RESUMEN
Noninbred albino rat experiments have shown that artificial ventilation in experimental acute pulmonary hypertension (ligation of the ascending aorta alone or in combination with anonymous veins, compression of the aortic arch to the spine with a special clamp without opening the chest, intravenous administration of a toxic dose of epinephrine) is a resolving factor for the development of pulmonary edema.
Asunto(s)
Edema Pulmonar/terapia , Respiración Artificial , Animales , Femenino , Hemodinámica/fisiología , Masculino , Edema Pulmonar/fisiopatología , RatasRESUMEN
The occlusion of the rat aorta's thoracic portion induces within 30 min hemodynamic shifts in major and minor circulation typical for a hypertensive incident. The occurring 4-5-fold increase of the lung venous pressure leads to no regular lung oedema and is of no major importance for its pathogenesis.
Asunto(s)
Enfermedades de la Aorta/fisiopatología , Agua Pulmonar Extravascular/fisiología , Hemodinámica/fisiología , Circulación Pulmonar/fisiología , Animales , Aorta Torácica , Presión Venosa Central/fisiología , Femenino , Ligadura , Masculino , Edema Pulmonar/etiología , Edema Pulmonar/fisiopatología , Venas Pulmonares/fisiología , Presión Esfenoidal Pulmonar/fisiología , Ratas , Ratas Endogámicas WKY , Factores de TiempoRESUMEN
Left ventricle (LV) function and systemic hemodynamic changes after coronary artery embolization by 15 microns radioactive microspheres were studied in anesthetized rats. Selective coronary embolization was produced by microsphere injection during ascending aorta occlusion in closed chest animal by using "L"-shaped wire. Maximal pressure (Pmax) developed was evaluated during ascending aorta occlusion. Coronary embolization evoked dose-dependent reduction in Pmax and dP/dtmax and then decrease in basal LV systolic pressure. dP/dt/P, with parallel increase in end diastolic LV pressure. Changes of cardiac output were bidirectional: after administration of relatively small amount of microspheres cardiac output increased. This method can be used for producing quantitative myocardial ischemia and we suggest that it may be a suitable model of the chronic heart failure.