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Biomedical subjects

K A Reimer

Publications and source records attributed to K A Reimer.

At least 109 records · Page 6Linked to original sources
PubMed1981

The transition to ventricular fibrillation induced by reperfusion after acute ischemia in the dog: a period of organized epicardial activation.

Ventricular fibrillation was induced in eight of 10 open-chest dogs by reperfusion after a 15-minute occlusion of the proximal circumflex coronary artery. Simultaneous recordings were made from 27 epicardial electrodes spaced over both ventricles. Analysis of the initial 1.5--2.5 seconds of the transition from sinus rhythm or ventricular tachycardia to fibrillation revealed that ventricular activation occurred in an orderly, rapidly repeating sequence in all hearts. Each activation from arose near the border of the ischemic-reperfused region and passed across the nonischemic portion of the ventricles to the opposite side of the heart as a single, organized wavefront. As the arrhythmia progressed, the time between the appearance of successive activation fronts on the epicardium decreased. Concurrently, the time for each activation front to traverse the ventricles increased. The stimulation increase in rate of appearance and decrease in conduction velocity for each successive cycle resulted in overlapping cycles in which a new activation front arose from the ischemic-reperfused region before the previous front terminated over the right ventricle. The overlap between successive activation fronts increased as the arrhythmia continued. Thus, ventricular activation during the transition to ventricular fibrillation arose near the border of the ischemic-reperfused region and was organized as it passed across the nonischemic tissue, but the body surface ECG appeared disorganized because of variable spacing between successive, coexistent activation fronts.

Acute Disease↗
PubMed1981

Myocardial infarct size and location in relation to the coronary vascular bed at risk in man.

Recent infarcts were compared with the anatomic boundaries of the involved vascular bed in human hearts to determine the amount and location of necrosis in relation to the myocardium at risk. The coronary arteries were injected with BaSO4 in 18 human hearts with 3-16-day-old infarcts. Thin (3-4 mm) slices were cut at 10-15 mm intervals, photographed, x-rayed and used for histologic analysis. Infarct outlines were traced from gross photographs using histologic confirmation of infarct boundaries, and the vascular bed was independently traced from the x-rays. Ischemic bed size and infarct size were then calculated by computerized planimetry. Infarct size ranged from 13-72% of the left ventricle (mean 30 +/- 3.6%) and was linearly related to the size of the occluded vascular bed (r = 0.93). However, the infarcts were always smaller than the occluded beds. They involved 50-88% of the ischemic bed (mean 69 +/- 3.0%) due to variation in the transmural extent of necrosis. A lateral zone of viable muscle within the ischemic bed was present but was consistently narrow (mean 1.7 +/- 0.3 mm) so that the infarcts involved 93 +/- 2.3% of the width of the bed at risk. Thus, ischemic bed size is a major determinant of infarct size in fatal human infarcts. When natural limitation of infarct size occurs, it is due primarily to limitation of the transmural extent of necrosis.

Barium Sulfate↗
PubMed1981

Lethal myocardial ischemic injury.

The biologic changes occurring in severely ischemic myocytes in vivo as the affected cells pass through the phase of reversible to the phase of lethal or irreversible injury are reviewed with special emphasis on the effect of ischemia on the production and utilization of highenergy phosphate, the destruction of the adenine nucleotide pool, and the appearance of signs of damage to the plasma membrane of the sarcolemma. Evidence is presented that indicates that the events occurring in severe ischemia in vivo are essentially identical to those found in total ischemia in vitro except that the biologic changes of ischemia develop more slowly in total ischemia in vitro than in severe ischemia in vivo. The slower time course of injury, together with the uniformity of injury provided by total ischemia in vitro, may allow for more precise identification of potential lethal cellular events in ischemic injury. The production of highenergy phosphates (HEP) from anaerobic glycolysis have been estimated in both in vivo and in vitro ischemia by the measurement of lactate accumulation, and total HEP utilization has been estimated from the depletion of stores of preformed HEP. The results show that between 80% and 90% of the HEP utilized by ischemic dog left ventricle is produced by anaerobic glycolysis. The onset of irreversibility is associated with marked depletion of the HEP and adenine nucleotide pools of the tissue and the cessation of energy production via glycolysis. The cessation of anaerobic glycolysis may be caused by the low sarcoplasmic, adenosine triphosphate (ATP) concentration of the dying myocyte. In addition to the foregoing changes, irreversibly injured tissue exhibits both ultrastructural and functional evidence of disruption of the plasmalemma of the sarcolemma. The possible relationships, causal and otherwise, between severe HEP depletion and membrane damage are discussed. Both HEP depletion (ATP < 3-8% of control) and membrane damage are considered to be objective signs of the presence of irreversible myocardial ischemic injury. However, at the present time, there is no proof that these changes are causally related either to each other or to cell death in severe in vivo ischemia.

Adenine Nucleotides↗
PubMed1980

Myocardial infarct size. Measurements and predictions.

Because patient prognosis is related in part to infarct size, therapies that could limit infarct size should be beneficial. The development of such therapies has been hampered by the lack of proven techniques to measure infarct size or to assess the effect of therapy in living patients. In addition, the evolution of ischemic cell death in human infarcts is not understood, and therefore the amount of ischemic myocardium that might be salvageable at various times after the onset of myocardial infarction is unknown. Experimental studies have contributed to our understanding of the evolution of acute myocardial infarcts. However, there is a continuing need for experimental and human anatomical studies to validate indirect in vivo techniques of estimating infarct size. In addition, reliable experimental models in which potential therapies can be tested are needed. In dogs, infarct size is predetermined in part by the amount of myocardium at risk and the amount of collateral flow in this risk region. Measuring these parameters should provide a framework within which the effects of therapy on infarct size can be assessed.

Animals↗
PubMed1980

Multiple coronary artery dissections in old age. A unique case.

A 70-year-old man died of alcoholic cirrhosis and long-standing pulmonary emphysema. Multiple independent dissecting aneurysms involved the distal epicardial branches of the right and left coronary arteries, but spared their proximal trunks. These dissections extended distally from vascular branch points in association with acute and chronic medionecrosis. Iatrogenic trauma superimposed on preexisting medial weakness may have accounted for what is, to our knowledge, a unique presentation of a rare condition.

Aged↗
PubMed1979

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.

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.

Animals↗
PubMed1979

[Role of changes in myocardiocytes in the development of acute heart failure in experimental myocardial infarct].

Some problems of the pathogenesis of the development of acute cardial insufficiency were studied on the material of 2-hour experimental myocardial infarction in dogs. Acute cardial insufficiency developed owing to additional load on the heart (partial stricture of the aorta) after ligation of the posterior circumflex branch of the coronary artery. It was found that 24 hours after the removal of the immediate causes of acute cardiac insufficiency (removal of clamps from the coronary artery and aorta) the symptoms of the contractile weakness of the left heart correlated directly with electron microscopic signs of increased degeneration of intracellular structures and did not depend on the level of energetic processes in cardiomyocytes and the structure and function of sarcolemma. The restoration of the bloodflow in the previously ligated coronary artery for 2 hours did not improve the condition of the cells in the ischemic zone but enhanced reparative processes in the non-ischemized zone of the left ventricle.

Acute Disease↗
PubMed1978

Experimental infarct size as a function of the amount of myocardium at risk.

Occlusion of the same coronary artery at the same anatomic site in a group of dogs results in significant variation in the size of the resultant infarcts. The present study shows that much of this variation can be explained by differences in the pattern of distribution of the occluded coronary artery. The relationship between the anatomic size of an occluded coronary bed and the the amount of necrosis resulting from 40 minutes of proximal circumflex coronary (LCC) occlusion and 3 days of reperfusion was determined in randomly selected dogs using an in vitro latex coronary injection technique. The amount of necrosis, calculated from serial histologic sections taken through the posterior papillary muscle (PP), correlated closely with the size of the occluded coronary bed: 5 dogs with small LCC beds (26 +/- 2%) had 10 +/- 3% PP necrosis; 5 dogs with medium-sized LCC beds (37 +/- 2%) had 33 +/- 1% necrosis; and 7 dogs with large LCC beds (42 +/- 1%) had 51 +/- 2% necrosis. The results show that much of the variability in infarct size among dogs subjected to coronary artery occlusion at the same anatomic site is a function of differences in ischemic bed size. Grouping dogs by occluded coronary bed size may improve the resolution of experimental studies testing the effect of various therapies on infarct size.

Animals↗
PubMed1978

Relation between high energy phosphate and lethal injury in myocardial ischemia in the dog.

The relationship between progressive depletion of high energy phosphate and the onset of lethal cell injury in ischemic myocardium following coronary occlusion has been evaluated. Myocardial ischemia was induced by proximal occlusion of the circumflex coronary artery for 15, 30, 40, or 60 minutes. Cell injury in the severely ischemic posterior papillary muscle (PP) was evaluated by electron microscopy and by measuring the capacity of slices of the injured PP to maintain electrolytes, resynthesize high energy phosphate, and exclude inulin during in vitro incubation. ATP content in the ischemic myocardium decreased to 35%, 9%, 7%, and 5% of control values after 15, 30, 40, and 60 minutes of ischemia, respectively, and was associated with a corresponding depletion of total adenine nucleotides. The loss of 65% of the ATP after 15 minutes of ischemia (reversible injury) was associated with only minimal ultrastructural changes and no significant defects of electrolytes in incubated slices. However, the depletion of over 90% of the ATP after 40 minutes of ischemia (irreversible injury) was associated with significant fine structural changes and markedly altered cell volume regulation. The results suggest a close relationship between the marked depletion of high energy phsophates and the development of lethal injury in acutely ischemic myocardium.

Adenosine Triphosphate↗
PubMed1977

Effect of the calcium antagonist verapamil on necrosis following temporary coronary artery occlusion in dogs.

Calcium metabolism may play an important role in the pathogenesis of myocardial ischemic injury. The effect of the sarcolemmal calcium flux inhibitor, verapamil, on myocardial necrosis was studied in dogs subjected to temporary coronary artery occlusion. One group of dogs was untreated. A second group was given 0.8 mg/kg verapamil intravenously over a 30 min period beginning 10 min prior to coronary occlusion. In a third group, the dose of verapamil was increased until complicated by hypotension or conduction abnormalities. Cardiac necrosis was produced in all dogs by 40 min of left circumflex coronary artery occlusion followed by 2--4 days of reperfusion. At the end of the experiment, animals were sacrificed and necrosis was quantitated histologically in transmural slices through the posterior papillary muscle. Pre-treatment with the lower dose of verapamil resulted in significantly less necrosis (14% treated vs 35% untreated) with minimal hemodynamic consequences. Higher does of verapamil were even more effective in limiting cardiac necrosis despite the development of hypotension and varying degrees of heart block.

Animals↗
PubMed1977

The wavefront phenomenon of ischemic cell death. 1. Myocardial infarct size vs duration of coronary occlusion in dogs.

Irreversible ischemic myocardial cell injury developes in an increasing number of cells as the duration of coronary occlusion is prolonged. The present study quantitates myocardial necrosis produced by 40 minutes, 3 hours, or 6 hours of temporary circumflex coronary occlusion (CO) followed by 2 to 4 days of reperfusion, or by 24 or 96 hours of permanent circumflex ligation in pentobarbital anesthetized open chest dogs. After 40 minutes of ischemia, myocyte necrosis was subendocardial but with increasing duration of coronary occlusion, irreversible injury progressed as a wavefront toward the subepicardium. Transmural necrosis was 38 +/- 4% after 40 min, 57 +/- 7% after 3 hours, 71 +/- 7% after 6 hours and 85 +/- 2% after 24 hours of ischemic injury. These results document the presence of a subepicardial zone of ischemic but viable myocardium which is available for pharmacologic or surgical salvage for at least three and perhaps six hours following circumflex occlusion in the dog.

Animals↗
PubMed1977

Infarct size reduction by propranolol before and after coronary ligation in dogs.

Coronary occlusion in the dog results in irreversible myocardial cell injury which develops first in subendocardial areas of severe ischemica and subsequently spreads into mid and subepicardial areas of moderate ischemia. The effect of propranolol on this progression of ischemic injury was evaluated. Three groups of dogs were studied: 1) untreated, 2) treated with propranolol before and throughout coronary ligation, and 3) treated with propranolol beginning three hours after ligation. Dogs were sacrificed 24 hours after coronary ligation and necrosis was quantitated from histologic sections of transmural slices through the posterior papillary muscle. Propranolol reduced infarct size by preventing necrosis in peripheral (subepicardial) areas of moderately ischemic myocardium. Pretreatment with propranolol reduced necrosis from 85 +/- 3% (untreated) to 52 +/- 4% (P less than 0.05). Delayed propranolol therapy was about half as effective as pre-treatment and reduced necrosis to 71 +/- 3% (P less than 0.05). Propranolol also limited microvascular injury so that perfusion defects, detected with the dye thioflavin S, were smaller in treated dogs.

Animals↗