Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of an intracoronary aminophylline infusion, adjusted to give a constant concentration of 25 microgram.cm-3 coronary blood, on the reactive hyperaemic responses following coronary occlusion for 4, 10, and 25 heart beats were investigated in anaesthetised, open-chest dogs. The vasodilator effect of intracoronarily-administered adenosine and the hyperaemic response after coronary occlusion for 10 and 25 heart beats were both significantly diminished under the influence of aminophylline. However, the decrease in the coronary dilator effect of adenosine amounted to 80%, whereas the hyperaemic response was diminished by only 20%. The hyperaemic response following a coronary occlusion for only 4 heart beats remained unchanged. The present results obtained with aminophylline suggest at least a partial involvement of adenosine in mediating reactive hyperaemia after sufficiently long periods of coronary artery occlusion.
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PMID:Effect of aminophylline on coronary reactive hyperaemia following brief and long occlusion periods. 60 74

Inhalation of the equimolecular mixture N2O - O2 rapidly achieves good analgesia in cases of coronary occlusion. This mixture was used with 51 patients (37 to 85 years old) with beneficial results on pain in 4 cases out of 5. This effect can be improved by giving a small amount of pethidine with the inhalation. In this way the respiratory depression of the full dose of narcotic analgesics is avoided. In halation of the mixture does not produce undesirable cardio-circulatory or respiratory changes. The oxygen content of the mixture increases patients' PaO2 without the risk of hyperoxia.
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PMID:[Nitrous oxide analgesia in myocardial infarction (author's transl)]. 60 76

Local oxygen partial pressure in terms of O2-availability and pulsatile intramyocardial pressure of the left ventricular myocardium of anaesthetized open-chest dogs have been measured simultaneously by means of a piezoelectric ceramic and a platinum electrode. The tissue PO2 decreases more slowly than the pulsatile intramyocardial pressure during a transient acute occlusion of the anterior descending branch of the coronary artery. The slow decrease in the tissue PO2 seems to be explicable by the assumption that the local myocardial contractile force decreases quickly due to an unknown factor during the acute coronary occlusion and that the O2-consumption of the local myocardial tissue is reduced in accordance with the rapid decrease in the contractile force.
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PMID:Effects of coronary occlusion on myocardial oxygen and pulsatile intramyocardial pressure. 61 87

The effect of sodium salicylate and acetylsalicylic acid (ASA) on myocardial ischaemic injury following acute coronary artery occlusion has been studied in thoracotomized dogs during basal conditions and during elevation of plasma free fatty acid (FFA) concentration induced by intravenous (i.v.) infusion of isoprenaline (0.075-0.15 microgram/kg/min). Ischaemic injury was measured as the sum of ST-segment elevations (sigmaST) in epicardial ECG recordings from 10-15 sites 15 min after occlusion. Both sodium salicylate and ASA (60 mg/kg) significantly reduced sigmaST both before and during isoprenaline infusion. Arterial concentrations of FFA were reduced by either drug during isoprenaline infusion, whereas in the basal state only a significant effect by sodium salicylate could be demonstrated. The reduction in epicardial ST-segment elevation during coronary occlusion could not be explained by reduced mechanical activity of the heart. It is suggested that the reduction by salicylates of myocardial ischaemic injury might be related to reduced utilization of FFA by the myocardium, although a FFA-nondependent mechanism cannot be excluded in the basal state.
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PMID:Effect of sodium salicylate and acetylsalicylic acid on epicardial ST-segment elevation during coronary artery occlusion in dogs. 61 55

Several invasive and noninvasive techniques used in determining the size of experimental myocardial infarction were evaluated after acute ligation of the left anterior descending (LAD) coronary artery in ten dogs. Systemic blood pressure, left ventricular end-diastolic pressure (LVEDP), and heart rate did not change significantly for up to 24 hours after coronary occlusion. Left ventricular wall motion abnormalities were detected by left ventriculography in the distribution of the LAD but these changes did not correlate well with the infarct weight determined at autopsy. On the other hand, the number of epicardial sites with ST-segment elevation of greater than or equal to 2 mm (mean 15.1 sites +/- 0.6 SEM) and the infarct area as measured by 99mTc-glucoheptonate (TcGH) myocardial imaging (15.7 sq cm +/- 0.6) did correlate strongly with the infarct weight (16.8 g +/- 0.7) determined by the nitroblue tetrazolium (NBT) technique (r = 0.91). TcGH myocardial scintigraphy and epicardial ST-segment mapping allowed early and accurate quantification of experimental myocardial infarcts ranging from less than 1 g to 28 g.
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PMID:Evaluation of methods for the quantification of experimental myocardial infarction. 61 95

In 14 dogs the effects on regional tension (Walton-Brodie gauges) and length (mercury-in-silastic) following 50% reduction (52.9 +/- 2.1) in coronary flow for two hours and reperfusion afterwards for one hour were addressed. Within five minutes of partial coronary occlusion, ejection tension in the ischemic zone decreased to 36.3 +/- 7.2% (P less than 0.001) and total tension to 64.4 +/- 5.7% of control (P less than 0.001) while phasic segment length increased to 165.2 +/- 16.3% control. No further significant changes in regional tension or length were observed throughout the two hour period of partial occlusion. Ejection tension remained positive and segment length maintained systolic shortening during the ejection phase throughout the period of occlusion. Following reperfusion, ejection tension in the ischemic zone increased from 35.1 +/- 5.9 to 87.0 +/- 22.0% (P less than 0.05) and total tension increased from 56.6 +/- 5.4 to 70.2 +/- 7.2% (P less than 0.02) while segment length decreased from 149.3 +/- 6.5 to 105.7 +/- 5.7% (P less than 0.001) within five to 15 min of reperfusion. The improvement in both regional tension development and segment length shortening was maintained throughout the one hour period of reperfusion. No significant changes were seen in the nonischemic zone. The present experimental study suggests that partial coronary occlusion producing a 50% reduction in coronary blood flow results in regional contractile changes. These changes are reversible at least twice as long as those following complete occlusion.
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PMID:Effects of reperfusion on the regional contraction of ischemic and nonischemic myocardium following partial coronary obstruction. 61 97

There is evidence that glucocorticoids reduce infarct size but their use in myocardial infarction remains controversial because of their potential adverse effects on healing of the infarct. To investigate the healing process, rats received either four parenteral doses of 50 mg/kg of methylprednisolone (MP) or saline 5 min, 3,6 and 24 hr after coronary occlusion and their hearts were examined by light and electron microscopy 48 hr and seven days after occlusion. At 48 hr, in five untreated rats, only 12 +/- 7% of injured myocytes showed the persistence of striations and a relatively intact sarcolemma despite loss of nuclei and hence appeared "mummified" whereas in six MP-treated rats 72 +/- 8% of myocytes exhibited this appearance (P less than 0.001). In treated rats there were fewer phagocytes than in controls. At seven days, in seven MP-rats, mummified cells were still more prominent than in five untreated rats and there were fewer phagocytes and less collagen. In conclusion, high dose of MP delays the inflammatory process and retards the disintegration of necrotic myocytes, resulting in impaired healing.
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PMID:Mummification of the infarcted myocardium by high dose corticosteroids. 61 98

An association of coronary artery occlusion, as determined by coronary arteriography with age, prevalence of risk factors and alcohol intake was studied in 1635 male and 371 female heart patients. The degree of coronary artery occlusion was positively related to elevated cholesterol, elevated triglycerides, diabetes, age and history of smoking for both male and female patients. Hypertension was related to the degree of occlusion only for female patients. Male and female patients who had a higher alcohol intake tended to have less extensive occlusion. No positive association was found between obesity and the degree of occlusion. When the patients were divided on the basis of age (less than 50 and greater than or equal to 50 years) the findings did not differ. The lack of finding a relation between obesity and occlusion or between hypertension and occlusion for males differs from the general findings of epidemiologic studies on the relation between these risk factors and coronary heart disease. The authors believe that this discrepancy may either be explained by the way they selected patients (i.e., they selected patients who underwent a diagnostic angiographic examination), or that obesity and hypertension are not directly related to coronary occlusion but influence occlusive disease through some secondary mechanism.
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PMID:Risk factors and angiographically determined coronary occlusion. 62 92

Myocardial creatine phosphokinase (CPK) activity and myocardial blood flow (MFB, 15 +/- mu microspheres) were measured at 24 hours after ligation of the left anterior descending coronary artery in nine untreated anesthetized dogs, in eight dogs pretreated with intravenous propranolol 5 mg/kg and in eight which had both pretreatment as well as infusion of propranolol (1.25 mg/kg/hour) after occlusion. Loss of CPK activity from the border and center zones of the myocardial infarct was similar in extent in dogs which had pretreatment but no infusion of propranolol as it was in the control group. Loss of CPK from the center zone was greater (P less than 0.005) in dogs receiving pretreatment followed by constant infusion of the drug. Propranolol had no significant effect on collateral blood flow to the border or center zone of the infarct. In separate experiments, there was no important difference in hemodynamic measurements, except a slower heart rate (P less than 0.01), when pretreated dogs were compared with control dogs up to 2 hours after coronary ligation. We conclude that propranolol given in this dose does not influence nyocardial damage, on the basis of regional myocardial blood flow or tissue CPK depletion values at 24 hr after coronary occlusion.
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PMID:Failure of high doses of propranolol to reduce experimental myocardial ischemic damage. 62 62

The effects of coronary occlusion and of subsequent propranolol and ouabain administration were examined in 12 conscious dogs. Overall left ventricular (LV) function was assessed by measurement of LV pressure and dP/dt, and regional myocardial function was assessed by measurements of segment length (SL), velocity of SL shortening and regional myocardial "work," i.e., pressure-length loops in normal and moderately and severely ischemic zones. Regional intramyocardial electrograms were measured at the same sites as function along with regional myocardial blood flow as determined by the radioactive microsphere technique. Coronary occlusion resulted in graded loss of function from the normal to severely ischemic zones, along with graded flow reductions and graded elevation of the ST segment. Propranolol, 1 mg/kg, depressed overall LV function and function in the normal zone more than in ischemic zones. Propranolol reduced flow to the normal zone and increased flow to ischemic zones, while not affecting ST-segment elevation significantly. In the presence of occlusion and propranolol, ouabain, 20 microgram/kg, improved overall LV function as well as regional function in the normal, moderately ischemic and severely ischemic zones. In addition, ouabain reduced ST elevation and increased blood flow further in moderately and severely ischemic zones. Most strikingly, ouabain returned normal systolic shortening to eight severely ischemic segments which were previously akinetic.
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PMID:Effects of a cardiac glycoside in combination with propranolol on the ischemic heart of conscious dogs. 62 66


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