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One of the hypotheses put forward concerning the mechanism of vasovagal syncope is that the vagal afferent fibres are activated during vigorous contractions against a partly empty left ventricle. The aim of the study was to confirm this hypothesis by using 2D echocardiography during a head-up tilt test. The study was carried out on 39 patients (17 male, 22 female, age range 21–64 years), all with a history of recurrent syncope. The patients were examined using a 2D echo to measure the end-diastolic and end-systolic volume before the head-up tilt test after the Westminster protocol (45min/60 grade) and every five minutes after tilting. T patients during head-up tilt test had a positive response and 32 proved negative. A reduction of both the end-diastolic and end-systolic volumes of the left ventricle was noticed. There was no significant difference in the degree of ejection fraction reduction. The difference in ejection fraction reduction between the two groups was similarly non-significant. It was also noticed that the patients with a positive response had more vigorous contractions than those with a negative test. The decision was therefore taken to use a different parameter for the left ventricle contraction, namely the LV posterior wall slope. As this parameter is partly dependent on time, its use in confirming the extremely vigorous nature of the contractions was considered appropriate. Only 6 patients were tested using this parameter. A tendency towards greater left ventricle posterior wall slope values, both before and during tilting was noticed in the group of patients with vasovagal reaction. Our data shows that vigorous contraction is probably less responsible for vasovagal syncope release than left ventricle volume reduction.
The myocardial infarct causes prolonged activation of the renin-angiotensin system and profoundly influences cardiac performance and renal excretory capabilities. The aim of the present study was to determine whether the myocardial infarct is also associated with an altered expression of AT1a receptors (AT1aR) mRNA in the heart and the kidney. To this end male Sprague-Dawley rats were subjected either to the left coronary artery ligation or to the sham surgery. Four weeks after the surgery the animals were sacrificed. In 11 infarcted and 10 sham-operated rats expression of AT1aR mRNA in the walls of the left and right ventricle of the heart, and in the renal cortex and renal medulla was determined by semiquantitative PCR method. In another group of 10 infarcted and 14 sham-operated rats the diameter of cardiomyocytes in the left and right cardiac ventricle was determined. The size of the infarct in the rats used for mRNA determination and for morphometric measurements was equal to 29.4 ± 1.8% and to 31.0 ± 1.2 % of the left ventricular wall, respectively. Expression of AT1aR mRNA was significantly greater in the left (P< 0.01) and right ventricle (P<0.03) of the heart in the infarcted than in the sham operated rats. AT1aR mRNA expression was also significantly greater (P<0.02) in the renal medulla of the infarcted rats than in the renal medulla of the sham operated rats whereas no significant difference was found in the renal cortex. The myocardial infarct was associated with a significant increase of diameter of cardiomyocytes of the left ventricle of the heart (P < 0.0001), however there was no significant correlation between changes in AT1aR mRNA expression and diameter of cardiomyocytes. The results provide evidence that the myocardial infarct results in significant and prolonged upregulation of AT1a receptors mRNA expression in the heart and in the medullary region of the kidney.
Chronic isoproterenol administration produces a rapid, highly reproducible rodent model of cardiac hypertrophy. Yet, despite widespread use of this model, the effects of isoproterenol on in vivo cardiac function and substrate metabolism are unknown. Isoproterenol (5 mg.kg-1.day-1) was infused for 7 days in male Wistar rats (n = 22). In vivo magnetic resonance imaging (MRI) showed that left ventricular mass increased by 37% and end-diastolic and systolic volumes increased by 33% and 73%, respectively, following isoproterenol infusion. Cardiac function at the base of the left ventricle was normal, but apical ejection fraction decreased from 90% to 31% and apical free wall thickening decreased by 94%, accompanied by increased fibrosis and inflammation. Myocardial palmitate oxidation rates were 25% lower, and citrate synthase and medium chain acyl-coenzyme A dehydrogenase activities were reduced by 25% and 29%, respectively, following isoproterenol infusion. Fatty acid transporter protein levels were 11-52% lower and triglyceride concentrations were 55% lower in isoproterenol-infused rat hearts. Basal glycolysis and glycogen concentration were not changed, yet insulin stimulated glycolysis was decreased by 32%, accompanied by 33% lower insulin stimulated glucose transporter, GLUT4, protein levels in rat hearts following isoproterenol infusion, compared with controls. In conclusion, isoproterenol infusion impaired in vivo cardiac function, induced hypertrophy, and decreased both fatty acid and glucose metabolism, changes similar in direction and magnitude to those found in the rat heart following moderate severity myocardial infarction.
Micro-anatomical changes in the aorta, pulmonary trunk, and left ventricle of Wistar rats were studied after the administration of streptozotocin. Twenty adult Rattus norvegicus were randomly assigned into two groups (control and diabetic) of ten rats each. Diabetes mellitus was experimentally induced in the diabetic group of rats by daily intra-peritoneal administration of multiple doses of 40 mg/kg streptozotocin dissolved in 0.1 M sodium citrate buffer for five consecutive days. The control group was given the equivalent volume of citrate buffer. The animals were monitored for four weeks after streptozotocin administration. Post sacrifice, the left ventricle, aorta, and pulmonary trunk were excised, weighed, and fixed by immersion in 10% formol saline. The tissues were processed for paraffin embedding, and sections of 6 µm thickness were produced and stained with H & E for general histological observations, and Verhoeff-van Gieson elastic fibre stain to demonstrate elastic fibres in these cardiovascular structures. The data obtained were analyzed with descriptive and inferential statistics. Histopathological and morphometric examinations of the stained sections showed a significant increase in the thickness of the tunica intima of aorta (t = –7.49; df = 9; p < 0.05) and pulmonary trunk (t = –10.81; df = 9; p < 0.05) in diabetic rats (14.59 ± 1.189 μm and 11.307 ± 0.863 mm, respectively) when compared to that of the control group (3.62 ± 0.353 μm and 3.22 ± 0.244 μm, respectively). In addition, the distribution of elastic and collagen fibres was sparse in the hearts of the diabetic group when compared to that of the control group. The findings of this study demonstrated that diabetes mellitus might cause some alterations in the microanatomy of cardiovascular structures. (Folia Morphol 2009; 68, 4: 207–214)
Several studies have reported an extensive regional heterogeneity in myocardial blood flow. The reported coefficients of variation for regional myocardial perfusion range from about 0.2 to 0.4 in normotensive animals. The spatial distribution of myocardial perfusion during haemorrhagic hypotension seems not to have been assessed. The goal of the present study was to determine the regional heterogeneity in myocardial blood flow within the rabbit left ventricle during normal conditions and after haemorrhagic hypotension. Radioactive microspheres were infused into the left ventricle in barbiturate anaethetized rabbits over either 30 or 120 sec. The haemorrhagic hypotension was induced by bleeding, so that mean arterial blood pressure was reduced to about 50% of control. The left ventricles were divided into samples of about 0.025 g each. Regional heterogeneity in the blood flow was expressed as the coefficient of variation corrected for the Poisspn distribution of microspheres (CVc). The CVc was 0.37 ±0.09 (mean±SD) during control and 0.41+0.11 after bleeding, the CVc obtained after bleeding being somewhat higher than during control (P<0.05). We obtained a high correlation coefficient (τ about 0.68) between regional perfusion values at control and after bleeding which indicates a stable perfusion pattern within the myocardium. We conclude that the regional distribution of coronary blood flow within the left ventricle is markedly heterogenous during control condition and that this pattern is not changed during haemorrhagic hypotension.
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