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

Midmyocardial and subendocardial pH monitoring was used as an indirect method for continuous evaluation of regional canine myocardial ischemia. Left ventricular midmyocardial pH (pHm) at 4 mm. depth was monitored in 10 dogs, under resting conditions, by means of a 5 mm. Beckman pH probe. pHm was 6.96 +/- 0.03, recorded at myocardial temperatures of 35 to 37 degrees C. Ischemia was then produced by snare occlusion of the proximal left main coronary artery for 2 minutes. pHm decreased to 6.87 +/- 0.03 (p less than 0.01) at 1 minute and 6.80 +/- 0.04 (p less than 0.005) in 2 minutes. When flow was restored, pHm returned toward normal within 2 minutes (pH 6.86 +/- 0.03) and at 5 minutes had returned to control values (pH 6.93 +/- 0.03). In another 5 dogs under similar conditions, pHm at 4 mm. and subendocardial pH (pHe at 8 mm.) were measured. Baseline pHm (6.97 +/- 0.01) and pHe (6.84 +/- 0.02) levels were significantly different (p less than 0.0005). After 2 minutes of ischemia, pHm was 6.82 +/- 0.03, whereas pHe decreased to 6.78 +/- 0.04 (p less than 0.1). Five minutes after snare release, pHe remained at 6.73 +/- 0.07; pHm (6.93 +/- 0.03) returned to control values. Both pHm (6.93 +/- 0.02) and pHe (6.84 +/- 0.09) levels were normal 15 minutes after release of the snare. The midmyocardium and subendocardium have different pH levels which can be monitored. Ischemia produces different pH patterns in these layers. pHm returns to control values within 5 minutes after 2 minutes of ischemia, whereas pHe remains depressed for at least 5 minutes. pH monitoring provides an accurate and simple method for on-line evaluation of endocardial ischemia.
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PMID:Monitoring of midmyocardial and subendocardial pH in normal and ischemic ventricles. 0 26

To assess possible coronary vasoconstriction in patients with ischemic heart disease, we measured coronary vascular resistance in 12 patients with normal hearts and 12 with coronary disease before and during the initial 50 seconds of cold pressor test, a stimulus known to produce systemic vasoconstriction. Control coronary vascular resistance was similar in the two groups, and although it did not change in patients with normal vessels, it rose by 27 per cent (P less than 0.005) in the group with coronary disease during the cold pressor test. In three of 12 patients with coronary disease coronary flow actually declined despite an increase in arterial pressure; in four, angina was precipitated. Phentolamine abolished increases in arterial pressure and coronary vascular resistance during the test in three patients with coronary disease. Adrenergically mediated coronary vascular tone may be an important determinant of coronary blood flow and may contribute to ischemia in patients with coronary disease.
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PMID:Reflex increase in coronary vascular resistance in patients with ischemic heart disease. 1 May 27

The indices of central hemodynamics and myocardial contractile function were studied in 35 dogs before and in different periods after the administration of drugs which block beta-receptors: propranolol, pindolol, and talinolol. The drugs blocking the beta-adrenergic receptors were administered against the background of an intact myocardium to 15 dogs and against the background of acute coronary insufficiency to another 15; acute ischemia was induced in 5 dogs to which the drugs were not given. It was established that beta-adrenergic blocking agents have a beneficial effect in the acute stage of myocardial ischemia; they exert a marked influence on the consumption of oxygen by the myocardium, intramyocardial tension, and the contractile capacity and rhythm of the heart. Talinolol produced the most favourable effect.
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PMID:[Effect of blockaders of cardiac beta-adrenergic structures on the central hemodynamics and contractile function of the myocardium in acute experimental coronary insufficiency]. 4 59

Phosphorylation rates of canine heart mitochondria isolated after various periods of myocardial ischemia after cardioplegic arrest were correlated with the myocardial ATP-, lactate- and undissociated lactic acid content as well as with interstitial H+-concentration. The following correlation coefficients were found: ATP: 0.87, lactate: 0.93, interstitial H+: 0.73. The calculated undissociated lactic acid content and the mitochondrial phosphorylation rate during ischemia showed a correlation coefficient of r = 0.95. Swelling measurements of mitochondria, isolated immediately after cardioplegic arrest, demonstrated that an undissociated lactic acid- and an ATP-concentration of 70 microM and 28 microM respectively are necessary for a half maximal swelling reaction under anaerobic conditions. The results suggest that the accumulation of undissociated lactic acid during myocardial ischemia could play an important role for mitochondrial damage in vivo.
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PMID:The role of ATP and lactic acid for mitochondrial function during myocardial ischemia. 4 43

Left atrial-to-aortic (La-A) assistance is effective in supporting the failing circulation. This study evaluated its effect in salvaging ischemic myocardium in both large and small infarct models. In a control group, good correlation was shown between measurements of infarct size by ST-segment mapping at 20 minutes, triphenyl tetrazolium chloride staining at 5 hours, and the distribution of radioactive microspheres (P less than 0.01). A servo controlled assist pump was used which controlled pump speed according to the left atrial pressure. This allowed greater degrees of bypass for prolonged periods with reduced risk of air embolism. La-A assistance reduced systolic left ventricular pressure, and reduced the pressure time index (P less than 0.05). La-A assistance did not reduce infarct size measured by ST-segment mapping in a large infarct model when instituted before occlusion or 20 minutes after occlusion. Triphenyl tetrazolium chloride staining, however, showed less severe and homogenous damage in the assisted group as compared to controls. Electron microscopy confirmed the patchy nature of the ischemia. In a small infarct model, La-A assistance reduced nST from 6.3 +/- 0.8 to 3.8 +/- 1.5 and ST from 4.9 +/- 0.6 to 2.7 +/- 0.9 (P less than 0.05). The endocardial to epicardial ratio in the ischemic area fell from 0.69 +/- 0.05 to 0.43 +/- 0.05 in the control group (P less than 0.05) and a similar fall occurred in the assisted groups. La-A assistance is thus effective in reducing myocardial ischemia in a small infarct model, but appears to be less effective in a large infarct model.
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PMID:The effect of left atrial-to-aortic assistance on infarct size. 6 5

Strength-interval curves and conduction times were determined in anesthetized dogs during and following myocardial ischemia using a computerized system capable of determining a 5 point strength-interval curve with conduction times within 20 seconds. At the peak incidence of ligation arrhythmias (5 minutes of ischemia), the falling limb of the strength-interval curve was shifted to the left and conduction time was prolonged, while at 15 minutes of ischemia, the strength-interval was shifted upward and conduction times had returned toward control. Lidocaine enhanced the upward shift of the strength-interval curve, contributing to the electrical stability of the myocardium during this phase of ischemia. During the first minute following abrupt reperfusion of the ischemic zone, there was a slight downward shift of the early part of the strength-interval curve, and conduction times tended to be shorter than control. Lidocaine enhanced the electrophysiological alterations following abrupt reperfusion; that is, it reduced excitation thresholds and increased the tendency to superconductivity. Thus, lidocaine enhanced electrical stability during acute ischemia but tended to exaggerate electrophysiologic defects observed during abrupt reperfusion.
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PMID:Time course of changes in ventricular excitability and conduction during myocardial ischemia and reperfusion in the dog: effect of lidocaine. 8 80

The electric stimulation of the lateral ventricular walls carried out in experiments on dog heart (open-thorax), as well as the analysis of the clinical, radiological and electrocardiographic data recorded in 462 cases with QRS macrovoltage led to the following conclusions: a) in 22% of the cases (hospital cardiologic examinations) this anomaly cannot be accounted for either by age, blood pressure or cardiac hypertrophy; b) a temporarily perturbed development of the ventricular depolarization, i.e. a "jerky" depolarization, not stagnant enough to produce an intraventricular block, may generate great negativity and positivity myocardial masses responsible for the appearance of large dipoles, namely of the increased QRS voltage; c) the coincident ischemia and macrovoltage of the QRS major wave, as well as the subsequent evolution of incipient CHD in a series of patients point to the hypothesis according to which the regional myocardial ischemia may induce a QRS macrovoltage by means of the above mechanism.
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PMID:Mechanisms and significance of QRS macrovoltage in the absence of cardiac hypertrophy. 10 95

The effects of nitroglycerin on regional left ventricular performance, assessed by echocardiographic techniques, were investigated in anesthetized, open-chest dogs during acute myocardial ischemia. During transient occlusion of the left anterior descending coronary artery, there was end-diastolic thinning and marked reduction in systolic thickening in the central ischemic zone. Similar changes of lesser degree were noted in the border zone. The normal zone was unaffected. Infusion of nitroglycerin during ischemia in dosages of 2.5--50 microgram/kg/min reduced left ventricular end-diastolic pressure without changing the abnormalities of systolic wall thickening. Effects of bolus injections of 20 and 50 microgram/kg of nitroglycerin were similar, although this also lowered aortic pressure. In a subgroup of animals in which nitroglycerin infusion was unaccompanied by tachycardia, there was also no evidence that ischemic dysfunction was altered. We conclude that nitroglycerin does not improve regional myocardial performance in acutely ischemic canine myocardium. The decrease in preload is probably entirely due to the peripheral effects of the agent.
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PMID:Effects of nitroglycerin on echocardiographic measurements of left ventricular wall thickness and regional myocardial performance during acute coronary ischemia. 10 86

Sixty-two autopsied hearts, with left ventricular hypertrophy (LVH) caused by mitral regurgitation (MR), aortic failure (AR), combined valvular disease (CVD), hypertension (HHD), or ischemia (IHD), and 23 control hearts with normal left ventricles were studied morphologically for analysis of modes of hypertrophy and for ECG-pathology correlation. Basic disorders modify the mode of hypertrophy; that is, elongated AR-type LV makes muscle fiber orientation in the outer layer more vertical, and globular MR-type LV makes it more horizontal than normal. High-voltage QRS correlates with hypertrophy of the outer layer which is often associated with that of the inner layer. ST depression and T changes correspond to relative deterioration of the inner and median layers, respectively.
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PMID:Histopathological study of hypertrophied myocardium of known etiologies with special reference to correlation of ECG changes. 14 36


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