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Query: UMLS:C0151814 (coronary occlusion)
3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship between ultrasonic attenuation and collagen content is examined in hearts from normal dogs and in hearts from dogs subjected to ischemic injury by coronary occlusion as an approach toward elucidating the physical mechanisms responsible for the attenuation of soft tissue. Increased ultrasonic attenuation is shown to correlate well with increased collagen concentration determined biochemically in regions of ischemic injury studied 2, 4, and 6 weeks following occlusion. Extrapolation of experimentally determined relationship between attenuation and collagen concentration suggests that collagen is responsible for not more than 15% of the attenuation observed in normal myocardium. These results indicate that collagen appears to be the principal determinant of the elevated attenuation detected in regions of myocardial infarction, but is apparently not the primary determinant of the attenuation of normal myocardium.
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PMID:The relationship between collagen and ultrasonic attenuation in myocardial tissue. 48 19

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

The effect of mild hemodilution (hematocrit, 19%) on ischemic and nonischemic regions of myocardium during acute coronary occlusion was studied in 41 pentobarbital-anesthetized, open-chest New Zealand white rabbits. Blood flow in the control area determined with radioactive microspheres was unaffected by occlusion and increased 61.8% following hemodilution. The endo/epi ratio remained at about 1.0. Occlusion decreased flow in the affected region to 41% of the control myocardium, and endo/epi ratio decreased significantly to 0.76. Hemodilution raised flow in this area 84.3%. Occlusion increased small vessel blood content (a measure of open capillary density) in the ischemic region significantly. Hemodilution further significantly increased this volume in the occluded area, although the increase in the control region was not significant. Relative tissue pO2, measured polarographically, declined significantly following occlusion in the affected area. Isovolemic hemodilution did not affect relative O2 tension in either area. The data indicate that during mild hemodilution, the O2 supply-demand status of both the occluded and nonoccluded myocardial regions is maintained.
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PMID:The effects of mild normovolemic hemodilution on regional flow, oxygenation, and small vessel blood content in the rabbit heart subjected to acute coronary occlusion. 49 27

We studied the effect of exercise training on the coronary collaterals that developed in response to gradual coronary occlusion in dogs. After their proximal left circumflex coronary artery occlusion, 33 dogs were randomly assigned to exercise or sedentary groups. Coronary collateral function was evaluted 5 weeks or 8 weeks later. The exercised dogs developed better epicardial collateral connections to the occluded left circumflex as judged by higher retrograde blood flow from the distal left circumflex and lower pressure drop across the collaterals. No difference in collaterals was apparent angiographically. Microsphere data indicated that exercise dogs were not better protected against tachycardia provoked subendocardial ischenia in the myocardium supplied by the collaterals.
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PMID:Exercise can promote coronary collateral development without improving perfusion of ischemic myocardium. 49 79

Acute occlusions of the left circumflex coronary artery were performed in open-chest dogs. A control group (n = 19) was compared with three groups (total n = 17) pretreated once daily with different doses of the cardioselective beta-blocking drug atenolol (ICI 66 082) given by mouth for 5 days. Only animals without coronary collateral vessels were examined, having a mortality rate of 100% in the control group. Arrhythmias and ventricular fibrillation during the first 30 min after coronary occlusion showed a biphasic distribution in time (phase 1a and 1b). A lower degree of beta-adrenoceptor blockade reduced the incidence of arrhythmias and ventricular fibrillation in phase 1a, but fibrillation occurred in all animals during phase 1b. A higher dose of the beta-blocking drug protected the animals from ventricular fibrillation, and arrhythmias in phase 1a were greatly reduced. At all times the ventricular fibrillation threshold in the group pretreated with atenolol was significantly higher than in the control group. In both groups a significant decrease in ventricular fibrillation threshold was found only during phase 1a. The greater sensitivity of phase 1a arrhythmias to beta-blockade and the lack of a decrease in ventricular fibrillation threshold during phase 1b might indicate differences in the genesis of arrhythmias and fibrillation in phases 1a and 1b.
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PMID:Prophylaxis of ventricular fibrillation after acute experimental coronary occlusion by chronic beta-adrenoceptor blockade with atenolol. 51 61

Effects of Theo-Esberiven, a coronary vasodilator, on the development of collateral circulation were investigated in dogs with their left anterior descending artery chronically occluded. The drug was administered i.v. at 0.1 ml/kg once a day for 1 to 4 weeks after the occlusion. Left circumflex coronary flow in dogs treated with the drug was increased over the value in control ones when measured one week after the occlusion. At the same time, the ratio of retrograde pressure to perfusion pressure, which correlates negatively with the collateral vascular resistance, significantly exceeded the value in control (P less than 0.05). On the basis of observations with blood vessel casts of hearts, distinct anastomoses between the circumflex and anterior descending arteries had already been observed in all preparations from dogs treated for 2 weeks in contrast to the findings seen in control ones. There were less histological changes in myocardial tissue obtained from dogs treated for one week than those in control ones. From these results, Theo-Esberiven appears possibly to accerelate the collateral development at the earlier stages after the coronary occlusion.
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PMID:Effects of theo-esberiven on the development of collateral circulation in dog hearts. 54 41

The time course of changes in VFT was determined during the 1st phase of arrhythmia following coronary occlusion and during consecutive reperfusion in five repeated periods of occlusion and reperfusion in 10 mongrel dogs (17--24 kg). VFT was determined using a square wave pulse series of 140 ms duration which was triggered by the R-wave of the ECG and placed into the vulnerable period of the cardiac cycle. After acute occlusion VFT decreased to a minimum level within a few minutes and then increased again slowly up to the control value which was reached about 20 min after the ligation. When the occlusions were repeated several times the extent of the decrease in VFT became increasingly less and its duration increasingly shorter until finally there was no significant decrease in VFT. Reperfusion after coronary occlusion led to an abrupt decrease in VFT within 1 min, followed by a rapid increase to the control value. This time course did not depend upon the number of prior occlusions. The results show that in the case of repeating short-term coronary occlusions one cannot expect comparable VFT time courses for the consecutive periods of occlusion except for the 1st and 2nd ones. Differing mechanisms leading to the occurrence of VF after coronary ligation and during reperfusion are discussed.
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PMID:Changes in ventricular fibrillation threshold during repeated short-term coronary occlusion and release. 58 6

In previous publications (1,2) the hypothesis was put forward that atheroma is caused by some pathogen or metabolic fault which impairs the transportability of cholesterol in the plasma. The lipoproteins containing the faulty metabolites are assumed to be incapable of traversing the capillary endothelium and continue to circulate uselessly in the blood stream, possibly giving rise to hypercholesterolaemia, until captured by lipophages which, if they can successfully complete their journey, void them into the gall bladder. The present paper takes the argument a step further by pointing out that the types of substances most likely to cause the described impairment are surfactants. A surfactant finding its way into the plasma could separate cholesterol from its carrier protein and itself become its carrier. The complex would still be kept in suspension in the plasma, but unable to cross biological barriers like the capillary endothelium. An important argument in favour of the hypothesis is that it can offer an explanation of the long-standing medical mystery of the connection between atheroma and the hardness or softness of the water supply. Infant deaths from coronary occlusion present a similar enigma. The paper points out that surfactants can conceivably find their way into infants' feeding bottles.
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PMID:Surfactants and atherogenesis. 59 83

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

The validity of a new noninvasive device, the cardiokymograph, was assessed as to its ability to detect regional myocardial wall motion by direct comparison of the analog tracing with that of an epicardial length gauge in 11 open-chest dogs. The correlation of the two methods was excellent both during control conditions and following changes induced by acute coronary occlusion. The average difference between the methods in timing of various cardiac events was only 6.2 +/- 1.9 ms at rest and 6.8 +/- 1.5 ms following ischemia (P = NS). Relative amplitude ratio correlations, determined for the four portions of the cardiac cyele (isovolumic systole, ejection, isovolumic relaxation, and diastole), were also excellent. The average correlation of the kymograph to the length gauge was r = 0.896 +/- 0.018 at rest (K = 0.977 LG + 0.033) and r = 0.932 +/- 0.013 following occlusion (K = 1.071 LG + 0.101). Thus, the cardiokymograph is a sensitive and accurate noninvasive method for detection of regional ischemic dysfunction and produces an analog tracing essentially identical to that of the epicardial length gauge.
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PMID:Noninvasive analysis of regional myocardial wall motion: cardiokymography. 59 68


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