Phasic right coronary artery blood flow in conscious dogs with normal and elevated right ventricular pressures.
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We studied phasic right coronary blood flow in well trained normal dogs and dogs with pulmonic stenosis. We installed electromagnetic flow transducers and pressure tubes under anesthesia to monitor right coronary blood flow, cardiac output, central aortic blood pressure, and right ventribular pressure. In normotensive dogs, systolic flow amplitude equaled early diastolic flow levels. The ratio of systolic to diastolic flow at rest was substantially greater in the right coronary bed (36+/-1.3%) than in the left circumflex bed (13+/-3.6%). Right diastolid flow runoff, including the cove late in diastole, resembled left circumflex runoff. Blood flow to the normotensive right (37+/-1.1 ml/min 100(-1) g) and the left (35+/-1.0 ml/min(-1) g) ventricular myocardium indicated equal perfusion of both cardiac walls. Throttling of systolic flow was related directly to the right ventricular systolic pressure level in the dogs with pulmonic stenosis. Retrograde systolic flow occurred in severe right ventricular hypertension. The late diastolic runoff pattern in dogs with pulmonic stenosis appeared the same as for the normotensive dogs. We obtained systolic to diastolic flow ratios of 1/3 the value of normotensive hearts in high and severe pulmonic hypertension. Electrocardiograms and studies of pathology suggested restricted blood flow to the inner layers of the right myocardium in the dogs with severe and high right ventricular hypertension. Normotensive and hypertensive peak hyperemic flow responses were similar, except for an increased magnitude of diastolic flow, with proportionately less systolic flow in hypertensive states. (+info)
Quantification of baroreceptor influence on arterial pressure changes seen in primary angiotension-induced hypertension in dogs.
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We studied the role of the sino-aortic baroreceptors in the gradual development of hypertension induced by prolonged administration of small amounts of angiotensin II (A II) in intact dogs and dogs with denervated sino-aortic baroreceptors. Short-term 1-hour infusions of A II(1.0-100 ng/kg per min) showed that conscious denervated dogs had twice the pressor sensitivity of intact dogs. Long-term infusions of A II at 5.0 ng/kg per min (2-3 weeks) with continuous 24-hour recordings of arterial pressure showed that intact dogs required 28 hours to reach the same level of pressure attained by denervated dogs during the 1st hour of infusion. At the 28th hour the pressure in both groups was 70% of the maximum value attained by the 7th day of infusion. Both intact and denervated dogs reached nearly the same plateau level of pressure, the magnitude being directly related both the the A II infusion rate and the daily sodium intake. Cardiac output in intact dogs initially decreased after the onset of A II infusion, but by the 5th day of infusion it was 38% above control, whereas blood volume was unchanged. Heart rate returned to normal after a reduction during the 1st day of infusion in intact dogs. Plasma renin activity could not be detected after 24 hours of A II infusion in either intact or denervated dogs. The data indicate that about 35% of the hypertensive effect of A II results from its acute pressor action, and an additional 35% of the gradual increase in arterial pressure is in large measure a result of baroreceptor resetting. We conclude that the final 30% increase in pressure seems to result from increased cardiac output, the cause of which may be decreased vascular compliance. since the blood volume remains unaltered. (+info)
Site of myocardial infarction. A determinant of the cardiovascular changes induced in the cat by coronary occlusion.
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The influence of site of acute myocardial infarction on heart rate, blood pressure, cardiac output, total peripheral resistance (TPR), cardiac rhythm, and mortality was determined in 58 anesthetized cats by occlusion of either the left anterior descending (LAD), left circumflex or right coronary artery. LAD occlusion resulted in immediate decrease in cardiac output, heart rate, and blood pressure, an increase in TPR, and cardiac rhythm changes including premature ventricular beats, ventricular tachycardia, and occasionally ventricular fibrillation. The decrease in cardiac output and increase in TPR persisted in the cats surviving a ventricular arrhythmia. In contrast, right coronary occlusion resulted in a considerably smaller decrease in cardiac output. TPR did not increase, atrioventricular condition disturbances were common, and sinus bradycardia and hypotension persisted in the cats recovering from an arrhythmia. Left circumflex ligation resulted in cardiovascular changes intermediate between those produced by occlusion of the LAD or the right coronary artery. Mortality was similar in each of the three groups. We studied the coronary artery anatomy in 12 cats. In 10, the blood supply to the sinus node was from the right coronary artery and in 2, from the left circumflex coronary artery. The atrioventricular node artery arose from the right in 9 cats, and from the left circumflex in 3. The right coronary artery was dominant in 9 cats and the left in 3. In conclusion, the site of experimental coronary occlusion in cats is a major determinant of the hemodynamic and cardiac rhythm changes occurring after acute myocardial infarction. The cardiovascular responses evoked by ligation are related in part to the anatomical distribution of the occluded artery. (+info)
Effect of portal-systemic anastomosis on renal haemodynamics in cirrhosis.
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In 12 patients with portal hypertension and repeated bleedings from oesophageal varices the central haemodynamics, portal pressure, and mean renal blood flow (RBF) were investigated immediately before and two to seven months after portal-systemic shunt. Cardiac output increased significantly, whereas arterial pressure was unchanged after operation. RBF, which was initially less than in controls, did not change. As portal pressure decreased significantly, a direct portal-renal, neural, or humoral reflex mechanism does not explain the subnormal RBF in cirrhosis. As plasma volume was large and unchanged after operation a "diminished circulating plasma volume" is an unlikely explanation. Therefore, on the basis of the present observations, previously postulated causes of renal hypoperfusion in cirrhosis need revision. (+info)
The respiratory responses of Carcinus maenas to declining oxygen tension.
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The degree of respiratory independence shown by Carcinus under conditions of declining oxygen tension is dependent on the animal's level of activity. Inactive Carcinus are capable of maintaining respiratory independence down to a Po2 of 60-80 mmHg. This is achieved primarily by an increase in ventilation volume such that the amount of oxygen made available at the respiratory surfaces remains constant over a wide range of oxygen tension. The Po2 at which this can no longer be maintained corresponds closely to the Po2 at which respiratory independence is lost. Under normoxic conditions the Po2 of the post- and prebranchial blood was 97 and 18 mmHg respectively. At the high oxygen tensions prevailing in the postbranchial blood the respiratory pigment is fully saturated. Under conditions of declining oxygen tension the heart rate remains more or less constant until the Po2 reaches 60-80 mmHg, the onset of bradycardia coinciding with the loss of saturation of the haemocyanin. Although cardiac output falls during hypoxia, the capacity rate ratio remains approximately constant, which enables the effectiveness of oxygen uptake by the blood to remain at a high level. (+info)
Reversal of severe pulmonary hypertension with beta blockade in a patient with end stage left ventricular failure.
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A 52 year old man with severe chronic left ventricular failure (New York Heart Association class IV) was considered unsuitable for cardiac transplantation because of high and irreversible pulmonary vascular resistance (PVR). In an attempt to produce symptomatic improvement, metoprolol was cautiously introduced, initially at 6.25 mg twice daily. This was slowly increased to 50 mg twice daily over a two month period and continued thereafter. After four months of treatment the patient's symptoms had improved dramatically. His exercise tolerance had increased and diuretic requirements reduced to frusemide 160 mg/day only. Assessment of right heart pressures was repeated and, other than a drop in resting heart rate, there was little change in his pulmonary artery pressure or PVR. His right heart pressures were reassessed showing a pronounced reduction in pulmonary artery pressure and a significant reduction in PVR, which fell further with inhaled oxygen and sublingual nitrates. He was then accepted onto the active waiting list for cardiac transplantation. A possible mechanism of action was investigated by assessing responses to beta agonists during treatment. Not only was there pronounced improvement in PVR but it was also demonstrated that beta receptor subtype cross-regulation may have contributed to the mechanism of benefit. (+info)
Validation of haemodialysis recirculation and access blood flow measured by thermodilution.
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BACKGROUND: Recirculation (R) and access blood flow (Qac) measurements are considered useful indicators of adequate delivery of haemodialysis. It was the purpose of this study to compare measurements of R and Qac obtained by two different techniques which are based on the same principle of indicator dilution, but which differ because of the characteristics of the injection and detection of the different indicators used. METHODS: Recirculation measured by a thermal dilution technique using temperature sensors (BTM, Fresenius Medical Care) was compared with recirculation measured by a validated saline dilution technique using ultrasonic transducers placed on arterial and venous segments of the extracorporeal circulation (HDM, Transonic Systems, Inc.). Calculated access flows were compared by Bland Altman analysis. Data are given as mean +/- SD. RESULTS: A total of 104 measurements obtained in 52 treatments (17 patients, 18 accesses) were compared. Recirculation measured with correct placement of blood lines and corrected for the effect of cardiopulmonary recirculation using the 'double recirculation technique' was -0.02 +/- 0.14% by the BTM technique and not different from the 0% measured by the HDM technique. Recirculation measured with reversed placement of blood lines and corrected for the effect of cardiopulmonary recirculation was 19.66 +/- 10.77% measured by the BTM technique compared with 20.87 +/- 11.64% measured by the HDM technique. The difference between techniques was small (-1.21 +/- 2.44%) albeit significant. Access flow calculated from BTM recirculation was 1328 +/- 627 ml/min compared with 1390 +/- 657 ml/min calculated by the HDM technique. There was no bias between techniques. CONCLUSION: BTM thermodilution yields results which are consistent with the HDM ultrasound dilution technique with regard to both recirculation and access flow measurement. (+info)
Factors mediating the hemodynamic effects of tumor necrosis factor-alpha in portal hypertensive rats.
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Nitric oxide, prostacyclin, and glucagon have been implicated in promoting the hyperdynamic circulatory state of portal hypertension. Recent evidence also indicates that increased tumor necrosis factor-alpha (TNF-alpha) production is involved in the pathogenesis of this hemodynamic abnormality. This study was aimed at investigating in rats with portal vein stenosis (PVS) the effects on splanchnic hemodynamics of blocking circulating TNF-alpha and the factors mediating the vascular action of this cytokine in this setting. Anti-TNF-alpha polyclonal antibodies or placebo was injected into rats (n = 96) before and 4 days after PVS (short-term inhibition) and at 24 h and 4, 7, 10 days after PVS (long-term inhibition). Short-term TNF-alpha inhibition reduced portal venous inflow and cardiac index and increased splanchnic and systemic resistance. Portal pressure was unchanged, but portal-systemic shunting was decreased. After long-term TNF-alpha inhibition, portal venous inflow and portal pressure were unchanged, but arterial pressure and systemic resistance rose significantly. Anti-TNF-alpha PVS rats exhibited lower increments of systemic resistance after Nomega-nitro-L-arginine methyl ester and indomethacin administration and lower serum levels of TNF-alpha, nitrates-nitrites, and 6-keto-PGF1alpha, both over the short and the long term. Serum glucagon levels rose after long-term inhibition. In conclusion, the specific role played by TNF-alpha in the development of the hyperdynamic state of portal hypertension appears to be mainly mediated through an increased release of nitric oxide and prostacyclin. Maintenance of the splanchnic hyperemia after long-term TNF-alpha inhibition could be due to a compensatory release of glucagon. (+info)