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OBJECTIVE: To evaluate if the extent of normal microflora disturbances differed between treatment with amoxycillin-clavulanate administered in an active form and cefuroxime axetil administered as an inactive prodrug. METHODS: Twenty-eight children, 0.5-5 years old, diagnosed with acute otitis media (AOM), were treated with either amoxycillin-clavulanate (13.3 mg/kg 3 times daily) or cefuroxime axetil (15 mg/kg twice daily) for 7 days. Saliva samples and nasopharyngeal swabs were collected before, directly after and 2 weeks after treatment. The saliva samples were quantitatively and qualitatively analyzed and the nasopharyngeal swabs were qualitatively analyzed. All isolated strains were tested for beta-lactamase production. RESULTS: Both treatment regimens gave rise to similar alterations of the normal oropharyngeal microflora. In both groups, the amount of Streptococcus salivarius was significantly reduced (P < 0.05). The most common causative pathogens of acute otitis were S. pneumoniae, Haemophilus influenzae and Moraxella catarrhalis. On the day of enrollment, approximately half of the patients, in both groups, were infected with more than one pathogen. The rate of infection or colonization with more than one potential pathogen was low on day 7 but recurred 2 weeks after treatment to similar levels as on day 0. The total number of patients with reinfection, recolonization or recurrence of pathogens on day 21 was 11/12 in the amoxycillin-clavulanate group and 4/7 in the cefuroxime axetil group. The most common beta-lactamase producer was M. catarrhalis. CONCLUSION: The local high concentration of antibiotics in the oropharynx immediately after intake of antibiotic suspensions seem to have little or no impact on the extent of disturbance of the microflora in this region. Children of this age group seem prone to either reinfection, recolonization or persistence of pathogens within 2 weeks after treatment. Furthermore, co-infection with more than one pathogen seems common in children with AOM and infection with beta-lactamase producing microorganisms occurs frequently.

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The utero-placental blood flow was investigated in anaesthetized normotensive pregnant rabbits after repeated administration of a high dose of the antihypertensive calcium antagonist felodipine and in untreated controls. By means of the microsphere technique blood flow was also determined in the lungs, skin, intestine, skeletal muscle and kidneys during chloralose anaesthesia. Felodipine reduced mean arterial blood pressure, which was associated with a marked reduction in vascular resistance in the skeletal muscle vascular bed, where blood flow was increased seven-fold. In contrast, blood flow to placentae and kidneys were reduced. The pronounced reduction in placental blood flow may limit foetal nutrition and hence explain reported foetal digital defects after administration of high doses of felodipine to pregnant normotensive rabbits.

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The changes in peripheral haemodynamics and regional resistances were studied during the rapid fall in mean arterial pressure (MAP) after surgical reversal of two-kidney, one clip renal hypertension in rats (RHR). The controls used were sham-declipped RHR and normotensive control rats (NCR). During the 2 h following renal artery declipping or sham-operation, MAP and heart rate (HR) were followed continuously. Finally, the regional blood flows in the kidneys, small intestine and skeletal muscle were determined by the microsphere technique. Declipping caused MAP to fall from 167 +/- 5 to 108 +/- 5 mmHg (n = 10) with a concomitant fall in HR from 424 +/- 11 to 363 +/- 14 beats/min (P less than 0.01). The calculated vascular resistances fell in the intestinal and declipped renal vascular beds by 50-60% compared with sham-operated rats (P less than 0.01). However, vascular resistances remained unchanged in skeletal muscle and in the untouched kidney. This indicates that the reduction in flow resistance varies in the different vascular beds, presumably reflecting a mixture of suppressed sympathetic activity and direct vasodilatory actions induced by mechanisms activated upon reversal of two-kidney, one clip renal hypertension by renal artery declipping.

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It is generally accepted that hypertensive cardiovascular complications can be prevented by treatment. However, during pregnancy, antihypertensive drugs might be hazardous in view of their influence on the fetus. Nevertheless, in spite of the diverging published results, even beta-blockers have been used in the pregnant patient. As our basic knowledge concerning the circulatory and fetal effects is minimal, we decided to elucidate the influence of the non-selective beta-blocker, propranolol, on the haemodynamic circumstances in hypertensive pregnant rats. Renal hypertension was induced by clamping both renal arteries 4 weeks before pregnancy. Shortly before term, cardiac output was determined with the dye-dilution technique and utero-placental blood flow was determined with the microsphere technique, both before and after propranolol injection. Mean arterial pressure and heart rate were registered continuously. The acute propranolol injection reduced mean arterial pressure by 26%. This was due mainly to a 32% decrease in cardiac output, which in turn was due to a 24% decrease in stroke volume and a 6% decrease in heart rate. Both myometrial and placental blood flow decreased significantly, by 45 and 50%, respectively. It was furthermore of interest to observe the significant increase in blood flow resistance in both myometrium and placenta. In conclusion, it can be stated that the non-selective beta-blocker propranolol, which lacks intrinsic stimulating activity, reduces mean arterial pressure mainly by a cardiac output decrease. The present results further indicate that the influence on peripheral blood flow might be caused by cardiac output changes as well as by direct effects on the uteroplacental vascular bed.

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Clinical as well as experimental studies have demonstrated a 70% reduction in utero-placental blood flow in pregnancies affected by severe hypertension (13, 19). In pregnant renal hypertensive rats, propranolol administration causes a further 50% reduction in utero-placental blood flow (16). The present study on renal hypertensive rats was performed in order to explore the acute effects on central haemodynamics and utero-placental blood flow of the non-selective beta-blocker pindolol, which also has an intrinsic beta-stimulatory effect. Renal hypertension was induced by partial clamping of both renal arteries in female Wistar rats 4 weeks before pregnancy. Some 2-4 days before expected parturition, cardiac output was determined with the dye-dilution technique and blood flow to the reproductive organs with the microsphere technique, both before and after acute pindolol administration. Mean arterial pressure and heart rate were recorded continuously during the experiment. After pindolol injection, mean arterial pressure fell by 22% due to a 38% reduction in total peripheral resistance. No significant changes in cardiac output, stroke volume or heart rate were found. Placental blood flow was significantly reduced, by 30%, whereas myometrial and ovarian blood flows were reduced by only 18 and 9%, respectively. Thus, the reduction in blood supply to the reproductive organs in renal hypertensive rats after acute pindolol administration was most pronounced in the placenta. This reduction in placental flow was, however, only about half as pronounced as after propranolol, which lacks intrinsic beta-stimulatory effects. This may suggest that vasodilating beta-receptors may play an important role in the maternal placental vascular bed.

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The aim of the present study on pregnant renal hypertensive rats was to investigate the effects on central hemodynamics and uteroplacental blood flow after chronic administration of pindolol, a nonspecific beta-adrenergic receptor blocking agent with intrinsic beta-stimulatory effect. Renal hypertension was induced by partial clamping of both renal arteries four weeks before pregnancy. Pindolol was administered with the food during the entire pregnancy period. Two to four days before expected delivery mean arterial pressure, heart rate, cardiac output, (dye-dilution technique) and utero-placental blood supply (microsphere technique) were determined. The chronic pindolol treatment reduced heart rate by 25 per cent while both mean arterial pressure and cardiac output remained unchanged. However, blood flow to uterus and placentae was reduced by 43 and 64 per cent, respectively, after pindolol treatment. Clinical as well as experimental studies (15, 16) demonstrate a reduced utero-placental blood supply when pregnancies are complicated by hypertension. As pregnancies with severe hypertension are associated with an increased frequency of intrauterine growth retardation and intrauterine asphyxia the present results indicate that the combination of hypertension and long-term treatment with beta-blockers might reduce utero-placental blood flow enough as to seriously interfere with fetal oxygen supply thereby increasing the risk of intra- and extra-uterine asphyxia.

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The main purpose of this study on rats was to examine the effect of pregnancy on experimental renal hypertension and cardiac size. Renal hypertension in the rats (RHR) was induced by standardized clamping of the left renal artery early in pregnancy (SRHR) or 4 weeks before mating (ERHR). As controls served non-pregnant RHR with the duration of hypertension matched to each above mentioned group, as well as non-pregnant and pregnant normotensive rats. Only 16% of the rats with renal artery clamping early in pregnancy (SRHR) developed hypertension in contrast to 41% of similarly operated non-pregnant rats and 56% of ERHR decreased their blood pressure to normal levels during pregnancy. Concerning left ventricular heart weight there was a slight increase in left ventricular weight during normal pregnancy in spite of a significantly reduced blood pressure. In both SRHR and ERHR an increased left ventricular heart weight was noticed during pregnancy even when arterial pressure was not increased. The present results suggest an antihypertensive effect of pregnancy and the existence of "trophic" influences and/or a volume induced adaptation of the heart causing an increased myocardial mass which is associated with pregnancy and partly independent of blood pressure influences.

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Impedance cardiography was used to study cardiodynamic changes throughout normal pregnancy. Stroke volume, heart rate and cardiac output were determined in fourteen normal primigravidae from early pregnancy until 6-25 weeks after delivery. To elucidate the influence of the patient's position on cardiac output, measurements were made in the supine as well as in the left and right lateral positions. Stroke volume and cardiac output increased up to the 28th week of pregnancy and then decreased during late pregnancy. These changes seemed to be independent of the patient's position. After delivery a further reduction in cardiac output due to a significant decrease in heart rate was found. No significant differences in cardiac output were found between right and left lateral position. However, during pregnancy as well as after delivery, cardiac output measured by impedance cardiography was significantly higher in the supine position than in the lateral positions. Thus, the impedance method does not seem to be reliable in measuring absolute values of stroke volume and cardiac output but may be used for relative measurements during pregnancy.

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An experimental study on pregnant rats was undertaken to explore whether renal hypertension interferes with uteroplacental blood supply and fetal weight. Renal hypertension was induced by standardized clamping of the left renal artery. Two days before expected delivery, blood flow to the reproductive organs was determined by microsphere technique in normal control rats, rats with short-standing renal hypertension induced early in pregnancy, and rats with established renal hypertension induced 4 weeks before pregnancy. Myometrial and placental blood supply was considerably reduced in renal hypertensive rats compared to that in normotensive pregnant rats, with the reduction in placental blood flow being as much as 68% in rats with established renal hypertension. Nevertheless, there was no reduction in fetal weights, placental weights, or number of fetuses in the litters. These findings suggest that the nutritional blood supply of the placenta normally has a considerable overcapacity, perhaps a necessary safety margin so that the fetus can manage the circulatory demands associated with delivery. If hypertension causes intrauterine growth retardation only by means of reduced placental blood flow, this reduction in flow obviously must be considerable.

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Central hemodynamics during late pregnancy were studied in normotensive rats and in rats with short-standing and "established" renal hypertension. In normal pregnancy cardiac output was increased 33%, due to increased stroke volume while mean arterial pressure and systemic resistance were reduced 17 and 40% respectively. The same changes, though less pronounced were noted during pregnancy in rats with short-standing renal hypertension, where cardiac output was increased 31%, due to equal increases in heart rate and stroke volume while systemic resistance was reduced only 27%. By contrast, no significant cardiac output increase, nor any resistance reduction was noted during pregnancy in rats with established hypertension. Thus, renal hypertension in rats seems to interfere with circulation during pregnancy mainly by restricting both the cardiac output increase and the systemic resistance reduction seen during normal pregnancy. This restriction seems to be more pronounced the longer the duration of hypertension.

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Total hand blood flow was measured by venous occlusion plethysmography in 14 healthy primigravid women. Consecutive measurements were made from the 15th week of pregnancy until term and after delivery. During pregnancy the mean hand blood flow, measured under standard resting conditions with the subjects supine, increased progressively from 7.7 in early pregnancy to 28.9 ml/100 ml/min at term. Simultaneously the peripheral vascular resistance decreased from 19.3 to 3.3 PRU100. When examined at 6--16 weeks after delivery hand blood flow and peripheral resistance were not yet returned to normal.

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1. Cardiac output, heart rate and mean arterial pressure were determined in two-kidney Goldblatt hypertensive rats of 4 weeks' duration, in matched normotensive controls and in declipped renal hypertensive rats 2 h-28 days after renal artery declipping. 2. After declipping mean pressure fell rapidly due to a corresponding reduction in total peripheral resistance, this being normalized after 1 day. Cardiac output and heart rate remained initially unchanged, but 1 day after declipping the former was significantly increased compared with output in renal hypertensive rats. 3. The initial normalization of total peripheral resistance must be ascribed to a subnormal vascular smooth muscle tone. The reason is that the hypertensive structural vascular changes are not yet significantly reduced and their presence implies an elevated flow resistance, even when vascular smooth muscle activity equals that in normotension. 4. This considerable 'overshoot' in vascular relaxation and lack of reflexogenic tachycardia, despite resetting of baroreceptors, suggest that peripheral as well as central mechanisms contribute to the rapid normalization of mean arterial pressure in two-kidney Goldblatt hypertension in rats, later stabilized by reversal of structural vascular changes.

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1. After 4.5 months of renal hypertension in rats renal artery 'declipping' was performed. Eight weeks afterwards paired hindquarter perfusions were performed on the declipped rats and normotensive control rats, exploring the relationships between mean arterial pressure and flow, from maximal vasodilatation to maximal vasoconstriction, induced by graded noradrenaline infusions. Left ventricular weights were measured. 2. Declipping caused a fall in mean arterial pressure from 180 to 135 mmHg, though still after 8 weeks the mean pressure was 19% higher than in normotensive control rats. 3. All parameters reflecting design and reactivity of the resistance vessels and left ventricular weight decreased significantly, but not as much as mean arterial pressure, and were still significantly increased compared with those of control rats. 4. This neither mean arterial pressure nor cardiovascular design was normalized 8 weeks after 'reversal' of long-standing renal hypertension, in contrast to short-standing renal hypertension where both are completely normalized 3 weeks after declipping.

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1. Mean arterial pressure, heart rate, cardiac output (dye-dilution technique), stroke volume, total peripheral resistance (TPR), utero-placental blood supply (microsphere technique) and foetal weights were determined 2 days before expected birth in normotensive control (NC) rats, spontaneously hypertensive (SH) rats, rats with short-standing renal hypertension induced early in pregnancy and rats with established renal hypertension induced 4 weeks before pregnancy. Non-pregnant rats in comparable states served as controls. 2. In normal pregnancy cardiac output increased by 33% and blood pressure and TPR decreased by 17 and 38% respectively. The same principal changes were noted in SH rats and those with short-standing renal hypertension, but no changes were found in rats with established renal hypertension during pregnancy. 3. Myometrial and placental blood supply was lower in all hypertensive groups compared with NC rats, the reduction being 46 and 36% in SH rats and in rats with established renal hypertension as much as 74 and 68% respectively. 4. In SH rats foetal weights were reduced compared with NC rats, but despite the 68% reduction of placental blood flow in rats with established renal hypertension foetal weights were here unchanged.

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The development of an increased ventricular wall mass was followed from birth until five weeks of age and also later in life in spontaneously hypertensive rats (SHR) which were compared with normotensive control rats (NCR). It was shown that the first signs of enhanced ventricular growth were already evident in SHR in the first week of life. At 10 months of age left ventricular weight was 68% higher in SHR than in matched NCR, at a mean pressure difference of 30%. Treatment of SHR with antihypertensive agents, like hydralazine, hydralazine-guanethidine, propranolol, or metoprolol, from three weeks up to 10 months of age reduced this gross increase in left ventricular weight by only about 10% while the mean pressure difference between SHR and NCR was reduced by 50 to 70%. It appears that the increase in left ventricular wall mass in SHR is initiated so early in life and is of such a character that it can only, to a fairly minor extent, be reversed or prevented by pressure-lowering procedures. Part of the explanation may be a substantial contribution of myocardial hyperplasia, in association with a genetically linked predisposal to structural cardiovascular adaptation, either 'inherent' in the effectors and/or caused by 'trophic' influences of a hormonal and/or transmitter nature.

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1. Cardiac output at rest, intra-arterial blood pressure and hand blood flow at maximal vasodilatation were studied in two groups of 18-25 year-old men: forty-four with mild blood pressure elevation were referred from a military enlistment centre, and twenty-nine normotensive volunteers were mainly recruited from the same enlistment centre. 2. The study group was characterized by a significantly higher cardiac index at rest, and a significantly higher blood flow resistance in the hand at maximal vasodilatation than the control group, indicating the presence of structural modifications in the resistance vessels of patients with mild blood pressure elevation. 3. The tendency to increased vascular resistance in the blood vessels of the hand at maximal vasodilatation was more pronounced in patients with a normal cardiac index than in those with a high index. This suggests inclusion in the study group of tense, anxious individuals with an elevated cardiac index but otherwise normal circulation, but does not exclude the possibility that these patients may develop structural changes later on.

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The cardiac output at rest, and the intra-arterial blood pressure and hand blood flow at maximal vasodilation were determined in two groups of men aged 18-22 years. 44 patients were referred from a military enlistment centre because of mild blood pressure elevation, and 29 normotensive volunteers were mainly recruited from the same enlistment centre. In addition, in a majority of subjects in both groups the auscultatory blood pressure of both parents was determined. The patients were characterized by a significantly higher cardiac index at rest, and a significantly higher vascular resistance in the hand blood vessels at maximal vasodilation than the controls, indicating the presence of structural alterations in the resistance vessels of these subjects with only very mild blood pressure elevation. The tendency to increased vascular resistance in the hand blood vessels at maximal vasodilation was more prominent in patients with a normal cardiac index than in those with a high index. This suggests inclusion in the patient group of tense, anxious individuals with an elevated cardiac index but otherwise normal circulation, but does not exclude the possibility that these patients may develop structural vascular changes later on. The parents' blood pressure was higher in the group of patients, both for patients with a normal and those with a high cardiac index, compared to the parents of the controls.

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After complete cardiovascular denervation mean arterial pressure (MAP) falls to almost equally low levels in spontaneously hypertensive rats (SHR) and normotensive control rats (NCR). This has earlier been suggested to indicate a dominance of neurogenic mechanisms in established SHR hypertension. -- In the present study, total peripheral resistance (TPR) remains, however, some 35 per cent higher in adult SHR than in NCR after pithing while cardiac output (CO), and stroke volume, is 35 per cent lower in SHR. These opposite differences in TPR and CO after denervation, resulting in equal MAP levels in SHR and NCR, seem rather to be a consequence of the rapidly established structural adaptation that affects all SHR high-pressure cardiovascular sections. Thus, the SHR precapillary resistance vessels display thickened walls and luminal narrowing, which keeps TPR higher than in NCR even during maximal vasodilatation. Due to hypertrophy, the SHR left ventricle exhibits a reduced myocardial stretch for a given filling pressure and stroke volume is consequently reduced more than in NCR after complete denervation. -- Paradoxically, therefore, rather than reflecting any dominance of neurogenic mechanisms in established SHR hypertension the MAP equalization in SHR and NCR after cardiovascular denervation emphasizes the hemodynamic importance of cardiovascular structural changes present in hypertension.

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