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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In canine hearts supported by cardiopulmonary bypass, isovolumic peak developed pressure (PDP, mm Hg) and myocardial oxygen consumption (MVO2, ml O2 X 10(-2)/beat/100 gm left ventricular [LV] weight) were determined at 5-ml increments of LV balloon inflation before and after either 2 hours of potassium cardioplegic arrest (ischemia, N = 7) or a comparable period of normothermic perfusion without ischemia (control, N = 6). The sensitivity of MVO2 as a marker of ischemic injury was compared with preservation of both adenosine triphosphate (ATP) stores and systolic pump function. Over a physiological range of end-diastolic volumes (5 to 35 ml) and end-diastolic pressures (0 to 18 mm Hg), the Frank-Starling curves were not depressed following both cardioplegic arrest and prolonged nonischemic perfusion. Although ATP stores decreased by 26% and 22% (ischemia and control groups, respectively; not significant), these levels did not distinguish the effects of cardioplegic arrest from prolonged perfusion. At the preinterventional measurement in both groups, PDP between 50 and 200 correlated with MVO2 from 3.0 to 10.0 (r = +0.84). Following cardioplegic arrest, postischemic MVO2 increased 137 +/- 6% when measured over the PDP range of 75 to 200 mm Hg (p less than 0.01). This change was not evident at a PDP of less than 75, in the empty beating heart, or in control hearts subjected to nonischemic extracorporeal perfusion. These data suggest that increased utilization of oxygen to develop physiological pressures may be a more sensitive indicator of ischemic injury than shifts in the pressure-volume relationship or depletion of adenine nucleotide stores.
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PMID:Oxygen utilization during isovolumic pressure-volume loading: effects of prolonged extracorporeal circulation and cardioplegic arrest. 396 17

Thirty patients who exhibited increased and 65 patients decreased spatial R wave amplitude during exercise testing were compared for left ventricular function and ischemic variables. Spatial R wave amplitude was derived from the three-dimensional Frank X, Y, Z leads using computerized methods. All patients had stable coronary artery disease and they were classified into two groups: one that attained a higher (n = 48) and one a lower (n = 47) median value of maximal heart rate during exercise (161 beats/min). Within these two groups, patients with increasing or decreasing spatial R wave amplitude during exercise were analyzed for differences in oxygen consumption, exercise-induced changes in spatial R wave amplitude, ST segment depression laterally (ST60, lead X), ST displacement spatially, left ventricular ejection fraction at rest, change in left ventricular ejection fraction with exercise and thallium-201 ischemia during exercise. Significant differences were demonstrated only in exercise-induced spatial R wave amplitude changes (p less than 0.0001). There was no significant correlation between exercise-induced change in heart rate and change in spatial R wave amplitude in either the group with increasing or the group with decreasing spatial R wave amplitude. It is concluded that changes in spatial R wave amplitude during exercise are not related to ischemic electrocardiographic or thallium-201 imaging changes or to left ventricular ejection fraction determined at rest or during exercise.
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PMID:Spatial R wave amplitude changes during exercise: relation with left ventricular ischemia and function. 403 Dec 71

We examined the influence of left ventricular end-diastolic pressure (LVEDP) on the mechanical interaction between ischemic and nonischemic areas during acute myocardial ischemia. Circumferentially oriented ultrasonic segment gauges were implanted in the midwall of the anterior apex and posterior apex of the left ventricle in seven anesthetized dogs. Stroke volume was measured with a flow probe around the ascending aorta in five of these animals. We varied LVEDP with vena caval occlusion and dextran infusions to three matched levels (7, 12, and 19 mm Hg) before and 30 min after complete occlusion of the mid left anterior descending coronary artery. With acute ischemia, the anterior apex or ischemic zone demonstrated marked segmental lengthening during isovolumetric systole (end-diastole to aortic valve opening) and akinesis during the ejection phase (aortic valve opening to closure). In the posterior apex or nonischemic area, isovolumetric shortening increased and ejection phase shortening decreased during acute ischemia when compared with those under control conditions at the same LVEDP. Thus, a portion of the shortening generated by the nonischemic area was expended in stretching the ischemic zone during isovolumetric systole, thereby reducing the amount of ejection phase shortening. As LVEDP was increased, there was a parallel decrease in both the amount of isovolumetric lengthening in the ischemic zone and the isovolumetric shortening in the nonischemic area. As a result, acute ischemia produced less of a reduction in ejection phase shortening in the nonischemic area and in stroke volume at high as compared with low LVEDP. We conclude that the ischemic zone imposes a mechanical disadvantage on the nonischemic area, the magnitude of which is directly proportional to the amount of isovolumetric lengthening or bulge in the ischemic zone. An increase in LVEDP during acute ischemia improves regional and global ventricular function by both the Frank-Starling mechanism in the nonischemic (but not the ischemic) area and by reducing the mechanical disadvantage that the ischemic zone imposes on the nonischemic area.
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PMID:Mechanisms of improving regional and global ventricular function by preload alterations during acute ischemia in the canine left ventricle. 404

At subsaturating concentrations of palmitoyl-CoA, the carnitine-dependent oxidation of the palmitoyl portion by uncoupled rat heart mitochondria was stimulated by ADP or ATP. This effect was traced to the prevention of acyl-CoA binding to adenine nucleotide translocase and the consequent sparing of acyl-CoA for acylcarnitine formation. Palmitoyl-CoA oxidation was stimulated by ITP also although ITP served neither as a transportable substrate nor as an inhibitor of ADP transport. ITP and other nontransportable nucleoside di(tri)phosphates prevented octanoyl-CoA binding to mitochondria. ITP was bound to mitochondria, and this binding was reversed by ADP, octanoyl-CoA, and carboxyatractyloside. Thus, besides a substrate site, there is a site on the translocase that binds nucleoside di(tri)phosphates, CoA and its esters, and atractylosides; inhibition of the translocase results, however, only from the binding of CoA esters of fatty acids and of atractylosides. We suggest that in O2-deficient hearts, when nucleotides decline and fatty acyl-CoA rises, the binding of the latter to the translocase becomes operational to slow fatty acylcarnitine production. By retarding the rise in amphipathic burden, this mechanism could protect heart against irreversible damage during brief periods of ischemia or hypoxia.
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PMID:Protective role of adenine nucleotide translocase in O2-deficient hearts. 633 Dec 5

Experimental animal investigations have shown that already after a few seconds of occlusion of a coronary artery a reduction in the systolic myocardial shortening and wall thickening takes place in the corresponding supply area. Following 1-2 minutes of ischemia systolic expansion occurs. Wall-thickness increase and myocardial shortening then take place during the isovolumetric relaxation phase. When at least 25% of the myocardium of the left ventricle becomes acutely ischemic the end-diastolic pressure and end-diastolic volume increase. As a rule an augmentation of myocardial contraction appears in the non-ischemic section of myocardium, which in part takes place through the Frank-Starling mechanism. With a gradual reduction of the coronary inflow, and a decline in the wall thickening of c. 50% of the control value, a significant reduction in blood flow took place only in the innermost quarter of the ventricular wall. With akinesia of the ischemic area, no reduction of the blood flow could be determined in the subepicardial region. Only with the occurrence of dyskinetic wall motion was a transmural reduction of blood flow effected. The ischemic contraction disturbances are fully reversible if coronary occlusion last only a few minutes. With a 15 minute occlusion the recovery time of the myocardial function can require several days (postischemic "stunned myocardium"). The first myocardial necroses occur after 20 minutes of ischemia, and after 3-6 hours of ischemia the infarction is complete.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamics in ischemia. Systolic phase]. 633 23

To examine the cardiac responses to selective septal ischemia, the septal artery was occluded intermittently in anesthetized open-chest dogs. Myocardial segment length was recorded continuously by an ultrasonic technique in the interventricular septum and the right and left ventricular free walls. At left ventricular end-diastolic pressure of 3.0 +/- 0.6 mm Hg, occlusion of the septal artery increased left ventricular end-diastolic segment length by 3.9 +/- 0.9% and stroke volume was maintained. After blood volume expansion to a left ventricular end-diastolic pressure of 7.2 +/- 1.4 mm Hg, occlusion of the septal artery did not increase end-diastolic dimensions and stroke volume decreased significantly but by less than 10%. At all levels of blood volume expansion, occlusion of the septal artery did not alter significantly the end-systolic segment length of the free wall of the left ventricle and the dimensions of the free wall of the right ventricle. The distance between the septum and the right ventricular free wall was unchanged in end-diastole and reduced in end-systole after occlusion of the septal artery. These observations indicate paradoxical movement of the ischemic septum. The ischemic septum seems to act as a passive diaphragm pump on the right ventricle without activation of the Frank-Starling mechanism in uninjured areas. In the left ventricle, the Frank-Starling mechanism is fully exploited with unaltered end-systolic dimensions of the uninjured myocardium because of the systolic bulging of the ischemia septum.
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PMID:Compensatory cardiac mechanisms evoked by septal ischemia in dogs. 684 57

The role of intracardiac volume in controlling electrocardiographic R-wave amplitude changes during acute myocardial ischemia was studied in 24 open-chest dogs. The R-wave amplitude in surface ECG leads 2, V5 and Frank X, Y and Z leads were correlated with hemodynamic, echocardiographic and angiographic changes in a 5-minute circumflex coronary artery ligation and reperfusion model. After coronary ligation, left ventricular end-diastolic diameter and volume increased progressively above control, reached a peak and plateau at 120--130 seconds after ligation and did not return to control levels until more than 5 minutes after release of the occlusion. In contrast, the R-wave amplitude showed a biphasic response to acute ischemia, reaching a nadir (sigma R = 18.2% below control) at 30 seconds after coronary ligation and only subsequently increased to reach a peak (sigma R = 52% above control) at 150 seconds after ligation. In addition, R-wave amplitude returned immediately to control levels within 10 seconds after reperfusion. In six other dogs, both venae cavae were occluded for a 30-second period, beginning 180 seconds after coronary ligation. Although intracardiac volume decreased markedly, R-wave amplitudes increased even more. Thus, the demonstration of discordance between alterations in intracardiac volume and R-wave amplitude in these studies suggests that factors other than intracardiac volume determine R-wave amplitude changes in the course of acute myocardial ischemia.
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PMID:R-wave amplitude variations during acute experimental myocardial ischemia: an inadequate index for changes in intracardiac volume. 722 82

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

Alternations of regional left ventricular myocardial function immediately after coronary artery branch ligation as related to the total left ventricular function were determined by utilizing left ventricular pressure-wall thickness loop in 6 anesthetized open-chest dogs. End-diastolic wall thickness was decreased immediately from 11.54+/-0.50 mm (standard error of the mean) of control to 10.99+/-0.50 mm in 5 to 10 min after ligation (p<0.05), while regional myocardial work calculated as the loop area, was also decreased from 27.5+/-6.1 to 19.3+/-5.8X10(3) dyn/cm (p<0.05), indicating that the local Frank-Starling curve at the myocardium was depressed during ischemia. At the site where the ligation did not have effect, end-diastolic wall thickness and the regional work did not change significantly. Analysis of the shape of the loop revealed that the myocardial shortening was incomplete during the systolic ejection phase, and that the myocardial relaxation occurred very early in the ventricular relaxation phase after ischemia without alterations in the isovolumic contraction phase. These findings are compatible with those reported on isolated cardiac muscle strips during anoxia. The left ventricular pressure-wall thickness loop is superior to the pressure-length loop in that the former can be applied easily for clinical purposes and that the former utilizes a more direct relationship of pressure to its generator than the latter. Thus, primary alterations of myocardial function during ischemia were clarified accurately by utilizing the present method in the left ventricle in situ.
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PMID:Alterations of myocardial function during early stages of mild experimental ischemia in dogs determined by left ventricular pressure-wall thickness loop. 742 Jul 35

During a 4 year period, 1,461 critically ill neonates were admitted to the newborn intensive care unit of the Newark Beth Israel Medical Center, and 507 (35 percent) had umbilical artery catheters inserted for physiologic monitoring. In five patients (1 percent) clinically significant limb ischemia developed as a result of catheter complications. Frank gangrene was observed in three patients; two died from the primary illness soon after the onset of gangrene and the third survived after leg amputation. The other two infants had advanced ischemia that responded favorably to catheter removal and heparinization. Irreversible limb ischemia in this setting is infrequent, and milder forms are usually unrecognized or undocumented. High placement of the catheter or the length of time it is in place were not related to complications. Limb ischemia occurred soon after catheter insertion rather than after its protracted use. Major complications may be reduced by placement of the catheter in the lower abdominal aorta or internal iliac artery, clinical awareness and observation and frequent noninvasive monitoring. Immediate catheter removal and intravenous anticoagulation are warranted if ischemia persists. From this study, we believe that the benefits derived from judicious umbilical artery catheterization outweigh any inherent risk.
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PMID:Clinically recognized limb ischemia in the neonate after umbilical artery catheterization. 742 16


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