Blood pressure changes in the pulmonary artery and the cardiac chambers during different forms of apnoea.
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Biomedical subjects
Publications and source records attributed to J Herget.
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In male rats, pulmonary hypertension was found 9, 17 to 18, and 30 wk after an intrapulmonary injection of 50 mg quartz dust suspended in saline. Pulmonary arterial blood pressure increased progressively with time, and in the oldest group, the weight of the right heart ventricle was increased.
The etiology of neuronal intestinal dysplasia remains largely unknown. There is, however, supporting evidence of the existence of Hirschprung's disease or chronic intestinal obstruction associated with neuronal intestinal dysplasia. With the aim of investigating the possible development of neuronal intestinal dysplasia linked to chronic intestinal obstruction, we have examined the enteric nervous system response to long-term obstruction in a rat model. Three different surgical techniques were tested in Wistar male rats. In animals that survived longer than the cutoff chronic intestinal obstruction point (6 weeks), full-thickness biopsies and acetylcholinesterase (AChE), NADH, hematoxylin-eosin, and anti-S100 protein stainings were performed. The results of our model indicate that chronic intestinal obstruction induced different degrees of enteric nervous system dysplasia, including histological features of neuronal intestinal dysplasia. The relationship between chronic intestinal obstruction and anomalies of the enteric nervous system, including neuronal intestinal dysplasia, needs to be further studied.
The possibility that changes in energy metabolism are involved in oxygen sensing during hypoxic pulmonary vasoconstriction was tested indirectly by measurement of hypoxic-pressor reactivity in lungs isolated from rats with low and high levels of plasma thyroxine. In the first study, male rats were treated for one week after thyroidectomy with 50 micrograms (n = 6) or 100 micrograms (n = 6) thyroxine per 100 g body weight (b.w.) daily or with solvent (n = 6). The lungs were isolated and perfused at constant flow with salt-albumin solution. They were ventilated with air +5% CO2 in a humid chamber at 38 degrees C. The dose-pressor response to hypoxia and angiotensin II were measured. In the second study, thyroidectomized male rats were treated similarly with 100 micrograms thyroxine (n = 7) or solvent (n = 6) and isolated lungs were perfused with homologous blood obtained from thyroidectomized blood donors treated in the same manner. Then the dose-pressor responses to hypoxia and K+ were elicited. The hypoxic-pressor responses were bigger in thyroxine than in solvent-treated rats. The response to angiotensin II and K+ was not affected by thyroxine treatment. The results are consistent with the idea that hypoxic-pressor reactivity varies directly with the metabolic rate of lung tissue.
The effect of chronic pretreatment with alpha-methyldopa on acute pulmonary hypertension induced by lung microembolization with Sephadex particles in the rat was studied. Alpha-methyldopa was administered twice a day for 10 days by oesophageal gavage (20 mg X kg-1 of body weight) prior to embolization. Rats were anaesthetized with urethane. A catheter was positioned in closed chest rats in the pulmonary artery and 50 microliter of Sephadex suspension in saline were injected. The control group was not pretreated with alpha-methyldopa. In a subgroup of control and pretreated rats, the cardiac output was measured by the dye dilution technique before and after lung microembolization. Rats pretreated with alpha-methyldopa had less pulmonary hypertension, higher cardiac output and more severe arterial hypoxaemia 15 min after lung microembolization than untreated animals. There was no difference in platelet counts prior and after embolization. We suggest that pulmonary hypertension after lung microembolization in the rat includes a vasoconstrictor component which can be suppressed by alpha-methyldopa, and that severe arterial hypoxaemia in pretreated rats is probably the result of a decrease of the ventilation/perfusion ratio in unobstructed areas, which in untreated rats may be prevented by active vasoconstriction.
Volume of carotid bodies was measured morphometrically in rats with experimental lung emphysema or silicosis. The mean volume of the left carotid body was 19.9 +/- (SD) 12.4 in 13 control rats, 30.7 +/- 12.5 in 9 rats with lung emphysema, and 41 +/- 18.9 . 10(6) micrometer 3 in 10 rats with lung silicosis. There was no correlation between carotid body volume and pulmonary arterial blood pressure. A good correlation was found between the volume of carotid body and partial pressure of oxygen in arterial blood. The functional meaning of the increase of volume of carotid bodies in rats with chronic respiratory insufficiency remains unclear.