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Biomedical subjects

J E Lowe

Publications and source records attributed to J E Lowe.

At least 199 records · Page 11Linked to original sources
PubMed1978

Reversible pulmonary oxygen toxicity in the primate.

In order to investigate the effects of high concentrations of oxygen on the lung, experiments were performed on 18 baboons exposed to a humidified environment of 95% oxygen for five days. Open lung biopsies for biochemical assay, histologic and electron microscopic analysis and measurement of tissue respiration were performed before and after oxygen exposure. Pulmonary function was evaluated by measurement of arterial blood gases, compliance, closing capacity (CC), functional residual capacity (FRC), total lung capacity (TLC), residual volume (RV) and vital capacity (VC) before and after exposure and then at seven and 14 days in the animals which recovered. Six baboons removed from the oxygen environment after 96--110 hours and exposed to room air died within three to 20 hours of profound hypoxemia (PaO2 40 +/- 6). The remaining 12 baboons were successfully weaned to room air over a three day period with a return of ABGs to control values (PaO2 89+/- 2). Electron microscopic analysis of alveolar membranes exposed to 120 hours of hyperoxia demonstrated endothelial cell swelling, interstitial alveolar membrane edema, and an increased predominance of Type II pneumocytes. Lung volume measurements showed significant decreases in TLC (25%), VC (34%), CC/TLC (28%) and dynamic compliance (47%). Biochemical studies indicated a shift toward anaerobic metabolism with a decrese in tissue oxygen consumption, reduced cytochrome oxidase activity, and increased lung lactic acid production. These changes were all found to be reversible in the 12 baboons slowly weaned back to room air.

Animals↗
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↗
PubMed1975

Semen characteristics in thyroidectomized stallions.

Three Quarter-horse stallions were surgically thyroidectomized at 18 months of age. Weekly semen collections were made from these and three control stallions from 25 to 39 months of age. Although the induced state of hypothyroidism in young stallions has a depressing effect on libido and general animation and can be corrected by thyroprotein supplementation, semen characteristics, testicular histology and fertility are not affected by the operation.

Animals↗