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Biomedical subjects

R B Jennings

Publications and source records attributed to R B Jennings.

At least 109 records · Page 6Linked to original sources
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↗
PubMed1978

Use of microporous expanded polytetrafluoroethylene grafts for aorta-pulmonary shunts in infants with complex cyanotic heart disease. A report of seven cases.

Seven cyanotic infants in our institution have undergone central aorta--pulmonary artery shunt operations with a microporous expanded polytetrafluoroethlene (PTFE) graft. All of these patients have had pulmonary atresia, in four cases associated with endocardial cushion type defects. Four patients have had excellent palliation for up to 13 months. Congestive heart failure and kinking of the pulmonary artery, frequently seen with other types of central aorta-pulmonary shunts, have not been a problem. Until further experience is gained with this procedure, however, we reserve its use to the occasional cyanotic infant in whom neither open-heart repair or the Blalock-Taussig shunt is feasible.

Aorta↗
PubMed1977

Occult lupus nephropathy: a correlated light, electron and immunofluorescent microscopic study.

Renal biopsies obtained from four adolescent girls who developed symptomatic thrombocytopenia with serologic evidence of systemic lupus erythematosus, without clinical signs of renal involvement, showed glomerular disease by electron and immunofluorescent microscopy with light microscopic changes in two cases. Subsequently, three of the patients developed proteinuria, and repeat biopsies from all four showed appearances ranging from resolution to significant glomerulitis. The findings illustrate the variable patterns of occult glomerulitis in lupus, and highlight the value of correlating light, electron and immunofluorescent studies in renal pathology.

Adolescent↗
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↗
PubMed1977

Subtotal cor triatriatum with left partial anomalous pulmonary venous return. Successful surgical repair in an infant.

A 10-week-old infant underwent successful repair of subtotal cor triatriatum associated with left-sided partial anomalous pulmonary venous return to the innominate vein. This unusual type of cor triatriatum represents an intermediate embryologic form between pure cor triatriatum and total anomalous pulmonary venous return. Important hemodynamic differences exist between this defect and pure cor triatriatum. Exact anatomic diagnosis prior to operation is highly desirable. To our knowledge, this case represents the first successful repair of this very rare congenital cardiac defect.

Electrocardiography↗
PubMed1976

On the nature of protection by propranolol against myocardial necrosis after temporary coronary occlusion in dogs.

Propranolol has been shown to reduce the extent of necrosis that develops after temporary coronary occlusion in dogs. To determine whether this protective action was related to beta adrenergic blockade or to direct effects, necrosis was quantitated in the posterior papillary muscle 2 to 4 days after 40 minute periods of coronary occlusion in anesthetized open chest dogs. Groups of dogs either were untreated or were pretreated with doses of d,l-propranolol, 0.005 to 5 mg/kg body weight, or doses of d-propranolol 2.5 or 5 mg/kg. Necrosis was greatly reduced in dogs treated with 5 mg/kg of d, l-propranolol. This protective effect was significant but quantitatively less with 0.5 and 0.05 mg/kg of d, l-propranolol. A dose of 0.005 mg/kg d, l-propranolol and d-propranolol failed to alter myocardial necrosis significantly. The dose-related reduction of necrosis with d, l-propranolol correlated with a similar dose relation for beta adrenergic blockade and suggested that a protective effect was related to beta blockade. The reduction of necrosis with 0.05 and 0.5 mg/kg of d, l-propranolol (a level at which direct "membrane stabilizing" effects are insignificant) suggested that direct effects were not essential for protection. The negative results with d-propranolol further support our conclusion that propranolol reduces myocardial ischemic injury through beta adrenergic blockade rather than through direct myocardial actions.

Animals↗