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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Contractile dysfunction is characteristic of the acutely ischemic myocardium. This study was undertaken to assess the temporal relations between the onset of cell anoxia and ischemic contractile failure in isolated, isovolumetric contracting rabbit hearts. High speed epicardial fluorescence photography using reduced nicotinamide adenosine nucleotide (NADH) was used to identify areas of cell anoxia. The onset of ischemia was correlated with deterioration of pressure generation over the course of sequential 60 second coronary arterial occlusions. In the isovolumetric contracting rabbit heart, areas of ischemia were detected 2 seconds after coronary occlusion. Significant reduction in peak systolic pressure occurred at 6 seconds of ischemic time and pressure continued to decrease throughout the 60 second period of coronary occlusion. NADH accumulation indicates imbalance of myocardial oxygen supply and demand and the cessation of oxygen utilization by the mitochondria. The results of this study indicate that ischemia is detectable within 1 to 2 seconds after coronary occlusion and that ischemic ventricular dysfunction occurs several seconds thereafter. Myocardial oxygen reserve is negligible.
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PMID:Temporal relation between onset of cell anoxia and ischemic contractile failure. Myocardial ischemia and left ventricular failure in the isolated, perfused rabbit heart. 22 47

This study was designed to determine whether quantitative alterations in ultrasonic attenuation are associated with myocardial changes occurring after acute ischemic injury. Five hundred seventeen regions of myocardium from 41 dogs were studied in vitro at five intervals after coronary occlusion: 15 min, 1 h, 6 h, 24 h, 3 days, and 6 wk. Quantitative indices of ultrasonic attenuation were determined from the measured frequency dependence of the ultrasonic attenuation coefficient characterizing each myocardial region over the range 2-10 MHz. Independent definition of regions of ischemic injury was provided by either creatine kinase depletion or colloidal carbon dye distribution. Results of this study indicate that ischemic myocardial regions investigated 15 min to 24 h after coronary occlusion demonstrated ultrasonic attenuation significantly decreased from nonischemic regions (P less than 0.05). In contrast, ultrasonic attenuation was significantly increased in zones of ischemia or infarction investigated at 3 days and 6 wk after coronary occlusion (P less than 0.05 and P less than 0.01, respectively). These results indicate that altered attenuation of transmitted ultrasound by myocardium in vitro is an early manifestation of ischemia.
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PMID:Changes in ultrasonic attenuation indicative of early myocardial ischemic injury. 42 Mar 17

We have recently detected accumulation of lysophosphoglycerides, catabolites of phospholipids, in ischemic myocardium early after coronary occlusion. In the present study we delineated effects of selected concentrations of albumin-bound lysophosphatidyl choline (LPC) comparable to those accompanying ischemia in vivo on action potentials of isolated canine Purkinje fibers. Lysophosphoglycerides induced concentration-dependent (0.75-3.0 mM) decreases in resting membrane potential, overshoot of phase 0, maximal velocity of upstroke (Vmax) of phase 0, and action potential duration. The highest concentrations (2.0-3.0 mM) induced fractionation of the action potential into several components, unresponsiveness to external stimulation, and enhanced automaticity at normal and reduced membrane potentials. LPC induced a rightward shift in the membrane response curve, a 40-fold prolongation of conduction time, and an increase in the ratio of effective refractory period to action potential duration such that the effective refractory period persisted beyond action potential duration, resulting in postrepolarization refractoriness. These electrophysiological alterations were entirely reversible after 70 minutes of perfusion without LPC, with the exception of a persistent depression in the Vmax of phase 0. Lysophosphatidyl ethanolamine (LPE) elicited alterations in action potentials indentical to those elicited by LPC. Furthermore, LPC (3.0 mM) induced comparable alterations in action potentials recorded from isolated rabbit papillary muscles. Since lysophospholipids accumulate early after myocardial ischemia, and since concentrations equivalent to those occurring in vivo induce electrophysiological alterations resembling those seen in ischemic myocardium in vivo, lysophosphoglycerides may be of major importance as biochemical mediators of malignant dysrhythmia induced by ischemia.
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PMID:Potential arrhythmogenic electrophysiological derangements in canine Purkinje fibers induced by lysophosphoglycerides. 42 75

The potential role of computerized transmission tomography (CTT) in the detection and quantitation of acute myocardial ischemic damage was assessed in 42 excised canine hearts at 2 hours, 8 hours, and 48 hours after coronary occlusion. The CTT scan detected by myocardial damage that was 2-48 hours old each time the presence of regional ischemia was confirmed by histochemical straining or epicardial electrocardiographic mapping. Intravenous administration of contrast material enhanced the x-ray attenuation of areas of ischemic damage of 8 and 48 hours duration compared with normal myocardium, but enhanced only normal myocardium in those of 2 hours duration. Volumetric estimation of the extent of damage from the CTT scans in dogs with ischemia of 48 hours duration showed a close linear relationship with the morphometric volume in the absence of contrast material. Quantitation of the area of ischemic damage from the CTT scan after contrast administration resulted in substantial underestimation of the volume of damaged tissue.
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PMID:Evaluation of myocardial ischemic damage of various ages by computerized transmission tomography. Time-dependent effects of contrast material. 44 46

The present study was done to quantitate the evolution of myocardial ischemic cell death within the framework of (1) the anatomical boundaries of the ischemic bed at risk and (2) the magnitude and transmural distribution of collateral blood flow. Myocardial ischemia was produced by proximal circumflex (LCC) occlusions in open chest dogs. Infarcts reperfused at 40 minutes, 3 hours, or 6 hours were compared with permanent infarcts. All dogs were sacrificed at 4 days. Regional myocardial blood flow was measured with 9-micrometer tracer microspheres before, and 20 minutes after, LCC occlusion. The location and size of the ischemic LCC bed at risk was determined by a dye injection technique. Infarct size was quantitated from multiple histologic sections. Necrosis involved 28 per cent, 70 per cent, and 72 per cent of the ischemic bed at risk in infarcts reperfused at 40 minutes, 3 hours, and 6 hours versus 79 per cent following permanent LCC ligation. Viable and potentially salvageable subepicardial muscle persisted for at least 3 hours after the onset of ischemia. Most of the salvageable myocardium was in the subepicardial region. In all groups, the lateral margins of necrosis were sharp in the subendocardial zone and were determined by the anatomical boundaries of the ischemic LCC bed at risk. LCC bed size ranged from 29 to 48 per cent of the left ventricle and thus contributed to variation in infarct size. However, infarct size, as a percentage of bed size, was determined by the transmural extent of necrosis within that bed (r = -0.97). This transmural extent of necrosis was related to subepicardial collateral flow after 3 hours (r = 0.92) and 6 or 96 hours (r = -0.85) but not after 40 minutes (r = -0.26) of ischemia. Thus, irreversible injury of ischemic myocardium developed as a transmural wavefront, occurring first in the subendocardial myocardium but ultimately becoming nearly transmural. Eventual transmural necrosis, and therefore over-all infarct size was determined by, and can be predicted from flow measurements obtained shortly after coronary occlusion.
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PMID:The "wavefront phenomenon" of myocardial ischemic cell death. II. Transmural progression of necrosis within the framework of ischemic bed size (myocardium at risk) and collateral flow. 44 73

We have investigated the rate of rise of myocardial PCO2 (PmCO2) after coronary artery occlusion using a new method for this measurement. Previous studies of PmCO2 have been limited by the slow response of the only available method, and no increase in MmCO2 prior to 3 minutes after occlusion has been found. We have implanted a miniature PCO2 electrode, with a 63% response time of 14 seconds, into the left ventricle of 14 open-chest dogs. After abrupt coronary occlusion, PmCO2 began to rise in 13.6 +/- 1.1 seconds in heparinized dogs and in 7.5 +/- 0.7 seconds in unheparinized dogs. The subsequent magnitude of the increase in PmCO2 was 24, 88, 171, and 222 mm Hg at 2, 5, 10, and 15 minutes after occlusion. The rate of rise of PmCO2 was essentially linear from 1 minute to 10 minutes at a rate of 18.3 mm Hg/min. The rate of rise was slower during the first 30 seconds after occlusion (6.1 mm Hg/min) and also from 30 seconds to 1 minute (9.7 mm Hg/min). This rate of rise is much greater than that previously observed and reflects the severe myocardial acidosis developing during ischemia. A rise in PmCO2 is one of the earliest metabolic changes that has been observed during myocardial ischemia.
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PMID:Rate of rise of myocardial PCO2 during early myocardial ischemia in the dog. 45 97

The risk of instantaneous death due to ventricular fibrillation was compared in resting and exercised dogs. Three weeks before testing, all dogs had bipolar left ventricular stimulating electrodes implanted and a reversible snare was placed around the anterior descending coronary artery. The dogs were randomly assigned to either an exercise (13 dogs) or a control (12 dogs) group. We measured ventricular fibrillation thresholds (VFTs) in all dogs before and after inducing ischemia by tightening the snare while the dogs stood at rest. The next day, nonischemic and ischemic VFTs were redetermined for control dogs at rest and for the exercise group during a treadmill run. No statistically significant changes were noted within and between groups in nonischemic or in ischemic VFTs at rest. In five exercise dogs, spontaneous ventricular fibrillation occurred during the first 8 minutes of the ischemic run, For the eight other exercise dogs, running increased the mean drop in VFTs during coronary occlusion by 23% (p less than 0.01). These data suggest that moderate dynamic exercise may greatly enhance the risk of ventricular fibrillation and sudden death in the presence of myocardial ischemia. In the absence of ischemia, exercise does not appear to increase vulnerability to ventricular fibrillation.
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PMID:Effect of submaximal exercise on vulnerability to fibrillation in the canine ventricle. 47 84

Intravenous infusion of acetylstrophanthidin to 6 dogs, after a 60 min left anterior descending coronary artery occlusion, was associated with a 43.0 +/- 10.5% decrease in the dose of digitalis needed to produce ventricular arrhythmias as compared to the pre-ischemic dose (97.5 +/- 8.0 microgram/kg). Reperfusion of the ischemic region for 2 h after a 90 min occlusion resulted in a 54.4 +/- 6.7% decrease in the arrhythmogenic dose. Direct intracoronary infusions of digitalis into the ischemic region, after a 90 min coronary occlusion followed by 2 h of reperfusion, was associated with a 47.7 +/- 6.4% decrease in the dose of digitalis needed to produce arrhythmias. The pre-ischemic (control) arrhythmogenic dose of digitalis via the intracoronary infusion method was 1.5 +/- 0.3 microgram/kg (mean +/- S.E.M. of 7 dogs). Sodium pump activity, estimated from the ouabain-sensitive 86Rb uptake in sodium-loaded ventricular slices, was significantly higher in slices obtained from the ischemic regions (6.84 +/- 0.30 nmoles 86Rb/mg dry wt. (mean +/- S.E.M.), than from the non-ischemic regions (3.43 +/- 0.64 nmoles 86Rb/mg dry wt.). Sensitivity of the sodium pump activity to the inhibitory effect of ouabain also was increased in the ischemic regions as indicated by a shift in the log dose--response curve to the left. Thus, it appears that there is an increase in myocardial sensitivity to the toxic effect of digitalis after temporary ischemia and it appears to be related to an increase in the sensitivity of the Na+,K+-ATPase or sodium pump to the inhibitory effect of digitalis.
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PMID:Ischemic-induced alterations in cardiac sensitivity to digitalis. 48 58

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

The patterns of regional contractile function were examined with ultrasonic crystals in "open-chest" anesthetized dogs. In normal myocardium, the base-line end-diastolic segment length (EDL) was 1.63 +/- 0.12 cm. and the mean systolic length (MSL) was 1.47 +/- 0.17 cm. Mean velocity of shortening over the first one third of systole (V1/3) was 15.9 +/- 2.3 mm. per second. Coronary occlusion induced regional ischemia with segmental dyskinesia (MSL = 1.84 +/- 0.12 cm). Reperfusion after 5 or 10 minutes of occlusion induced rapid recovery of contractile function that was independent of catecholamine release, as demonstrated in animals pretreated with 6-OH dopamine. After initial recovery, however, contractile function deteriorated. There were an increase in EDL (from 1.73 +/- 0.11 to 1.78 +/- 0.11; p less than 0.001) and the appearance of early systolic dyskinesia. V1/3 diminished from 5.6 +/- 4.6 to -6.6 +/- 2.5 mm. per second (p less than 0.005). Thus reperfusion damage, defined as late deterioration after recovery from brief periods of ischemia, may be partly distinct from ischemic damage per se. It is possible that the deterioration of myocardial function which accompanies reperfusion of previously ischemic myocardium may be a contributing factor in the transient myocardial dysfunction that is occasionally seen following cardiopulmonary bypass.
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PMID:Contractile damage from reperfusion after transient ischemia in the dog. 63 43


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