Biomedical subjects
D Heath
Publications and source records attributed to D Heath.
Effects of phenobarbitone, cinnarizine, and zoxazolamine on the development of right ventricular hypertrophy and hypertensive pulmonary vascular disease in rats treated with monocrotaline.
The results of this experiment suggest that the addition of zoxazolamine to the diet may prolong the survival and reduce the incidence of right ventricular hypertrophy and hypertensive pulmonary vascular disease in male rats given a single subcutaneous injection of monocrotaline. Phenobarbitone and cinnarizine were ineffective.
Effect of chlorphentermine on the lipids of rat lungs.
Chronic administration of chlorphentermine to rats resulted in a reduction of body weight compared to a normal control group. The weight of the heart, liver, kidney, and spleen was less in the treated group while the weight of the lungs was increased significantly. There was no change in the ratio of right ventricular to left ventricular weight in the rats treated with chlorphentermine, supporting the views that this drug does not cause pulmonary hypertension. Biochemical analysis showed that the increase in the weight of the lungs was due to the accumulation of phospholipid. All classes of phospholipid were affected, but particularly phosphatidyl choline, the tissue concentration of which increased nine times. Chlorphentermine also increased the proportion of palmitate present in pulmonary phosphatidyl choline. Histological examination of the lung after treatment with chlorphentermine showed evidence of this drug-induced lipidosis. No conclusion can as yet be reached as to the mechanism involved in the accumulation of phospholipid in the lung after chlorphentermine.
Clara cells in the llama.
A study was made by light and electron microscopy of the Clara cells of two llamas born and bred at an altitude of 4,720 m in the Peruvian Andes. The Clara cells were numerous and prominent with big apical caps, many of which had been extruded into the terminal bronchioles. On electron microscopy the caps were found to contain vesicular endoplasmic reticulum. Previous studies have shown this to contain dipalmitoyl lecithin, a known pulmonary surfactant. Acute exposure to a simulated altitude of 4,270 m has been reported to increase surface tension in lung extracts of mice. Hence it may be that an animal, such as the llama, chronically exposed to high altitude requires a persistent secretion of pulmonary surfactant.
Atherosclerotic human carotid sinus.
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A pulmonary hypertension-producing plant from Tanzania.
An African youth who had died from primary pulmonary hypertension was suspected of having ingested a herbal remedy containing the seeds of the local plant Crotalaria laburnoides. Consequently powdered seeds of this plant were fed to 20 Wistar albino rats for 60 dyas to see if this would induce ventricular hypertrophy and associated hypertensive pulmonary vascular disease. At the end of the experimental period right ventricular hypertrophy, medial hypertrophy of the pulmonary trunk and 'muscular pulmonary arteries', and muscularization of the pulmonary arterioles had developed in a proportion of the test animals. These are the morbid anatomical features pathognomonic of a raised pulmonary arterial pressure and show that the seeds of Crotalaria laburnoides contain an agent capable of inducing pulmonary hypertension in rats. This study suggests the value of seeking a history of ingestion of herbal remedies and drugs in cases of unexplained pulmonary hypertension in man.
Hypertensive pulmonary vascular disease.
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Pulmonary veno-occlusive disease.
Pulmonary veno-occlusive disease has recently been recognized as a distinct pathological entity and a cause of pulmonary arterial hypertension. Twenty previously reported cases and a new patient are here reviewed. The majority presented with breathlessness and in the early stages of the disease, when the abnormal signs were not striking, some patients were wrongly diagnosed as suffering from an anxiety state. The condition usually has an insidious onset but is remorselessly progressive and since no effective treatment is available at present, invariably fatal and the majority of patients have died within two years. The fully developed clinical picture is dominated by symptoms and signs of pulmonary arterial hypertension, similar to those found with other diseases causing a raised pulmonary arterial blood pressure. However, some patients with pulmonary veno-occlusive disease show, in addition, signs of pulmonary venous and capillary hypertension, which can lead to its clinical recognition when associated with a normal left atrial blood pressure. In this condition the pulmonary wedge pressure would appear to be unreliable as a record of the left atrial blood pressure. Pulmonary angiography and lung scanning will differentiate pulmonary veno-occlusive disease from massive thromboembolic pulmonary arterial hypertension but not from primary pulmonary arterial hypertension or micro thromboembolism. Although in some patients it should now be possible to recognise pulmonary veno-occlusive disease in life, there will be others where, even after full investigation, it will still be impossible to differentiate the condition from primary pulmonary arterial hypertension or micro thromboembolism and in these the diagnosis will only be made when the distinctive histological pattern of the disease is demonstrated. In pulmonary veno-occlusive disease there is a widespread occlusion of the pulmonary veins and venules by a loose intimal fibrosis which is often basophilic. Recanalization of the occluded veins is common and in some cases may be very striking. These occlusive lesions in the pulmonary veins lead to an elevation of pulmonary arterial pressure with associated disease of these vessels, and are also responsible for chronic oedema of the elveolar walls with subsequent development of interstitial pulmonary fibrosis. In the present case organised thrombi were present in the pulmonary arteries in addition to the pulmonary venous lesions.
Enzyme activities in red and white muscles of guinea-pigs and rabbits indigenous to high altitude.
The activities of several enzymes functioning in different areas of fuel catabolism were measured under standardized conditions, using crude homogenates of sartorius and ventricular muscle from outbred guinea-pigs and rabbits indigenous to high or low altitude. The activities of sartorius and myocardium were found to reflect the metabolic patterns known to be associated with white and red muscle. Both species had right ventricular hypertrophy at high altitude. The enzyme activities in the high altitude guinea-pig were not significantly different from those in the sea level animals. In the high altitude rabbit, compared with the low altitude rabbit, the activities of glyceraldehyde-3-phosphate deydrogenase and phosphofructokinase were greater in both the sartorius and myocardium. In addition, mitochondrial glycerol-3-phosphate dehydrogenase activity was greater in the sartorius at high altitude, while aspartate aminotransferase and beta-hydroxyacylcoenzyme A dehydrogenase activities were greater in the myocardium at high altitude. Succinate dehydrogenase activity was comparable at the two altitudes for both tissues. There was a greater proportion of skeletal muscle type lactate dehydrogenase in the high altitude rabbit myocardium but no difference was found with the guinea-pig.
The pathology of the lung in paraquat poisoning.
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Letter: Ruptured aneurysm of splenic artery in pregnancy.
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The influence of age and sex on the response of the right ventricle, pulmonary vasculature and carotid bodies to hypoxia in rats.
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The pathogenesis and structure of paraquat-induced pulmonary fibrosis in rats.
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The ultrastructure and time sequence of the early stages of paraquat lung in rats.
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Extensibility of the human carotid sinus.
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The heart and pulmonary vasculature of the llama (Lama glama).
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