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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intraruminal administration of 0.25 g of 3-methylindole (3MI; skatole/kg of body weight) to seven young calves generally caused mild respiratory signs and lesions, accompanied by only slight changes in cardiopulmonary function. Moderate depression, trembling, and irregular respiratory rate were observed between postadministration hours (PAH) 6 and 12. By PAH 24 at this dosage, abnormal clinical signs were not present. Statistically significant (P less than or equal to 0.05) changes observed in blood gas data from the seven calves were a decrease in aortic oxygen tension at PAH 12, increases in free-flowing venous oxygen tension in the intervals between PAH 6 and 12 and between PAH 6 and 24, and an increase in occluded venous oxygen tension at PAH 24. All calves had increases (although generally not statistically significant) in heart rate, cardiac output, cardiac index, stroke volume, and stroke index after 3MI administration. Mean aortic and pulmonary arterial pressure changes were generally small and variable. At necropsy, the lungs of the calves did not collapse when the thorax was opened. Patchy areas of consolidation (0.5 cm in diameter) were scattered throughout the parenchyma. Pulmonary edema or emphysema was not observed grossly. Microscopically, the alveolar septae were irregularly thickened because of edema, infiltration by polymorphonuclear and mononuclear cells, and vascular congestion. Interstitial lesions were patchy in distribution and severity and corresponded to the areas of consolidation observed grossly. Alveolar epithelial hypertrophy and hyperplasia were present, and an occasional focus of alevoli contained fluid of edema. Degeneration of individual hepatocytes was observed in scattered areas of the liver, especially in the periportal areas. It was concluded that differences in 3MI dosage response may exist between young calves and adult cattle in which calves are more resistant to the pulmonary cytotoxicity of 3MI.
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PMID:Pathophysiologic studies of calves given 3-methylindole intraruminally. 51 32

Blood loss of sufficient magnitude to over-ride compensatory mechanisms and result in a lowering of arterial pressure will ultimately lead to irreversible circulatory collapse. Identification of the organ or tissues which may trigger a terminal cascade remains controversial. The weight of evidence supports the view that cardiac performance deteriorates with prolonged oligemic hypotension, although this may not be the initiating or sole reason for irreversible failure of the circulation. Controversy regarding the heart as an important target organ is no doubt in part due to the multiplicity of preparations and protocols, and variety of methods used to characterize cardiac function. We have used ventricular function curves to calibrate LV performance in terms of pump function, while arterial pressure remains at a pre-determined level. With this approach, a progressive decline in stroke volume for a given LV end diastolic pressure is consistently observed in hemorrhagic shock (AP, 30 mmHg). If arterial pressure is briefly re-elevated at 30 minute intervals, permanent deterioration is prevented. However, if the hypotension is sustained for 2 hours, LV performance remains depressed following pressure re-elevation. Among the mechanisms responsible for deterioration of performance, coronary perfusion pressure (CPP) exerts a pivotal role. Thus, no LV depression occurs after 2 hours of shock provided CPP is maintained at normotensive levels. But if myocardial O2 availability falls below 10 ml/min/100 gm of heart, both O2 uptake and extraction decline and this is uniformly accompanied by cardiac failure. This likely reflects mitochondrial damage and impaired aerobic metabolism. These changes are potentiated by the appearance of metabolic acidosis and failure of sympathetic neurohumoral activity. Both factors directly reduce myocardial contractility, but assume much greater importance during shock. While E. coli endotoxin has been shown to reduce cardiac performance, the relative importance of bacterial products which may enter the circulation during hemorrhagic shock in uncertain. Reduced O2 availability, metabolic acidosis and adrenergic failure appear the major determinants of diminished cardiac performance and thereby may contribute to irreversible collapse of circulatory function.
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PMID:Cardiac performance in hemorrhagic shock. 55 6

After a two-hour period of regional intestinal shock (arterial inflow pressure 30 to 35 mm Hg; electrical stimulation of regional vasoconstrictor fibers at 6 Hz) a pronounced cardiovascular derangement is observed as reflected in a rapid fall in arterial blood pressure. In this study, central hemodynamics and lung function were investigated to elucidate if functional changes in the thoracic organs might explain the cardiovascular collapse. No alteration of pulmonary function was observed. A negative inotropic influence on the heart was, however, noted as judged by a decreased left ventricular stroke volume and left ventricular maximal pressure change in the face of an increased left ventricular end diastolic pressure. Based on earlier observations with the same shock model, it is proposed that the cardiac effects were caused by cardiotoxic material released from the hypoxic gut.
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PMID:Cardiac and pulmonary function in regional intestinal shock. 68 92

Electron and light microscopic studies were performed on rabbit brain to re-examine the structural changes of endothelial cells and perivascular glia following ischemia. Although swelling of perivascular glia occurred, earlier findings of extreme perivascular glial swelling and bleb formation leading to luminal collapse and plugging could not be confirmed. Ischemic brains, however, had a higher proportion of small-diameter capillaries than controls. It is felt that structural changes in ischemic capillary walls in themselves are not sufficient to explain failed cerebral reperfusion, or the no-reflow phenomenon.
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PMID:Reassessment of cerebral capillary changes in acute global ischemia and their relationship to the "no-reflow phenomenon". 83 56

Longitudinal stretch of the rabbit basilar artery produces local injury followed by prolonged circular constriction. After stretching and rapid release in vitro localized constrictions promptly occurred. This could be prevented by prior treatment with cyanide or calcium-free solution. Once produced, constrictions persisted for more than 72 hours. Previously induced constriction was not reversed by treatment for two hours with cyanide or by removing calcium. Histological observation indicated that constricted areas were associated with a discrete circumferential rupture of the internal elastic lamina and disruption and thinning of the underlying media. Specific catecholamine fluorescence at the adventitio-medial junction was unchanged in constricted areas. The relationship between smooth muscle cell length and resting tension of artery segments with and without constrictions was compared. Segments with constrictions had a shorter muscle length for any given resting tension, which confirms that constriction was not due to passive collapse of the vessel wall. These findings suggest that injury of cerebrovascular smooth muscle may result in essentially irreversible vasoconstriction. Such a mechanism could contribute to the pathogenesis of prolonged cerebral vasospasm after SAH or traumatic injury to the cerebrum.
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PMID:An in vitro study of prolonged vasospasm of a rabbit cerebral artery. 126 10

A new cardiac output regulation method for the moving actuator total artificial heart (TAH) has been developed without using an extra compliance chamber or any transducer. The left and right ventricular sacs are alternately pumped by the pendulous moving actuator, with the left sac attached to the actuator and a free right ventricle. Preload sensitive cardiac output response is achieved by adjusting heart rate just below the level needed to generate atrial collapse, while maintaining full-fill and full-ejection conditions. The motor current waveform analysis detects mild atrial suction related to the amount of venous return. In addition, the structural characteristic of the pendulous moving actuator allows for manipulation of the left and right ventricular output difference by adjusting the asymmetry of stroke angle to either the left or right. In mock circulatory system tests, cardiac output increased from 5 to 9 L/min, with left atrial pressure (LAP) maintained at approximately 5 mmHg higher than right atrial pressure (RAP) over a physiologic range of preload (0-12 mmHg of RAP) and afterload [80-120 mmHg of aortic pressure (AoP)].
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PMID:Cardiac output regulation in the moving actuator total artificial heart without a compliance chamber. 145 Apr 84

Left atrial booster pump function produces variable effects on cardiac output. Generally, cardiac output decreases by only 15-20% when atrial fibrillation occurs, however, in some cases, hemodynamic collapse occurs through loss of left atrial contraction. We evaluated the relative significance of left atrial booster pump function in acute or chronic load and in myocardial ischemia using the left ventricular volume curve. Blood entering into the left ventricle during the left atrial contraction phase (FVLA) represents the left atrial volume work, and the ratio of FVLA to the left ventricular filling volume during one cardiac cycle (%FVLA) represents the relative significance of left atrial booster pump function in cardiac output. In dog experiments, we calculated the change in FVLA and %FVLA by measuring the the left ventricular internal minor axis diameter and using Pombo's method. We also measured the change of the left atrial segment length as a direct indicator of left atrial contraction. In the acute change in preload, FVLA changed with stroke volume, but %FVLA remained unchanged. The change in FVLA correlated with the direct indicator of the left atrial excursion; the extent of the left atrial segment length (LASL). During acute change of left ventricular afterload, both FVLA and %FVLA were unchanged. In regional myocardial ischemia, both FVLA and %FVLA were increased, suggesting an increase in the left atrial booster pump function. In clinical study, we calculated FVLA and %FVLA from the left ventricular diameter using M-mode echocardiography. In chronic volume overloading (aortic regurgitation), FVLA increased while %FVLA was maintained unchanged. The same FVLA-%FVLA relationship was observed in acute volume loading. In cases of left ventricular hypertrophy (LVH) and old myocardial infarction (MI), both FVLA and %FVLA were increased, suggesting the increased left atrial booster pump function. In these cases, the left ventricular rapid filling velocity decreased, suggesting that impairment of rapid filling caused the increase of left atrial preload and hence increased left atrial volume work. The results of this study show that in old MI and in LVH, both left atrial volume work and the relative significance of left atrial booster pump function increase. We concluded that prevention of atrial fibrillation may be very important in these diseases.
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PMID:[Left atrial booster pump function in left ventricular blood filling: clinical and experimental analyses]. 184 34

Many patients with hypertrophic cardiomyopathy experience postprandial exacerbation of their symptoms. The vasodilation associated with eating may be deleterious in hypertrophic cardiomyopathy, especially during exercise. To examine the hemodynamic effects of a meal in hypertrophic cardiomyopathy, 11 patients were studied with invasive hemodynamic monitoring during exercise testing in the fasting state and 45 min after a 740 kcal (3,100 J) meal. The meal induced a decrease in systemic vascular resistance index at rest (mean +/- SD, -17 +/- 14%), increases in mean right atrial (31 +/- 21%), mean pulmonary artery (14 +/- 14%) and mean pulmonary capillary wedge (17 +/- 14%) pressures and an increase in cardiac index (18 +/- 10%) due to an increased heart rate without any significant change in stroke volume. During postprandial exercise, heart rate, rate-pressure product, cardiac index and cardiac filling pressures were higher than during fasting exercise and one patient had a decrease in exercise blood pressure compared with the fasting test. Five patients with postprandial exacerbation of symptoms in everyday life had a lesser increase in systemic arterial pressure and stroke volume during both exercise tests and a smaller increase in cardiac index after the meal than did the six patients without postprandial symptom exacerbation, suggesting more severe cardiac disease. It is concluded that patients with hypertrophic cardiomyopathy have an abnormal hemodynamic response to food, in which stroke volume fails to increase and pulmonary capillary wedge and pulmonary artery pressures increase. These adverse changes persist during postprandial exercise and may predispose to exertional collapse in certain patients.
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PMID:Effects of a meal on hemodynamic function at rest and during exercise in patients with hypertrophic cardiomyopathy. 185 10

Effects of betaxolol, a cardioselective beta-adrenoceptor antagonist, on blood pressure and hypertensive complications in stroke-prone spontaneously hypertensive rats (SHRSP) were investigated. Betaxolol was provided in a dose of 33 +/- 1.8 mg/kg/day, orally in drinking water, throughout the experimental period. The chronic treatment with betaxolol inhibited the development of hypertension in SHRSP and reduced values of blood urea nitrogen, creatinine, total cholesterol, free cholesterol, triglyceride, phospholipid and HDL-cholesterol in serum. Treatment with betaxolol apparently inhibited the incidence of hypertensive lesions such as cardiac fibrosis, mesenteric vasculitis, proliferative and/or necrotic vasculitis and glomeruli showing collapse or vasculitis in the kidneys. To shorten the time before the onset of hypertension and the subsequent stroke, SHRSP were kept on a SP diet containing 0.39% Na instead of the F-2 diet. When the SHRSP were kept on the SP diet, all of the control SHRSP had cerebral apoplexy and severe hypertensive lesions in the heart and kidney. When betaxolol was chronically administered to SHRSP, cerebral apoplexy and hypertensive lesions in the heart and kidney were inhibited, but the effect on blood pressure was slight. Treatment with betaxolol reduced serum creatinine levels. Our observations show that betaxolol reduces blood pressure and potently inhibits hypertensive complications in SHRSP.
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PMID:[Antihypertensive effects of betaxolol, a cardioselective beta-adrenoceptor antagonist, in stroke-prone spontaneously hypertensive rats (SHRSP)]. 197 70

To determine whether myocardial dysfunction contributes to vascular collapse in anaphylactic shock, we examined left ventricular (LV) contractility, coronary blood flow, and myocardial lactate metabolism during antigen challenge in eight dogs that were sensitized to ragweed pollen extract (anaphylaxis group). Findings in the anaphylaxis group were contrasted to those in another group of dogs in which mean blood pressure was decreased to the same extent by arteriolar vasodilation with nitroprusside. The animals were examined under nonhypoxic conditions while anesthetized and ventilated. LV mechanics were examined with subendocardial crystals placed primarily along the anterior-posterior minor axis of the LV. During antigen challenge, a depression in LV contractility was observed in the anaphylaxis group as assessed by fractional dimensional shortening, stroke volume, and the slope of the end-systolic pressure-dimension relationship. During anaphylaxis, moreover, coronary vasodilation rather than coronary vasoconstriction was observed, and evidence of myocardial ischemia as assessed by altered myocardial lactate metabolism was not found. Our results indicate that depressed LV contractility occurs in anaphylactic shock. The results further suggest that the mechanism may be due to a direct effect of mediators of anaphylaxis on the myocardium to produce systolic dysfunction.
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PMID:Left ventricular contractility is depressed in IgE-mediated anaphylactic shock in dogs. 200 Sep 70


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