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)

Myocardial cell pH was measured with 5, 5 dimethyl-2, 4-oxazolidinedione (DMO) in intact anesthetized dogs by a transient indicator dilution technique. Bolus injections of labeled DMO, vascular, extracellular and water indicators were made into the left anterior descending coronary artery, and blood samples were collected from the great cardiac vein. The steady state distribution of DMO between cells and plasma was calculated from the mean transit times of the indicator. Normal myocardial cell pH averaged 6.94 and changed by 58% of the concomitant alterations in plasma pH after infusions of acid or alkali. Myocardial ischemia induced by inflation of a balloon tip catheter in the left anterior descending coronary artery resulted in progressive decreases in cell pH to 6.59 by 1 hour. Infusions of sodium carbonate diminished intracellular acidosis. Hemodynamic studies during 4 hours of ischemia with blood pH at 7.55 to 7.60 indicated a significantly reduced left ventricular end-diastolic pressure and increased stroke volume by comparison with findings in animals given infusions of saline solution. Ventriculograms revealed improved wall motion in the ischemic segment after infusion of alkali. Precordial mapping showed a significant reduction in the number of leads with S-T segment elevation as well as in the sum of S-T segment elevations, but R wave amplitudes did not differ from those in control studies. Calculations of extracellular space, tissue water and cation content revealed a reduced gain of cell sodium ion and loss of cell potassium ion during ischemia after alkali treatment. The latter may account for the S-T segment responses, whereas enhanced ventricular performance may be related to reduced competition of hydrogen ion with calcium ion for binding sites on contractile protein.
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PMID:Myocardial ischemia and cell acidosis: Modification by alkali and the effects on ventricular function and cation composition. 0 59

In 8 patients affected with acute myocardial infarction verapamil was highly effective in controlling ventricular extrasystoles. Theoretically the drug ought not to be effective if the extrasystoles were related to fast cardiac fibers characterized by a rapid inward Na+ current. The result suggests that in acute myocardial ischemia ventricular extrasystoles are related to slow inward Ca++ currents.
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PMID:Effects of verapamil in ventricular premature beats of acute myocardial infarction. 7 83

Cardiac lymph was obtained from 12 normal dogs (group 1) for two consecutive 2-h control periods and from 7 dogs (group 2) for 2 h before and 2 h after occlusion of the circumflex branch of the left coronary artery. Lymph composition was studied with reference to pH, red blood cell (RBC) concentration, total protein content, potassium and sodium ion concentrations, and creatine phosphokinase (CPK) and acid phosphatase enzyme activities. No significant difference was noted in any variable between the two groups during the firts 2-h period. In group 1, no significant changes occurred in any variable as a result of the passage of time alone. In group 2, 2 h of myocardial ischemia produced increases of 53.3 plus or minus 5.1% in lymph flow, 67 plus or minus 5% in protein content, and 418 plus or minus 27% in the RBC concentration, suggesting increased blood capillary permeability. Lactate rose 120.5 plus or minus 27%, potassium concentration increased 16.9 plus or minus 2.4%, acid phosphatase increased 30 plus or minus 3%, and CPK rose 61.6 pluse or minus 10.9%, suggesting ischemic injury of myocardial cells. These changes in lymph were statistically significant (P LESS THAN 0.05) and reflect both capillary and myocardial cell abnormalities.
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PMID:Cardiac lymph flow and composition in acute myocardial ischemia in dogs. 23 6

We prospectively studied the clinical, biochemical (including creatine phosphokinase (CPK) isoenzymes) and electrocardiographic features of exertional heat stroke in 13 patients (group 1) and severe heat exhaustion in 14 patients (group 2). Despite initial presentations with severe hyperthermia, tachycardia and hypotension, only one patient with heat stroke had myocardial ischemia. The CPK isoenzymes were not indicative of myocardial damage in any patient. The patients with heat stroke were somewhat more dehydrated than those with heat exhaustion as measured by differences in serum creatinine, sodium and osmolality, and the former (group 1) had a significantly lower initial glucose level (P less than 0.05). Although significant differences in potassium were not observed in the pretreatment samples, at 12 hours the serum potassium was significantly lower in group 1 (P less than 0.05). This suggests that this group may have been more potassium-depleted at the time of heat stroke. Prompt recognition and vigorous therapy were successful in rapidly lowering high temperatures and in preventing serious complications.
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PMID:Cardiovascular and metabolic manifestations of heat stroke and severe heat exhaustion. 42 71

A prospective study in 12 adult male patients undergoing coronary-artery revascularization was conducted to compare the effects of a morphine versus a halothane anesthetic technique on several indices of myocardial oxygen supply and demand. Indices reflecting myocardial contractility, preload, afterload, and heart rate were measured. Undesirable increases in systemic and pulmonary capillary wedge pressure were minimized using sodium nitroprusside as needed. In the period after sternotomy but before revascularization, patients anesthetized with morphine (mean 2.1 mg/kg) had significant (P less than .05) increases in rate-pressure product, tension-time index, blood pressure, and heart rate, as well as relative myocardial ischemia, evidenced by significant ST-segment depression in the V5 lead of the EKG and a decreased diastolic pressure-time index/tension-time index compared with patients anesthetized with halothane (mean .75 per cent inspired). Few difficulties associated with myocardial depression were seen in patients anesthetized with halothane. Halothane, at least in a well-monitored environment, is safe for use in patients without severe ventricular dysfunction undergoing coronary-artery revascularization.
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PMID:Indices of myocardial oxygenation during coronary-artery revascularization in man with morphine versus halothane anesthesia. 43 35

There have been many reports about ventricular arrhythmias during acute coronary occlusion. Nevertheless, it is only recently that interest has been taken in the occurrence of ventricular arrhythmia after reperfusion following coronary occlusion. To investigate the mechanism of the latter kind of arrhythmia, we studied the effect of changing the duration of occlusion time on the recovery time courses of the VMRT (Ventricular Multiple Response Threshold), and of the A-V differences in the serum K+ concentration across the heart. The time course of delta K+ recovered soon after reperfusion, while changes in VMRT needed more time for recovery to the initial state. Concerning heart rate, blood pH, and the levels of Na+, Cl-, and Ca++, no significant changes were detected. There was no relation between the time courses of VMRT and those of the A-V differences in serum K+. Consequently, time courses in VMRT were dependent upon the duration of coronary occlusion time. A possible explanation for these results may be that the longer the duration of the preceding occlusion time, the more severe the myocardial damage due to myocardial ischemia.
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PMID:An experimental study of release arrhythmia: Occlusion time-dependent changes in ventricular fibrillation threshold. 49 23

In 70 patients with thyrotoxicosis and in 24--with ischemic heart disease with energy-dynamic cardiac insufficiency a study was made of electrolyte metabolism in the blood plasma, erythrocytes and 24-hour urine. The sodium and potassium content in erythrocytes rose, and sodium gradient diminished in the patients examined, this being related to the development of energy-dynamic cardiac insufficiency.
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PMID:[Electrolyte metabolism in thyrotoxicosis with energy-dynamic cardiac insufficiency]. 52 44

Verapamil, at a dose of 1 mg/kg, was given intravenously to anesthetized cats one hour after coronary artery occlusion. Verapamil significantly reduced mean arterial blood pressure, but produced an increase in heart rate, partially offsetting the reduction in myocardial oxygen demand resulting from the reduction in pressure. Verapamil failed to prevent the elevations in the S-T segment of the electrocardiogram observed in cats subjected to myocardial ischemia (MI) and given only the vehicle for verapamil (i.e., 0.9% NaCl). Moreover, verapamil also did not prevent the accumulation of creatine phosphokinase (CPK) activity in the circulating blood after MI. Nevertheless, verapamil significantly prevented the loss in CPK and in amino-nitrogen observed in the ischemic region of the myocardium, indicating some protective effect on myocardial integrity. The major effects of verapamil on electrolyte content of ischemic myocardial tissue were a decrease in sodium and an increase in potassium. However, calcium gain by the heart was not prevented by verapamil. Verapamil, therefore, exerts a partial degree of protection of the ischemic myocardium but exerts some other effects which do not help prevent the spread of ischemic damage in the myocardium.
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PMID:Influence of verapamil on cellular integrity and electrolyte concentrations of ischemic myocardial tissue in the cat. 52 60

The effects of propranolol on periinfarction block, myocardial ischemic injury and left ventricular performance following anterior descending coronary artery occlusion were studied. Experiments were made in 14 dogs anesthetized with pentobarbital sodium. Two minutes of reversible myocardial ischemia was induced by occlusion of descending left coronary artery. The severity of myocardial ischemia estimated by summing S-T segment elevation (sigma ST) from epicardial ECG mapping, heart rate, femoral arterial pressure and left ventricular (LV) dp/dt was determined before, during coronary occlusion alone and following propranolol infusion (0.25 mg/Kg) and coronary occlusion. Periinfarction block aspects on epicardial ECG appeared in four dogs following five repeated coronary occlusions. Propranolol infusion before coronary occlusion prevented the periinfarction block in every animal. The decrease of myocardial ischemia (sigma ST elevation), heart rate, arterial blood pressure and LV dp/dt following propranolol and coronary occlusion might be partly due to the beneficial effect of this drug on periinfarction block.
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PMID:Effect of propranolol on experimental periinfarction block and myocardial ischemia. 59 24

To study the action of aspirin upon the myocardium per se, independent of thrombosis, coronary occlusion with a balloon catheter was induced in 53 anesthetized dogs divided into two groups. One group (N = 20) was treated daily with aspirin (600 mg/dog) for seven days and another (N = 33) was untreated. Left ventricular hemodynamics and precordial ECG mapping were used to assess the influence of myocardial ischemia over a four hour period. There were no significant differences in left ventricular function or extent of injury as judged by ECG mapping between the two groups. However, there was a significant decrease in the incidence of ventricular fibrillation in the treated dogs (5% vs 39%). Serial plasma samples for free fatty acid determination showed a significant rise in the untreated group. Aspirin blocked the FFA increment in the treated animals. Tissue samples from the ischemic area of left ventricle exhibited a significant reduction of the sodium and water increments, as well as a lesser potassium loss in the treated animals compared to the controls and may have been the basis for the lower incidence of arrhythmias. Since infusion of 51Cr labelled platelets showed no myocardial accumulation of platelets in either group, microthrombi did not appear to contribute to the observed differences.
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PMID:Antiarrhythmic effects of aspirin during nonthrombotic coronary occlusion. 63 Jun 76


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