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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renal veins of Sprague-Dawley rats were ligated following intravenous infusion of various dilutions of pooled dog sera. Ten minutes later, the occluded venous segment in each animal was opened, and the presence or absence of a clot was observed. After injection of saline, no clot developed. For each pool of dog sera, a "minimal thrombosis-inducing dose" (MTD) was established. This dose was about ten times higher in females than in males; castration of females reduced it to approximately the male level. Treatment of castrated females with Premarin (a conjugated estrogen preparation) returned the dose to the normal female range. Testosterone treatment of normal females reduced the dose, but to a somewhat less extent than did castration. Endocrine manipulation had little effect on the minimal thrombosis-inducing dose of males. The results obtained in this study appear to be relevant to epidemiological data in human populations, an indication that primary artery thrombosis (coronary occlusion, cerebrovascular accident) is less common in women during the reproductive ages than in men; but after the menopause, the incidence rapidly increases in the female population.
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PMID:Effect of sex hormones on the serum-induced thrombosis phenomenon. 525 51

Acute experiments on 27 dogs were conducted to examine the effect of intravenous nitroglycerin, sodium nitroprusside and phentolamine on the hemodynamics and regional contractility of the left ventricle under conditions of experimental coronary occlusion. Nitroglycerin was the most effective agent versus the other drugs in decreasing the elevated diastolic pressure in the left ventricle whereas sodium nitroprusside showed the most pronounced hypotensive effect in relation to systemic arterial pressure. All these drugs produced indirect favourable chrono- and inotropic effects especially marked with phentolamine. The effect of nitroglycerin and sodium nitroprusside on the cardiac output may vary to a great extent: a decrease in the stroke volume occurred in the presence of the remaining high degree of peripheral vascular resistance and a fall in the elevated and diastolic pressure in the left ventricle, an increase in the stroke volume was observed in the case of a considerable drop in the overall peripheral vascular resistance and the persisting endodiastolic overburden of the left ventricle.
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PMID:[Comparative evaluation of the effect of nitroglycerin, sodium nitroprusside and phentolamine on hemodynamics and myocardial contraction during coronary occlusion in the dog]. 641 46

This study of 1,718 men with bypass surgery from 1970 to 1974 in Milwaukee has indicated that the following factors are significantly associated with five-year survival: left ventricular end-diastolic pressure (LVEDP), plasma cholesterol level, coronary occlusion score, age, and left ventricular function (LVF). The 31 men with a previous stroke had a high risk (five-year survival was 32%). To serve as a guide to patient risk, a logistic model is used to predict five-year survival. These probabilities are tabulated for all combinations of LVEDP, age, LVF, occlusion score, and plasma cholesterol level.
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PMID:The probability of surviving coronary bypass surgery. Five-year results from 1,718 patients. 696 34

In acute experiments on 32 dogs the authors studied the time course of the contractile function of the myocardium after coronary occlusion in the area of ischaemia and in segments of the left ventricle far removed from the ischaemic zone. Local contractility was studied with the aid of M-echographic method through changes in the thickness of the ventricular wall during the contraction. As a result of experimental investigation the authors distinguish 3 types of myocardial asynergy: hypokinesia, hypokinesia with elements of dyskinesia in the initial part of the ejection period and dyskinesia. A quantitative assessment of the degree of asynergy is offered on the strength of the amplitude of movement of the ischemized wall, percentage of its maximum systolic thickening and the local phase structure of the myocardial contraction. The most sensitive index of the state of general contractility of the left ventricle after limited ischaemia of the myocardium proved to be the end diastolic pressure and the ratio between the stroke work of the left ventricle and the end diastolic pressure.
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PMID:[Contractility of ischemic and intact regions of the myocardium during experimental occlusion of the coronary vessels]. 715 9

Regional function parameters under myocardial ischemia are frequently clearly changed when the parameters as the stroke volume, cardiac output, ejection fraction and the like are still unchanged by a compensation mechanism. Length changes can be measured regionally and phasically by means of a mercury wire strain gauge. The active shortening during the ejection time in relation to the total length change in this region is a possibility for the registration of the relative systolic shortening (delta LS%). Changes will be quantified still clearer and earlier if in the x-y display a vector representation of the regional displacements with the pressure in the left ventricle takes place. The plane of this vector decreased already a few seconds after the coronary occlusion. This is therefore a special early change in ischemia. The important for the estimation of therapeutic measures and other indirect measuring methods is accentuated.
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PMID:[Evaluation of regional heart function by means of local changes in pressure and direction in the vector cardiogram]. 721 Jul 62

Three basic mechanisms may be involved in the control of cardiac function during acute coronary occlusion: (1) neural; (2) hormonal (circulating catecholamine); and (3) intrinsic (e.g. Frank--Starling law). The response of intact, sedated (Innovar-Vet, 0.08 cc/kg), chronically instrumented dogs to a 5 min left circumflex coronary occlusion was tested to delineate the relative roles of each of the above mechanisms. First, 6 innervated and 6 cardiac denervated dogs were examined. The major difference between groups was that the occlusion-induced tachycardia was significantly smaller in the denervated dogs than in the normally innervated animals (+10 +/- 7 vs +27 +/- 4/min, respectively, (mean +/- S.D.)). Changes in the first time derivative of left ventricular pressure (d(LVP)/dt) were similar (--898 +/- 556 vs --796 +/- 274 mm Hg/sec, denervated vs innervated). Decreases in stroke volume and mean arterial pressure were also similar in the two groups. The occlusion-induced tachycardia was compared in a second group of denervated dogs (n = 5) before and after administration of propranolol to examine the role of circulating catecholamines, and, by exclusion, to observe the response of the heart per se, independently of extrinsic control factors. The heart rate response was similar in both cases (+8 +/- 4 vs +6 +/- 4/min, unblocked vs blocked). Finally, blood pressure was prevented from falling during coronary occlusion in 3 normally innervated dogs by coupling the femoral artery to a reservoir of saline suspended above the animals. Blunting the input to the baroreceptors in this manner did not significantly change the size of the occlusion-induced tachycardia. We conclude that during acute coronary occlusion in dog: (1) the major role of the cardiac nerves involves modulating changes in the chronotropic state of the heart; (2) changes in d(LVP)/dt result principally from intrinsic phenomena linked to ischemia-induced alterations in myocardial performance; (3) changes in circulating catecholamines play only a minor role in controlling the heart during acute coronary occlusion in denervated dog; and (4) receptors located within the heart figure significantly in the etiology of the occlusion-induced tachycardia.
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PMID:Neural, hormonal and intrinsic mechanisms of cardiac control during acute coronary occlusion in the intact dog. 726 97

To determine whether additional hypertrophy would be beneficial or maladaptive in cardiac failure, the effects of insulin-like growth factor (IGF-1) were investigated in rats with left ventricular (LV) dysfunction. In normal rats, 3 mg/kg per d of recombinant human IGF-1 for 14 d augmented LV wt (32%) and increased LV/body wt ratio (P < 0.01). 2 d after coronary occlusion, rats were randomized to IGF-1 (3 mg/kg per d) or placebo. After 2 wk, IGF-1-treated rats showed significant increases in LV wt (13%) and LV wt/tibial length ratio, but LV/body wt ratio was unchanged. By microangiography, compared with controls (n = 12) IGF-1-treated rats (n = 16) showed increased LV end-diastolic volume (19%) and stroke volume (31%) (both significant normalized to tibial length, but not to body wt). Average infarct size did not differ between groups. The LV ejection fraction (EF) was not significantly different between groups, but estimated cardiac output was higher in treated rats; there was a significant interaction for the EF between infarct size and treatment (P = 0.029) and a trend for EF to be higher in treated rats with large infarctions (EF 33.4 vs 25.1% in controls). Myocyte cross-sectional areas in noninfarcted LV zones tended to be larger in treated rats (232.1 vs 205.4 microns 2; P = 0.10), but there was no difference in capillary density and collagen content did not differ between groups. In conclusion, IGF-1 administration caused hypertrophy of the normal heart in vivo. When stimulated by IGF-1, the severely dysfunctional heart in evolving myocardial infarction is capable of undergoing additional hypertrophy with evidence of improved function, suggesting a beneficial effect. Further investigation of the potential role of growth factor therapy in heart failure appears warranted.
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PMID:Insulin-like growth factor-1 enhances ventricular hypertrophy and function during the onset of experimental cardiac failure. 786 Jul 46

The role of changes in preload in maintaining stable hemodynamics during coronary obstruction was assessed in the presence of myocardial ischemia due to occlusions of the left anterior descending (LAD) and left circumflex (LCX) coronary arteries. Changes in preload (mean left atrial pressure) to maintain a constant stroke volume after coronary occlusion were examined in 18 anesthetized dogs (LAD occlusion in 9 dogs, LCX occlusion in 9 dogs). The level of ischemia was assessed sonomicrometrically. Ventricular function curves relating left atrial pressure to stroke volume were assessed during a control state and after 1 min of coronary occlusion. The extent of preload reserve after coronary occlusion was examined on the ventricular function curves and was defined as the change in mean left atrial pressure required to maintain stroke volume at the level of the control state under conditions of regional ischemia. Ischemic size was determined by a stereo-angiogram after the animals were sacrificed. The extent of preload reserve (X) was linearly related to the ischemic size (Y) in both LAD (Y = 0.90 + 0.16X, r = 0.76, p < 0.001) and LCX (Y = -1.79 + 0.19X, r = 0.79, p < 0.001) occlusions. The slopes of the regression lines in LAD and LCX occlusions were the same. The X intercepts of these lines were -5.6% and 9.4% of the left ventricular weight in LAD and LCX ischemia (p < 0.001), respectively. Thus, the presence of systolic wall motion abnormalities due to coronary occlusion can be compensated for hemodynamically by changes in the preload reserve.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of preload reserve in myocardial ischemia--the relation between preload reserve and ischemic size differs between anterior descending and circumflex coronary artery occlusions in a canine model. 828 9

Changes of ischemic myocardium following coronary occlusion, including active and passive functions, and adaptive changes of non-ischemic surviving myocardium have been summarized under the term "left ventricular remodeling" post myocardial infarction. An increase in left ventricular volume may be a consequence, and associated with an adverse prognosis. Although left ventricular dilatation may increase stroke volume and, thus, be compensatory at first, in about one-fifth of patients it ultimately results in progressive dysfunction and heart failure. Major determinants of this process are time, infarct size, infarct location, global left ventricular function assessed 4 days after infarction by radionuclide ejection fraction and right heart catheter (stroke volume), and morphology of the infarct-associated coronary artery. The surviving myocardium hypertrophies and may also dilate structurally. Depression of left ventricular ejection fraction chronically after the infarct is due to deterioration of wall motion of chamber segments initially classified normal by radionuclide analysis. Biochemical changes may also occur, including reduction of phosphocreatine, prolongation of time to peak Cai2+, and changes in myosin isoforms. Systemic or local humoral factors may be involved in these changes, however, clear evidence is still lacking. Perfusion of surviving myocardium may be altered under various conditions due to morphologic and functional changes of coronary vasculature. Successful prevention of heart failure and death by angiotensin converting enzyme inhibitors in asymptomatic patients with left ventricular dysfunction post-myocardial infarction has supported the pathophysiologic concepts of remodeling.
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PMID:Ventricular remodeling after myocardial infarction. Experimental and clinical studies. 835 28

This article reviews the evidence that myocardial stunning during surgical reperfusion after coronary revascularization or heart transplantation is not strictly due to myocardial injury sustained during ischemia, but results from pathophysiological events triggered by reperfusion (reperfusion injury). In sheep, left ventricular (LV) dP/dt and stroke work were reduced up to 50%, and 60% to 70% necrosis was observed in the area at risk during 3 hours reperfusion following coronary occlusion and cardioplegic arrest on bypass. Reperfusion with leukocyte depleted blood, or pharmacological blockade of either thromboxane or leukotriene receptors, provided significant improvements in LV function and myocardial blood flow, with a 40% to 50% reduction in necrosis. Similar results have been obtained using animal heart subjected to 2 to 3 hours arrest at either 4 degrees C or 15 degrees C, simulating cardiac preservation and reperfusion after transplantation. Diastolic pressure was significantly elevated, and increases in the time constant for relaxation of LV pressure and coronary vascular resistance were noted. These indices of myocardial stunning were reversed after blocking neutrophil-endothelial cell interaction with monoclonal antibodies against CD18 or ICAM-1 receptors, and significant improvements were also obtained after either thromboxane or leukotriene receptor blockade. We conclude that immediate postoperative myocardial stunning results largely from reperfusion injury that occurs due to an acute inflammatory response to ischemia and reperfusion, and that stunning can be largely reversed with appropriate pharmacological intervention.
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PMID:Myocardial stunning and reperfusion injury in cardiac surgery. 846 24


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