulmonary vessel resistance did not lead to normalization of pulmonary haemodynamics.The mentioned impact partially removes the neurogenic component of multicircuit and multifactorial regulation of pulmonary circulation. Therefore, along with pulmonary artery denervation, further search for pharmacological agents selectively influencing pulmonary vessels remains a problem of current importance.
Asunto(s)
Hipertensión Pulmonar , Animales , Desnervación , Humanos , Hipertensión Pulmonar/etiología , Hipertensión Pulmonar/cirugía , Monocrotalina , Arteria Pulmonar/cirugía , Resistencia VascularRESUMEN
This review contains the data concerning the mechanisms of spontaneous fibrinolysis in pulmonary vessels and possibilities of its acceleration in pulmonary embolism. The spontaneous fibrinolysis system is known to be sequential and multifactorial, with the interaction of accelerators (t-PA and u-PA) and inhibitors (alpha-2-antiplasmin, PAI-1, TAFI). The fibrinolytic processes take place in case of prevailing reactions of accelerating factors over inhibiting ones. The endothelium of pulmonary vessels possesses pronounced antithrombogenic and profibrinolytic properties, therefore, the processes of fibrinolysis in the pulmonary vascular bed normally occur more intensively than in the vessels of the systemic circulation. The membrane proteins of the endothelium annexins A2 activate plasminogen, whereas thrombomodulin inhibits the activity of PAI-1. The main approaches to increase the fibrinolysis intensity in conditions of pulmonary embolism may be aimed at elevating the activity of fibrinolytic enzymes (enhancing the synthesis of annexins A2, the use of NMDA-receptor antagonists) and suppressing its inhibitors (the use of monoclonal antibodies to alpha-2-antiplasmin, as well as plasminogen activator inhibitor-1 (PAI-1) and thrombin-activatable fibrinolysis inhibitor (TAFI). Promising directions for future research can be the synthesis of a new generation of tissue-type plasminogen activators, and investigations of the possibility of clinical application of antithrombin and thrombomodulin, angiotensin converting enzyme inhibitors and cortisol antagonists. To meet these challenges, it is necessary to develop new models of venous thrombosis and acute pulmonary embolism in different animal species, with the assessment of the changes in the venous haemodynamics and pulmonary microcirculation on the background of administration of a new class of fibrinolytic agents.
Asunto(s)
Carboxipeptidasa B2 , Embolia Pulmonar , Aceleración , Animales , Carboxipeptidasa B2/farmacología , Fibrinólisis , Fibrinolíticos/farmacología , Embolia Pulmonar/tratamiento farmacológicoRESUMEN
In acute experiments in anesthetized rabbits the changes of the pulmonary hemodynamics following 60 s myocardial ischemia in the region of the descendent left coronary artery were studied in control animals and after the blockade of α-adrenoreceptors by phentolamine or ß-adrenoreceptors by propranolol. Following myocardial ischemia in control animals the pulmonary artery pressure and flow decreased, the pulmonary vascular resistance did not change, the left atrial pressure elevated; the cardiac output decreased more than pulmonary artery flow. Following myocardial ischemia after the blockade of ß-adrenoreceptors the pulmonary artery pressure decreased more than in control animals, the pulmonary artery flow was decreased in the same level as in the last case. The pulmonary vascular resistance was diminished, the left atrial pressure increased; the pulmonary artery flow and cardiac output decreased in the same level. Following myocardial ischemia after the blockade of ß-adrenoreceptors the pulmonary artery pressure and pulmonary vascular resistance decreased more than after the blockade of α-adrenoreceptors, the left atrial pressure did not change. In both cases the pulmonary artery flow decreased in the same level and its changes were correlated with venous return shifts. The differences of the pulmonary artery changes following myocardial ischemia after the blockade of α- and ß-adrenoreceptors are caused not only the different pulmonary vascular resistance changes, but also the left atrial pressure.
Asunto(s)
Antagonistas Adrenérgicos alfa/farmacología , Antagonistas Adrenérgicos beta/farmacología , Pulmón/irrigación sanguínea , Isquemia Miocárdica/fisiopatología , Arteria Pulmonar/fisiopatología , Animales , Presión Sanguínea/efectos de los fármacos , Gasto Cardíaco/efectos de los fármacos , Vasos Coronarios/efectos de los fármacos , Vasos Coronarios/fisiopatología , Pulmón/efectos de los fármacos , Pulmón/fisiopatología , Contracción Miocárdica/efectos de los fármacos , Isquemia Miocárdica/metabolismo , Miocardio/metabolismo , Miocardio/patología , Fentolamina/farmacología , Propranolol/farmacología , Arteria Pulmonar/efectos de los fármacos , Conejos , Receptores Adrenérgicos alfa/metabolismo , Receptores Adrenérgicos beta/metabolismo , Resistencia Vascular/efectos de los fármacosRESUMEN
In acute experiments in anesthetized cats myocardial left ventricular ischemia caused the decreasing of the arterial pressure, cardiac output, superior and inferior vena cava flow and venous return. The diminishing of the superior vena cava flow was caused by the decreasing of the cardiac output, increasing of the vascular resistance and decreasing of the blood flow in the region of the brachiocephalica artery. The inferior vena cava flow decreased following the diminishing of the cardiac output and abdominal aorta blood flow, while vascular resistance in this region did not change. In acute experiments in anesthetized rabbits following myocardial ischemia after the blockade of N-cholinoreceptors the superior and inferior vena cava flow decreased in the same level as in control animals. Following myocardial ischemia after the blockade of α-adrenoreceptors the superior and inferior vena cava flow decreased more significant, than in control animals.
Asunto(s)
Hemodinámica/efectos de los fármacos , Isquemia Miocárdica/fisiopatología , Vena Cava Inferior/fisiopatología , Vena Cava Superior/fisiopatología , Antagonistas Adrenérgicos alfa/farmacología , Animales , Presión Arterial/efectos de los fármacos , Presión Sanguínea/efectos de los fármacos , Tronco Braquiocefálico/efectos de los fármacos , Tronco Braquiocefálico/fisiopatología , Gasto Cardíaco/efectos de los fármacos , Gatos , Antagonistas Colinérgicos/farmacología , Isquemia Miocárdica/tratamiento farmacológico , Conejos , Receptores Adrenérgicos alfa/metabolismo , Receptores Colinérgicos/metabolismo , Resistencia Vascular/efectos de los fármacos , Vena Cava Inferior/efectos de los fármacos , Vena Cava Superior/efectos de los fármacosRESUMEN
In acute experiments in anesthetized rabbits the pulmonary hemodynamics changes were studied following 60 s myocardial ischemia in the region of the descendent left coronary artery in control state and after the blockade of M- or N-cholinoreceptors and acetylcholine infusion. Following myocardial ischemia in control animals the pulmonary artery pressure and flow decreased, the pulmonary vascular resistance was not changed. Following myocardial ischemia after the blockade of M-cholinoreceptors by atropine the changes of pulmonary hemodynamics were the same as in control animals, the cardiac output decreased twice as more as in control animals. Following myocardial ischemia after the blockade of N-cholinoreceptors by hexamethonium the pulmonary hemodynamics changes were the same as in the control rabbits. Following myocardial ischemia after the acetylcholine infusion the pulmonary artery flow decreased more than the cardiac output, the pulmonary vascular resistance was diminished. The disbalance of the cardiac output and pulmonary artery flow changes has revealed the significance of the adreno-cholinergic interaction in the changes of the pulmonary vessels capacitance and resistive functions following myocardial ischemia.
Asunto(s)
Acetilcolina/metabolismo , Pulmón/metabolismo , Isquemia Miocárdica/metabolismo , Miocardio/metabolismo , Receptores Colinérgicos/metabolismo , Animales , Antiarrítmicos/farmacología , Atropina/farmacología , Presión Sanguínea/efectos de los fármacos , Gasto Cardíaco/efectos de los fármacos , Vasos Coronarios/fisiopatología , Bloqueadores Ganglionares/farmacología , Hexametonio/farmacología , Pulmón/irrigación sanguínea , Pulmón/efectos de los fármacos , Pulmón/fisiopatología , Isquemia Miocárdica/fisiopatología , Miocardio/patología , Arteria Pulmonar/fisiopatología , Conejos , Resistencia Vascular/efectos de los fármacosRESUMEN
In acute experiments in rabbits the changes of the pulmonary hemodynamics following myocardial ischemia in the region of the descendent left coronary artery were studied in normotensive animals and after the infusion of histamine or isoproterenol. Following histamine intravenous in fusion the pulmonary artery pressure and pulmonary vascular resistance were increased, however the pulmonary artery flow decreased. In these conditions myocardial ischemia caused the returning of the elevated pulmonary artery pressure to normal level following the diminishing of the pulmonary artery flow to the same level as in normotensive rabbits. Meanwhile the pulmonary vascular resistance remained elevated. Following isoproterenol intravenous injection the isoproterenol artery pressured and flow, pulmonary vascular resistance were decreased. In these conditions myocardial ischemia caused the decrease of the isoproterenol artert pressure, more, than in normotensive rabbits, which was the result of diminishing left atrial pressure, however, the pulmonary artery flow and pulmonary vascular resistance decreased in both cases to the same level. Thus we concluded, that following myocardial ischemia in rabbits with decreased arterial pressure, the changes of pulmonary artery pressure depend on pulmonary artery flow and left atrial pressure changes. The shifts of the pulmonary artery flow depend on venous return ones and does not correlated with pulmonary vascular resistance changes.
Asunto(s)
Hemodinámica , Pulmón/irrigación sanguínea , Isquemia Miocárdica/inducido químicamente , Isquemia Miocárdica/fisiopatología , Arteria Pulmonar/fisiopatología , Animales , Presión Arterial , Presión Sanguínea/fisiología , Circulación Coronaria/fisiología , Vasos Coronarios/fisiopatología , Histamina/toxicidad , Humanos , Isoproterenol/toxicidad , Pulmón/fisiopatología , Masculino , Isquemia Miocárdica/complicaciones , Conejos , Resistencia Vascular/fisiologíaRESUMEN
In acute experiments in anesthetized cats the changes of the left atrial pressure, left ventricular myocardial contractility, its relaxation, venous return and cardiac output were studied after catecholamines or acetylcholine and histamine intravenous injection. When arterial pressure was elevated and venous return with cardiac output increased to the same level, the left atrial pressure decreased if the left ventricular myocardial contractility and its relaxation rate were increased equally. However, the left atrial pressure elevated, if left ventricular myocardial relaxation increased less than myocardial contractility. When arterial pressure was depressed, the left atrial pressure decreased if left ventricular myocardial contractility decreased less than myocardial relaxation diminished. If left ventricular myocardial contractility decreased significantly, the left atrial pressure increased. In the last case the value of cardiac output was more, than venous return one. The data suggest that after injection of the pressor and depressor vasoactive drugs, if the shifts of the venous return and cardiac output are equal, the changes of the nature and value of the left atrial pressure are dependent on the relation of the left ventricular myocardial contractility and its relaxation rate.
Asunto(s)
Función del Atrio Izquierdo/efectos de los fármacos , Corazón/efectos de los fármacos , Hemodinámica/efectos de los fármacos , Vasoconstrictores/administración & dosificación , Vasodilatadores/administración & dosificación , Acetilcolina/administración & dosificación , Animales , Función del Atrio Izquierdo/fisiología , Presión Sanguínea/efectos de los fármacos , Gasto Cardíaco/efectos de los fármacos , Gasto Cardíaco/fisiología , Gatos , Epinefrina/administración & dosificación , Corazón/fisiología , Hemodinámica/fisiología , Histamina/administración & dosificación , Inyecciones Intravenosas , Contracción Miocárdica/efectos de los fármacos , Contracción Miocárdica/fisiología , Norepinefrina/administración & dosificación , Ventiladores MecánicosRESUMEN
In acute experiments in anesthetized rabbits the changes of the pulmonary hemodynamics following myocardial ischemia in the region of the descendent left coronary artery were studied in control animals and after the blockade of alpha-adrenoreceptors by phentolamine or N-cholinoreceptors of autonomic ganglia by hexamethonium. Following myocardial ischemia in control animals the pulmonary artery pressure and flow decreased, the pulmonary vascular resistance was elevated not significantly, the cardiac output decreased more than pulmonary artery flow. Following myocardial ischemia after the blockade of alpha-adrenoreceptors the pulmonary artery flow and cardiac output decreased in the same level and the pulmonary vascular resistance was decreased. In these conditions the pulmonary artery pressure decreased more than in control animals, meanwhile the pulmonary artery flow was decreased in the same level as in the last case. Following myocardial ischemia after the blockade of N-cholinoreceptors the pulmonary hemodynamics changes were the same as they were following myocardial ischemia in the control rabbits, the cardiac output decreased more than pulmonary artery flow. The disbalance of the cardiac output and pulmonary artery flow changes in the case of myocardial ischemia was caused by the pulmonary vessel reactions following activations of the humoral adrenergic mechanisms.
Asunto(s)
Antagonistas Adrenérgicos alfa/farmacología , Hexametonio/farmacología , Isquemia Miocárdica/metabolismo , Fentolamina/farmacología , Receptores Adrenérgicos alfa/metabolismo , Receptores Colinérgicos/metabolismo , Animales , Presión Sanguínea/efectos de los fármacos , Gasto Cardíaco/efectos de los fármacos , Vasos Coronarios/efectos de los fármacos , Vasos Coronarios/metabolismo , Vasos Coronarios/fisiopatología , Modelos Animales de Enfermedad , Ganglios Autónomos/efectos de los fármacos , Ganglios Autónomos/metabolismo , Ganglios Autónomos/fisiopatología , Bloqueadores Ganglionares/farmacología , Hemodinámica/efectos de los fármacos , Masculino , Isquemia Miocárdica/fisiopatología , Arteria Pulmonar/efectos de los fármacos , Arteria Pulmonar/metabolismo , Arteria Pulmonar/fisiopatología , Conejos , Resistencia Vascular/efectos de los fármacosRESUMEN
In acute experiments in anesthetized rabbits, changes of the pulmonary hemodynamics following myocardial ischemia in the region of the descendent left coronary artery were studied in control animals and after the infusion of adrenaline and phenylephrine. The pulmonary artery pressure was increased following infusion of these drugs; however, it decreased to normal level in the condition of myocardial ischemia. Meanwhile the pulmonary vascular resistance was elevated to the same level in both cases. Following adrenaline infusion, the pulmonary artery blood flow and venous return increased and, in the condition of myocardial ischemia, they decreased to normal level, but the left atrial pressure was decreased. Following phenylephrine infusion, the pulmonary artery blood flow and venous return did not change and, in the condition of myocardial ischemia, these parameters decreased lower than normal level but the left atrial pressure was elevated. Thus we concluded that equal values of the pulmonary artery pressure in both cases were caused by changes of different character in the left atrial pressure. The differences of the changes character and values of the pulmonary artery flow under experimental myocardial ischemia following the infusion of adrenaline and phenylephrine were caused by different shifts of the venous return.
Asunto(s)
Presión Sanguínea/fisiología , Hipertensión/fisiopatología , Pulmón/irrigación sanguínea , Isquemia Miocárdica/fisiopatología , Animales , Presión Sanguínea/efectos de los fármacos , Modelos Animales de Enfermedad , Epinefrina/administración & dosificación , Hemodinámica/fisiología , Humanos , Isquemia Miocárdica/inducido químicamente , Fenilefrina/administración & dosificación , Arteria Pulmonar/fisiopatología , ConejosRESUMEN
In acute experiments in anesthetized rabbits, changes of the pulmonary hemodynamics following myocardial ischemia in the region of the descendent left coronary artery were studied as well as in control animals and after the blockade of beta-adrenoreceptors. The myocardial ischemia decreased the left ventricular myocardial contractility, cardiac output and arterial pressure, decreased the pulmonary artery pressure and flow. Following myocardial ischemia, the pulmonary artery pressure decreased less than pulmonary artery blood flow as the result of elevating of the left atrial pressure, meanwhile pulmonary vascular resistance was not changed. Following myocardial ischemia in animals after the blockade of the beta-adrenoreceptors, the pulmonary flow decreased the same as in control animals. However, the pulmonary artery pressure was decreased twofold more significantly than in control animals, and its diminishing was in the same degree as the pulmonary artery flow. Following myocardial ischemia after the blockade of the beta-adrenoreceptors, the pulmonary vascular resistance decreased whereas the left atrial pressure did not change significantly because the myocardial contractility decreased less than in control animals.
Asunto(s)
Antagonistas Adrenérgicos beta/farmacología , Oclusión Coronaria/fisiopatología , Ventrículos Cardíacos/efectos de los fármacos , Isquemia Miocárdica/fisiopatología , Propranolol/farmacología , Arteria Pulmonar/fisiopatología , Animales , Presión Sanguínea/efectos de los fármacos , Gasto Cardíaco/efectos de los fármacos , Ventrículos Cardíacos/fisiopatología , Hemodinámica/efectos de los fármacos , Modelos Animales , Contracción Miocárdica/efectos de los fármacos , Conejos , Receptores Adrenérgicos beta/metabolismo , Resistencia VascularRESUMEN
The character and values of changes of the pulmonary hemodynamics and venous return following acetylcholine, histamine and isoproterenol intravenous injection were studied in acute experiments on the anesthetized cats. After depressor drugs injection the character and values of changes of pulmonary artery pressure and flow were different. In 67% cases the pulmonary artery pressure was decreased, and in 33%--it was elevated, meanwhile the pulmonary artery flow was decreased in 48% cases and it was increased in 52%, i.e., in the equal number of observations. Thus, following depressor drugs intravenous injection, hemodynamic mechanisms of the changes of pulmonary artery pressure and flow are different. The character and values of changes of the pulmonary artery pressure are correlated with the changes of pulmonary vascular resistance and are not dependent with the left atrial pressure shifts. The changes of the pulmonary artery blood flow are caused by the changes of the venous return and are not correlated with the changes of the right and left atrial pressure.
Asunto(s)
Presión Sanguínea/efectos de los fármacos , Arteria Pulmonar/fisiología , Vasoconstrictores/farmacología , Animales , Velocidad del Flujo Sanguíneo/efectos de los fármacos , Presión Sanguínea/fisiología , GatosRESUMEN
It was found that changes of resistance, capacity and exchange vessel functions of the skeletal muscle depended on values of amplitude and frequency of perfusion blood flow in acute experiments on cats. Amplitude-frequency characteristics of hemodynamic parameters of these functions were nonlinear. Ranges of amplitude and frequency variation with significant shifts of these parameters were determined. Conditions of perfusion (constant flow or constant pressure) changed volume and direction of haemodynamic parameter shifts under the amplitude-frequency modulation of the pulsatile blood flow. The pulsatile blood flow oscillations exerted maximum influence on hemodynamic parameters of exchange vessel function. The author has proposed the wave regulation conception of organ vessel functions.
Asunto(s)
Presión Sanguínea/fisiología , Músculo Esquelético/irrigación sanguínea , Músculo Esquelético/fisiología , Animales , Velocidad del Flujo Sanguíneo/fisiología , Gatos , Femenino , Masculino , PerfusiónRESUMEN
Myocardial ischemia caused inhibition of myocardial contractility, increased pressure in the left atrium, reduced cardiac output and reduced systemic blood pressure. The decrease in cardiac output is due to a combination of the myocardial contractility reduction and that of the outflow of blood from the pulmonary vascular bed. Hemodynamic changes in the arterial part of the systemic circulation are accompanied by shifts in its venous part: reduced blood flow in the anterior and posterior caval veins and a decrease in venous return. The determining factor for reducing the flow of venous blood to the heart during myocardial ischemia is a decrease in cardiac output. Myocardial ischemia of the left ventricle is accompanied by a decrease in pressure and blood flow in the pulmonary artery. The data obtained suggest that the degree of reduction of these indicators of pulmonary hemodynamics depends on the elevated pressure in the left atrium resulting from reduction of the left ventricle contractility. The degree of hemodynamic disorders in systemic and pulmonary circulation in myocardial ischemia depends not only on the size of the zone of myocardial ischemia of the left ventricle, but also on the duration of cessation of its blood supply. We suggest that the time factor is a decisive one with respect to severity of hemodynamic disorders occurring only at a certain, critical, size of the zone of myocardial ischemia.
Asunto(s)
Gasto Cardíaco , Ventrículos Cardíacos/fisiopatología , Isquemia Miocárdica/fisiopatología , Circulación Pulmonar , Animales , Velocidad del Flujo Sanguíneo , Presión Sanguínea , Gatos , Arteria Pulmonar/fisiopatologíaRESUMEN
The character and values of changes of the pulmonary and systemic hemodynamics following epinephrine, norepinephrine and angiotensin intravenous injection were studied in acute experiments on the anesthetized cats. After catecholamines injection pulmonary blood flow was always increased, meanwhile pulmonary artery pressure can be elevated (in the most observations) or decreased. In the cases of angiotensin administration the pulmonary blood flow could be augmented or decreased; pulmonary artery pressure had been increased or decreased independently from the character of changes of pulmonary flow. Thus, linear correlation between shifts of the pulmonary artery pressure and pulmonary blood flow had not been revealed. The changes of the pulmonary artery pressure were not correlated with the pulmonary vascular resistance ones; however they had strong relationship with the changes of the left atrial pressure. If the left atrial pressure was decreased the pulmonary artery pressure elevation was less, comparing with its values in experiments, where the left atrial pressure was increased; in the case of depressor shifts of pulmonary artery pressure, the left atrial pressure was also decreased. The character and values of the pulmonary blood flow changes were strongly correlated with the changes of the venous return; however they had no linear correlations with the right and left atrial pressures and pulmonary vascular resistance changes. Thus we concluded, that hemodynanics mechanisms of the pulmonary artery pressure and flow changes following vasoactive pressor drugs injection changes are different.
Asunto(s)
Velocidad del Flujo Sanguíneo/efectos de los fármacos , Pulmón/irrigación sanguínea , Arteria Pulmonar , Resistencia Vascular/efectos de los fármacos , Vasoconstrictores/farmacología , Animales , Presión Sanguínea/efectos de los fármacos , GatosRESUMEN
The character and values of changes of the pulmonary and systemic hemodynamics following neurogenic stimuli application on the cardiovascular system were studied in acute experiments on the anesthetized cats. Vagus nerve stimulation reduced the heart rate and decreased myocardial contractility in result, right and left atrial pressure increased, whereas pulmonary pressure and flow, venous return, cardiac output and venous return decreased. Pulmonary pressure reached maximal level and returned to the initial value earlier than the pulmonary flow. On the contrary, pulmonary pressure, following neurogenic pressor stimuli, reached maximal level and returned to the initial value later than the pulmonary flow; the sign of the changes of the pulmonary pressure could be positive or negative, whereas pulmonary flow were always increased. The venous return did not change, and for this reason it could not cause the increasing of pulmonary flow which was elevated following increasing of the heart rate and myocardial contractility. The shifts of the pulmonary pressure were correlated with the pulmonary resistance those, which were increased after the stellate ganglion stimulation and decreased following carotid reflex; they did not change in case of sciatic nerve stimulation. The shifts of the pulmonary pressure did not depended on the decreased right and left atrial pressures. When the pulmonary flow was always increased, the cardiac output following electrical stimulation of the stellate ganglion and sciatic nerve was elevated, and it was decreased following carotid reflex, i. e. linear correlation between these parameters were not found. Pulmonary and systemic arterial pressure changes were more obvious in case of direct neurogenic stimuli application comparing with reflectory ones; in both cases, the positive chrono- and inotropic cardiac effects were similar.
Asunto(s)
Velocidad del Flujo Sanguíneo , Gasto Cardíaco , Frecuencia Cardíaca , Pulmón/irrigación sanguínea , Contracción Miocárdica , Animales , Presión Sanguínea , Gatos , Estimulación Eléctrica , Nervio Ciático , Ganglio Estrellado , Nervio VagoRESUMEN
In acute experiments on anesthetized cats, intravenous injection of the pressor drugs (epinephrine and norepinephrine) and depressor drugs (acetylcholine, histamine, isadrin) caused different changes of right and left atrial pressures. Following catecholamine injection, right atrial pressure decreased in most cases, whereas left atrial pressure increased. In case of injection of the depressor drugs, right atrial pressure increased in most cases, and left atrial pressure decreased. Thus, changes of atrial pressures following intravenous injections of pressor and depressor drugs were reciprocal. The percent changes of the right atrial pressure in case of intravenous injections of pressor drugs were lesser than in the left atrial pressure. In case of intravenous injection of depressor drugs, if both right and left atrial pressures were decreased, then the percent changes of the right atrial pressure were more significant than in the left atrial pressure. If both right and left atrial pressure were increased their percent changes were equal. The increasing of inferior vena cava flow following catecholamine injection was less significant if atrial pressures were increased, whereas in case of depressor drugs injection superior vena cava flow was less significant if atrial pressures were increased. The character of changes of the right and left atrial pressures had no linear correlation with the directions of the shifts of the venous return and cardiac output.
Asunto(s)
Función del Atrio Izquierdo/fisiología , Función del Atrio Derecho/fisiología , Vasoconstrictores/administración & dosificación , Vasodilatadores/administración & dosificación , Presión Venosa/efectos de los fármacos , Animales , Determinación de la Presión Sanguínea , Gatos , Inyecciones Intravenosas , Volumen Sistólico/efectos de los fármacos , Vena Cava Inferior/fisiología , Presión Venosa/fisiologíaRESUMEN
In acute experiments on anesthetized cats, intravenous injection of epinephrine and norepinephrine caused different changes of right and left artrial pressures. These shifts mostly (82%) had similar directions: in these experiments, both right and left atrial pressures could be decreased (I group of animals) or increased (II group). The number of animals in these groups was equal. However, in 18% of the experiments, right atrial pressure was decreased, while left atrial pressure was increased. The changes of the left atrial pressure was, as a rule, more significant as compared with right atrial pressure shifts. In the I group of animals, systolic right atrial pressure was not changed, and systolic left atrial pressure was decreased. In the II group of animals, systolic pressure in both atria was augmented. Diastolic pressure was decreased in both atria in all the animals. When the atrial pressures were decreased, the increases of the superior and inferior vena cava flows, venous return and cardiac output were more significant as compared with animals in which the atrial pressures had been elevated. The changes of the superior and inferior vena cava flows were more obvious in animals following epinephrine injection as compared with animals in which norepinephrine was injected. The right atrial pressure returned to the initial level more rapidly than the left atrial pressure, and the time dynamics of the shifts of the right atrial pressure was similar to that of the superior vena cava flow. The temporal changes of the left atrial pressure were identical to the time changes of the cardiac output. We concluded that character of changes of the mean, systolic, and diastolic right and left atrial pressures following catecholamines injections was not correlated with the direction of venous return and cardiac output shifts, and was depending on intracardiac hemodynamics.
Asunto(s)
Función Atrial/efectos de los fármacos , Epinefrina/farmacología , Hemodinámica/efectos de los fármacos , Norepinefrina/farmacología , Animales , Presión Sanguínea/efectos de los fármacos , Gasto Cardíaco/fisiología , Gatos , Epinefrina/administración & dosificación , Atrios Cardíacos/efectos de los fármacos , Inyecciones Intravenosas , Norepinefrina/administración & dosificación , Vena Cava Inferior/fisiología , Vena Cava Superior/fisiologíaRESUMEN
In acute experiments on anesthetized cats, intravenous injection of the norepinephrine and angiotensin caused different changes of right atrial pressure in intact animals (decreasing--I group, of animals, and increasing--II group). After right and left vagus nerves had been cut, the right atrial pressure in the I group of animals decreased, but its changes were lesser than in intact animals due to slowing down of the increase of the right ventricular myocardial contractility and venous return. The latter was the result of severe diminution of the increase of the superior vena cava flow compared with the intact animals, meanwhile the value of the inferior vena cava flow did not change. In the II group animals after vagotomy and intravenous injection of the noripinephrine and angiotensin the sign of the right atrial pressure became negative, i. e. the direction of its shifts changed to the opposite, compared with intact animals. In this case, the changes of the sign of the right atrial pressure was caused by the removal of the reflectory inhibitory vagal influences on the heart, because the values of the right ventricular myocardial contractility and venous return were the same as in intact animals of the group, due to decreasing of the value of the superior vena cava flow and increasing of the shifts of the inferior vena cava flow. The vagotomy alone caused also different changes (decreasing or increasing) of right atrial pressure following increasing of the right ventricular myocardial contractility, meanwhile the changes of the venous return were insignificant. Direct electrical stimulation of both the right and the left vagus nerves caused the increasing of the right atrial pressure and decreasing of the right ventricular myocardial contractility and venous return. Thus we concluded, that different changes of the right atrial pressure in animals following intravenous injection of the pressor vasoactive drugs could be the result of different manifestations of the vagal afferent impulsation, which has influence on the sympathetic tonic discharges on the vessels of the regions of the superior and inferior vena cava, and the vagal reflectory inhibitory influences on the heart.
Asunto(s)
Angiotensinas/administración & dosificación , Norepinefrina/administración & dosificación , Nervio Vago/fisiología , Vasoconstrictores/administración & dosificación , Función Ventricular , Función Ventricular/fisiología , Animales , Función del Atrio Derecho/efectos de los fármacos , Función del Atrio Derecho/fisiología , Presión Sanguínea/efectos de los fármacos , Presión Sanguínea/fisiología , Gatos , Atrios Cardíacos/inervación , Ventrículos Cardíacos/inervación , Función Ventricular/efectos de los fármacosRESUMEN
Changes of the right atrial pressure, superior and inferior vena cava flows, right ventricular myocardial contractility (first derivate of right ventricular pressure, dP/dt max) following i.v. injection of acetylcholine, histamine and isoproterenol, were studied in acute experiments on anaesthetized mongrel cats with artificial lung ventilation and opened chest. The right atrial pressure in those cases could be increased (I group of animals) or decreased (II group). In maximal shifts of right atrial pressure following acetylcholine injection, the superior vena cava flow increased but the inferior vena cava flow decreased in equal proportion. When the right ventricular myocardial contractility decreased more than the right atrial pressure was augmented, and when the cardiac negative inotropic effect was weak, the right atrial pressure was reduced. After histamine injection in both groups of animals, right ventricular myocardial contractility was increased on the same level, and changes of the inferior vena cava flow were insignificant. The right atrial pressure was elevated following greater increase of superior vena cava flow. Isoproterenol caused the positive cardiac inotropic effect and augmenting of the superior vena cava flow in both groups of animals. The right atrial pressure was elevated if the inferior vena cava flow increased and, on the other hand, when the inferior vena cava flow decreased the right atrial pressure was reduced. Thus different maximal changes of the right atrial pressure following i.v. injection of acetylcholine, histamine and isoproterenol could be explained by different hemodynamic mechanisms of the interaction between superior and inferior vena cava flow shifts and changes of the right ventricular myocardial contractility.
Asunto(s)
Función del Atrio Derecho/efectos de los fármacos , Presión Sanguínea/efectos de los fármacos , Hemodinámica/efectos de los fármacos , Vasodilatadores/farmacología , Acetilcolina/farmacología , Animales , Función del Atrio Derecho/fisiología , Gatos , Hemodinámica/fisiología , Histamina/farmacología , Isoproterenol/farmacología , Contracción Miocárdica/efectos de los fármacosRESUMEN
Changes of the right atrial pressure and systemic haemodynamics following action of catecholamines (epinephrine and norepinephrine) were studied in acute experiments on anaesthetised mongrel cats with artificial lung ventilation and opened chest. Maximal changes of the right atrial pressure took place on the 12th-16th second following catecholamine administration. In that case, the atrial pressure could be decreased or increased. At the moment of maximal changes of the right atrial pressure, the venous return and the right ventricular myocardial contractility (the first derivative of the right atrial pressure, dP/dt max) increased more if the right atrial pressure decreased, as compared with the animals whose right atrial pressure augmented. The findings suggest that at the time of the maximal changes of the right atrial pressure following action of catecholamines, there may be a direct connection of the right atrial pressure with interrelation of venous return and the right ventricular contractility. The right atrial pressure, however, is a dependent parameter but it does not determine the venous return.