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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the effects of methylprednisolone sodium succinate (MPSS) on 60 minutes of myocardial ischemia during profound (5 degrees C) topical cardiac hypothermia (ice chips) in a canine right heart bypass preparation. The ventricular function curve shifted to the right and downward, but not significantly, after ischemia, and stroke work declined significantly for both control and treated dogs. Contractility (rate of rise of left ventricular pressure and maximum velocity of the contractile element) declined for both groups but not significantly. Total coronary flow, oxygen consumption, and metabolism of lactate and pyruvate were not different for control and treated dogs. Ultrastructure of the outer and inner myocardium did not demonstrate benefit from MPSS. Intracellular and extracellular edema of moderate severity was slightly worse in the subendocardium, and reversible mitochondrial injury of a mild to moderate degreee was symmetrically present. Ice-related injury was not noted. We were unable to deomonstrate that pretreatment with MPSS favorably alters cardiodynamics or ultrastructure after 60 minutes of profound topical cardiac hypothermia.
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PMID:Topical cardiac hypothermia: the effect of methylprednisolone sodium succinate. 65 47

The changes in left ventricular (LV) dynamics induced by brief periods of ischemia (100 seconds) and subsequent reperfusion were analyzed in conscious dogs. Global LV ischemia, induced by partially occluding the left main coronary artery, reduced LV flow homogeneously and impaired LV function as reflected by decreases in LV stroke "work" (89 +/- 4% M +/- SE), systolic shortening (72 +/- 4%), velocity of shortening (56 +/- 6%), LV systolic pressure (34 +/- 5%), and dP/dt (59 +/- 6%). Regional LV ischemia, induced by occluding either the left circumflex or anterior descending coronary artery completely, reduced flow to the ischemic segment (82 +/- 3%) while decreasing segment work (96 +/- 5%), shortening (82 +/- 3%), and velocity of shortening (70 +/- 5%), with minimal depression of overall LV function. In both groups the extent of shortening was reduced more rapidly and greater (P less than 0.01) than shortening velocity. Moreover, with localized ischemia, segment work was reduced more (P less than 0.01) than shortening. With reperfusion, a transient overshoot in function above preischemic control levels was observed in both groups (global work increased by 60 +/- 12% and regional work by 28 +/- 4% above control). This overshoot was not dependent on adrenergic mechanisms, but was prevented by inhibiting reactive hyperemia. Thus myocardial ischemia induces a dissociation between extent and rate of myocardial shortening. A further dissociation between shortening and work is apparent with regional ischemia. After reperfusion there is a transient overshoot in function which appears to be dependent upon the associated reactive hyperemia.
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PMID:Initial myocardial adjustments to brief periods of ischemia and reperfusion in the conscious dog. 65 61

To evaluate the influence of glucose infusate administered with insulin and potassium on left ventricular function during 4 h of ischemia, as well as mechanism of action, four groups of intact anesthetized dogs were studied. Acute regional ischemia was induced with a balloon tip catheter in the left anterior descending artery and infusates were begun after 20 min of ischemia. A threefold increase of plasma glucose concentration was associated with improved left ventricular function during ischemia, compared to animals receiving isovolumic saline. There was a significant decline of left ventricular end-diastolic pressure associated with elevation of stroke volume and ejection fraction to control levels, as determined by indicator dilution. In a separate subgroup studied by cineangiography, shortening of the ischemic anterior wall, after an initial decline, was increased in response to glucose but there was no evidence of extension of injury. Ischemic tissue exhibited a smaller gain of water as well as Na+ per gram dry weight as compared to ischemic controls. On precordial electrocardiogram mapping there was a significant decrease in the sigmaST (sum of ST elevation) as well as NST (number of ST segment elevations), but the reduction of R wave amplitude was not different from controls. To further evaluate long-term effects, eight controls and six treated animals underwent myocardial ischemia and were sacrificed after 4 mo. Calculated area and weight of scar, as well as degree of wall thinning, were similar in both groups. The glucose-treated animals had a significant decrease of plasma FFA in contrast to controls which manifested a significant rise. To examine the postulate that the decrease in FFA was important to therapeutic action, a third group was infused with Intralipid (Cutter Laboratories, Inc., Berkeley, Calif.) and heparin, simultaneously with the glucose infusate, to effect an elevation of plasma FFA during ischemia. Changes in myocardial function and electrolyte composition, as well as precordial electrocardiogram mapping, were similar to that of animals receiving glucose alone. Because serum osmolality was increased approximately 40 mosmol during the glucose infusion, the potential role of hyperosmolality was assessed by infusion of 20% mannitol during acute ischemia in a fourth group. After a transient small increase, there was a moderate decline in function by 4 h, suggesting that the response to glucose is not dependent upon extracellular osmolality. Thus, it is concluded that during the initial hours after the onset of myocardial ischemia the glucose infusate improves ventricular performance without evidence of arrhythmia induction or intensification of ischemic injury. Evolution of irreversible necrosis appears to be delayed rather than prevented under the circumstances of this study.
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PMID:Sustained effect of glucose-insulin-potassium on myocardial performance during regional ischemia. Role of free fatty acid and osmolality. 65 87

The effectiveness of beta-histine-HCL in modifying the size of developing myocardial infarcts was tested in the surgically ligated dog. Branches of the left coronary artery were ligated and a 6-hour continuous intravenous infusion of 0.24 mg/kg/min of beta-histine was administered from 0 to 120 min after ligation. The effect of this treatment was evaluated histologically in studies on acute ischemia by the use of the hematoxylin-basic fuchsin-picric acid stain for early myocardial ischemia. The treatment was also evaluated grossly in a study on chronic ischemia where the dogs were permitted to survive for 30 days before sacrifice. In these experiments the size of infarcts found in the beta-histine-treated animals was compared with those found in the saline controls. Both studies showed that the control ligations produced a large uniform area of ischemia or infarction that was greatly reduced or prevented by immediate treatment with beta-histine. Also, beta-histine was capable of significantly reducing the size of developing infarcts for up to 120 min after ligation.
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PMID:Modification of the size of developing infarcts in the ligated dog heart by betahistine-HCL. 66 41

Insulin was administered to two patients whose diminished myocardial contractility made it difficult to terminate cardiopulmonary bypass. In both instances, bypass was successfully terminated shortly after the insulin injection. These clinical observations led to experiments under the controlled conditions provided by the isolated, working rat heart preparation. The recovery of contractility after 30 minutes of severe ischemia was assessed in all 11 control and 11 insulin-treated hearts. Myocardial performance, as judged by the product of heart rate and peak systolic blood pressure, was significantly greater in the insulin-treated hearts. These clinical observations and experimental findings suggest the need for more extensive study of the potential value of insulin in treating depressed contractility after prolonged myocardial ischemia.
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PMID:Insulin therapy for depressed myocardial contractility after prolonged ischemia. 66 28

Experimental studies of the myocardial action potentials following coronary artery occlusion have shown that the resulting regional ischemia is reflected by characteristics changes in the shapes of the action potentials in the ischemic region. The principal changes are decreases in the magnitude of the resting potential and in the action potential duration. Action potentials with prolonged durations have been observed in the infarcted regions of experimental animals after the development of inverted T waves in the surface electrocardiogram (ECG). We use such abnormal action potentials in our digital computer model to study the effects of acute myocardial ischemia and infarction on the surface ECG. The heart is represented in sufficient detail to allow variations in the location and size of the ischemic injury and in the distribution of the severity of injury within the injured region. The evolution of acute infarctions is simulated by progressively modifying the abnormal action potentials assigned to the injured region. Calculated standard 12 lead ECGs and torso isopotential surface maps for simulated acute ischemia and infarction are in good agreement with patient data reported in the literature. Typical simulations include anterior and inferior transmural ischemia and infarction and anterior subendocardial ischemia. The model is used to examine relationships between torso surface potentials during ventricular activation and recovery and the site and size of the ischemic injury.
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PMID:Simulation studies of the electrocardiogram. II. Ischemia and infarction. 66 62

To determine the effect of ischemia on myocardial clearance of thallium-201 (201Tl), we studied 12 dogs with ischemia produced after the injection of Tl. Tl was given I.V. 10 minutes before left anterior descending (LAD) coronary artery ligation. 85Sr-microspheres (MS) were administered 5 minutes later, and control biopsies were obtained from the myocardium. The LAD was tied and repeat biopsies obtained from the ischemic zone (IZ) and normal zone (NZ) 15 minures and 2 hours later. 46Sc-MS were given just before the final giopsy. Tl activity in the IZ was not significantly different from that in the NZ either before LAD occlusion or 15 minutes and 2 hours later. Tl clearance at the end of 2 hours was not significantly different (27 +/- 5% vs 28 +/- 5%, IZ vs NZ respectively) between the two zones. The half-time of Tl clearance from both the IZ and NZ was calculated at 4.5 hours (consistent with previously reported normal values). This occurred despite a decrease in regional myocardial blood flow to 24 +/- 6% of control (P less than 0.01) in the IZ and an increase to 47 +/- 14% of control (P less than 0.01) in the NZ during the study. We conclude that myocardial ischemia does not alter the normal rate of Tl clearance from the myocardium.
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PMID:The effect of ischemia on thallium-201 clearance from the myocardium. 66 69

Both vasodilator and inotropic agents improve cardiac function in ischemic heart failure. However, since vasodilators may reduce coronary perfusion pressure and inotropic interventions may increase myocardial oxygen consumption (MVO2), both may increase myocardial ischemia. Accordingly, we determined myocardial blood flow and MVO2 in a canine model of failure induced by propranolol and volume load combined with acute coronary ligation. Both nitroprusside and digitalis reduced ventricular diastolic pressure (LVDP) and increased myocardial blood flow in the ischemic subendocardium. Decreased systolic wall tension also caused a significant reduction MVO2. The benefit of nitroprusside in failing hearts was obtained even with the addition of critical obstruction of the main left coronary artery (LCA). The role of preload reduction is emphasized by the contrasting results with nitroprusside in hearts with low LVDP: (1) decreased myocardial blood flow in ischemic subendocardium, and (2) left ventricular decompensation in animals with critical LCA obstruction. Thus, reduction of LVDP, which decreases subendocardial ischemia, is essential for the beneficial effects of vasodilators and inotropic interventions in ischemic heart failure. Decreased MVO2 caused by reduced heart size may also have a salutary role.
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PMID:Mechanisms of beneficial effects of vasodilators and inotropic stimulation in the experimental failing ischemic heart. 68 93

The relationship between progressive depletion of high energy phosphate and the onset of lethal cell injury in ischemic myocardium following coronary occlusion has been evaluated. Myocardial ischemia was induced by proximal occlusion of the circumflex coronary artery for 15, 30, 40, or 60 minutes. Cell injury in the severely ischemic posterior papillary muscle (PP) was evaluated by electron microscopy and by measuring the capacity of slices of the injured PP to maintain electrolytes, resynthesize high energy phosphate, and exclude inulin during in vitro incubation. ATP content in the ischemic myocardium decreased to 35%, 9%, 7%, and 5% of control values after 15, 30, 40, and 60 minutes of ischemia, respectively, and was associated with a corresponding depletion of total adenine nucleotides. The loss of 65% of the ATP after 15 minutes of ischemia (reversible injury) was associated with only minimal ultrastructural changes and no significant defects of electrolytes in incubated slices. However, the depletion of over 90% of the ATP after 40 minutes of ischemia (irreversible injury) was associated with significant fine structural changes and markedly altered cell volume regulation. The results suggest a close relationship between the marked depletion of high energy phsophates and the development of lethal injury in acutely ischemic myocardium.
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PMID:Relation between high energy phosphate and lethal injury in myocardial ischemia in the dog. 68 46

Modern clinicians encounter considerable difficulties in the diagnosis and treatment of ischemic heart disease which is first of all due to insufficient knowledge of the main mechanisms of the development of coronary insufficiency, myocardial dystrophy, myocardial necrosis, and cardiosclerosis. From the point of view of molecular cardiology, myocardial hypoxia cannot be considered as the foundation for ischemic disease. Metabolic insufficiency of the heart both of coronary and non-coronary origin should also be taken into account. Apart from ischemic (coronary) disease, ischemia of the myocardium alongside with metabolic disorders occurs in most diverse conditions and diseases. Therefore, in future this diagnosis will be reconsidered towards a more accurate determination of the causes of these disorders. Examples from clinical practice are presented for the discussion os such causes and mechanisms. A classification of the causes of metabolic heart deficiency and its outcomes is proposed.
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PMID:[Pathogenesis and classification of ischemic heart disease]. 68


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