Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to determine the incidence of ST-segment depression during anesthesia and operation. Graded exercise testing has demonstrated a high correlation between ST-segment depression and myocardial ischemia. Therefore, 11 patients without and 29 patients with known coronary-artery disease were monitored during surgical procedures with a commercially available exercise electrocardiographic monitor (Viagraph). Comparisons were made between this device, which monitored lead V5, and the standard operating room monitor, which monitored lead 11. Eleven of 29 patients in the disease group demonstrated significant ST depression. Nine of the 11 ischemic episodes were not recognized on the standard operating room monitor. Retrospective review of anesthetic records of those 11 patients with ST-segment depression revealed rate--pressure product values greater than 11,000 for ten of them. Postoperatively, three of the 11 patients with significant ST-segment depression had changing electrocardiograms compatible with ischemia. None of the control group demonstrated significant ST-segment depression. The incidence of ischemia was 38 per cent during anesthesia and operation in the coronary-artery-disease group. Lead V5 analysis is superior to lead 11 analysis in detecting ST-segment depression. The period in which intubation is performed is one of the highest-risk intervals during anesthesia and operation, particularly when it is associated with an increased rate--pressure product.
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PMID:Myocardial ischemia during non-cardiac surgical procedures in patients with coronary-artery disease. 49 52

The purpose of this study was to determine whether a quantitative relationship existed between a reduction in regional myocardial blood flow, measured by radiolabeled microspheres, and the degree and type of changes in myocardial activation recorded in bipolar left ventricular subepicardial and subendocardial electrograms, in open-chest dogs following acute coronary artery occlusion. We found that the degree of regional myocardial ischemia was related quantitatively to the reduction in amplitude recorded with bipolar electrograms in the subepicardium and subendocardium, and to the increase in duration of subepicardial electrograms. Other characteristics measured in electrograms did not relate to the degree of ischemia. Despite a comparable reduction in regional myocardial blood flow, subepicardial conduction delay exceeded that recorded in the subendocardium, which often exhibited accelerated conduction.
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PMID:Relationship between changes in left ventricular bipolar electrograms and regional myocardial blood flow during acute coronary artery occlusion in the dog. 49 40

Twenty-two cat hearts were perfused according to Langendorff technique and myocardial regional ischemia was induced by occlusion of left anterior coronary artery. Separation of particulate (bound) from soluble (free) fraction, and subsequent fractionation into plasma membranes, lysosomes, sarcoplasmic reticulum, and mitochondria were performed by sucrose density gradient ultracentrifugation. By ischemia for 60 min, particle-bound activity of cathepsin D decreased from 4.2 +/- 0.24 U/mg protein to 3.2 +/- 0.31 U/mg protein (p less than 0.01). Likewise, the particle-bound activity of beta-glucuronidase decreased from 11.9 +/- 0.92 U/mg protein to 6.2 +/- 1.28 U/mg protein (p less than 0.01). Accordingly, free/bound activity ratios of cathepsin D increased from 0.8 to 1.9 and beta-glucuronidase from 0.9 to 2.8, respectively. Conspicuous fall from 12.8 +/- 0.6 U/mg protein to 8.0 +/- 0.97 U/mg protein (p less than 0.01) in absolute specific activity of cathepsin D bound to the lysosomal fraction, presents definitive evidence of lysosomal release of the acid hydrolases during the early phase of myocardial ischemia. Electron microscopic observation of the ischemic myocytes revealed ultrastructural alterations of the lysosomes suggestive of autophagic degradation of various subcellular organelles.
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PMID:Lysosomal hypothesis in evolution of myocardial infarction. Subcellular fractionation and electron microscopic cytochemical study. 50 30

It is shown that the diffusion capacity of the capillary channel diminishes in myocardial ischemia. In unchanged or increased capillary permeability this effect may only be explained by a functional shunt of the affected cardiac area. Intracoronary administration of a carrier of biologically active substances in the form of microspheres of modified Sephadex does not aggravate irregularity in the blood supply to the zone of ischemia, which is evidence of the adequacy of the organ reserves of the functional shunt in this situation.
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PMID:[State of the microcirculation in myocardial ischemia and its alterations after depositing bioresorbing microspheres of Sephadex in the coronary bed]. 50 68

Potassium (34 mEq/L) cardioplegia was induced with cold blood (CBK) in three groups of six dogs undergoing 60 minutes of myocardial ischemia at a systemic temperature of 27 degrees +/- 2 degrees and a myocardial temperature of 7 degrees +/- 2 degrees C (crushed ice). Group 1 (CBK) animals were reperfused initially with 400 ml cold blood over 8 to 10 minutes at increasing pressures of up to 75 mm Hg. Group II (CBK-K) dogs were reperfused in the same manner as Group I with the addition of potassium chloride, 30 mEq/L. In Group III (CBKG-KG) glutathione, 30 mg/100 ml, was added to both the pre- and postischemic perfusions with CBK. After 30 minutes of reperfusion control studies were repeated. Heart rate, peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of contractile element, pressure-volume curves, coronary flow distribution, muscle stiffness, and heart water were not significantly different from control values. Total coronary flow and myocardial uptake of oxygen, lactate, and pyruvate did not serve to separate the three groups; the same was true for right ventricular creatine phosphate, adenosine triphosphate, and adenosine diphosphate during ischemia and recovery. Ultrastructural myofibrillar lesions were noted in all groups. thus, postischemic cardioplegia and use of a physiological reducing agent do not enhance CBK cardioplegia with topical and systemic hypothermia.
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PMID:Cold-blood potassium cardioplegia: evaluation of glutathione and postischemic cardioplegia. 50 72

Right ventricular hemodynamics were evaluated in 179 patients with coronary artery disease to determine the effects of chronic ischemia on right ventricular diastolic pressure. Abnormal right ventricular filling pressures occurred only in patients with an abnormal right ventricular systolic pressure or an abnormal left ventricular end-diastolic pressure. Of the 63 patients whose right ventricle was stressed by an increased systolic load secondary to passive pulmonary hypertension, 44 (72 percent) had an abnormal right ventricular end-diastolic pressure. In this group obstruction of vessels serving the right ventricular free wall or septum, or both, was almost universal (43 of 44, 98 percent) and a significantly increased incidence of inferior infarction (P less than 0.05) was noted. Such obstruction was significantly less frequent in patients with normal filling pressures (10 of 17, 59 percent; P less than 0.001). Compared with patients with coronary artery disease, patients with passive pulmonary hypertension due to aortic stenosis or mitral stenosis had significantly greater degrees of pulmonary hypertension (P less than 0.05) yet slightly lesser elevations of right ventricular end-diastolic pressure. These data suggest that in patients with ischemic heart disease the right ventricle exhibits diastolic dysfunction at lower levels of afterload stress than it would with normal coronary blood flow.
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PMID:Right ventricular diastolic pressure in coronary artery disease. 50 30

Hypertensive crises were studied in 80 patients. In severe cases the ECG provided evidence of systolic overloading of the left ventricle with intensification of coronary circulation and development of acute myocardial ischemia. Phase analysis showed prolongation of the mechanical systole with increase of the myocardial index. In more complicated cases there was a more evident hypodynamic syndrome with marked myocardial insufficiency. Hemodynamic disturbance were marked by a sharply increased peripheral resistance with a heterogenous reaction of the cardiac output. Blood supply to the cerebral tissue reduced sharply with an increase in the resistance of cerebral vessels. Renin activity was directly related to the severity of the crisis. A sharp onset of cerebral and cardiac ischemia was marked by changes in the antigen albumin. Timely diagnosis and differentiated treatment made it possible to avoid vascular complications in hypertensive crisis.
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PMID:[Clinical aspects of hypertensive crises]. 51 73

The effect of repeated local ischemia and reperfusion on myocardial metabolism and ventricular performance was studied in 12 open-chested pigs fasted overnight. Myocardial ischemia was induced by reduction of the flow in the left anterior descending coronary artery to 40% of control during 30 min. After 35 min of reperfusion a second 30-min occlusion period was started, again followed by a 35-min reperfusion period. At the end of both reperfusion periods coronary flow and coronary resistance had returned to control values. During control there was lactate uptake, but no significant uptake of glucose, free fatty acids (FFA), triglycerdies, glycerol and inosine. During the first occlusion period the heart released lactate and inosine, and used glucose and FFA. At the end of the first reperfusion period lactate uptake approached control values, but inosine was still released by 10 of the 12 animals. In the second ischemic period, glucose and FFA were again taken up. Lactate and inosine were released, but the production was much smaller than during the first occlusion period. Depletion of myocardial glycogen and high-energy phosphates could be responsible for this quantitatively different response. Necrosis may have played a role, although enzyme release was minimal and only observed after the second occlusion period. Heart rate, peripheral resistance and ventricular filling pressure were virtually unchanged throughout the course of the experiments. Maximum rate of fall of left ventricular pressure (min LVdP/dt) decreased during ischemia and did not recover during reperfusion. Changes in min LVdP/dt and cardiac output were more closely related than changes in max LVdP/dt and cardiac output. This model cannot be used for the study of interventions during myocardial ischemia in which the animal serves as its own control.
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PMID:Myocardial substrate utilization and hemodynamics following repeated coronary flow reduction in pigs. 52 55

The effect of verapamil on ST changes was evaluated in 10 selected patients with acute myocardial infarction admitted to the Coronary Care Unit within 8 hours after the onset of symptoms. To evaluate the extent of ischemia it has been used the magnitude and direction of the ST vector derived from X, Y and Z leads of the Frank vector system. After a control period of 2 hours, during which the changes of the ST vector magnitude were assessed, each patient received 0.1 mg/Kg verapamil intravenously, ST vector magnitude (STVM), ST azimuth (STAZ), ST elevation (STEL), heart rate, systemic blood pressure and pressure-rate product were assessed 5, 15, 30, 45, 60, 75, 90, 105 and 120 minutes after the administration of the drug. Verapamil produced a significant progressive decrease in STVM (from a mean of 254 +/- 44 muV at the end of the control period, to 139 +/- 25 muV after 2 hours; P < 0.01). Systolic blood pressure decreased significantly throughout the trial; the most significant decrease was registered immediately after the infusion of verapamil (from a mean of 134 +/- 3 mmHg to 121 +/- 3 mmHg; P < 0.001). Pressure-rate product declined slightly. No significant change in STVM was observed in 10 control patients with acute myocardial infarction examined over a 4 hours period. The apparent protective effect of verapamil in myocardial ischemia is discussed in relation to its calcium-antagonistic properties in excitable tissues.
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PMID:[Effects of acute infusion of verampil on the ST segment elevation measured with the Frank orthogonal leads in patients with acute myocardial infarct]. 54 89

The hypothesis was investigated that cigarette smoking obstructs the blood flow response that develops as a protection against tissue damage in an organ subjected to ischemia (reactive hyperemia). Forearm blood flow was recorded at rest and following forearm ischemia before and after cigarette smoking in healthy male and female volunteers. The experiments were also repeated after pre-treatment of the subjects with indomethacin, a prostaglandin synthesis inhibitor. Before pre-treatment with indomethacin, ischemia induced a reactive hyperemia amounting to 20 +/- 4 ml/100 ml tissue. This hyperemia was significantly (p less than 0.01) reduced by cigarette smoking, to 12 +/- 3 ml/100 ml tissue. After indomethacin, which in itself lowered the reactive hyperemia to 8 +/- 2 ml/100 ml tissue, smoking did not elicit any effect. It is suggested that smoking counteracts reactive hyperemia in tissues by interfering with the same physiological mechanism as indomethacin, i.e. with the vascular formation of PG. The possible significance of this observation in relation to cigarette smoking and ischemic heart disease is stressed.
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PMID:Cigarette smoking, prostaglandins and reactive hyperemia. 55 Jan 58


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