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D Pelling

Publications and source records attributed to D Pelling.

24 records · Page 2Linked to original sources
PubMed1970

Haemodynamic and other studies in the renoprival hypertensive rat.

1. The optimal conditions for the development of hypertension after total nephrectomy were defined in the rat. Under these conditions, haemodynamic changes were then studied before and for 3 days after total nephrectomy in the unanaesthetized animal and compared with mock-nephrectomized controls.2. Changes in cardiac output were followed with an electromagnetic flowmeter chronically implanted on the ascending aorta, and mean arterial pressure with an indwelling aortic cannula.3. Haematocrit fell in animals developing hypertension, due to plasma volume expansion. Restriction of administered saline did not reduce the fall in haematocrit without also preventing development of the hypertension.4. Cardiac output and stroke volume increased significantly on the second and third days after nephrectomy. Peripheral resistance remained unchanged and pulse rate tended to fall.5. The increase in cardiac output appeared to be more than could be accounted for by anaemia alone, and it is suggested that plasma volume expansion was partly responsible.6. In another group of rats developing renoprival hypertension a correlation was found between changes in plasma volume and arterial pressure over the three days.7. Renoprival hypertension was accompanied by a slight but significant reduction in oxygen consumption in comparison with the controls.8. No relationship was found between the changes in blood pressure, and plasma sodium and potassium levels.9. It is concluded that the observed rise in cardiac output associated with renoprival hypertension as induced in this study was not attributable to anaemia nor to a rise in metabolic rate. The implications of this situation are discussed in relation to a theory of the pathogenesis of hypertension and the findings of other workers.

Animals↗
PubMedDate not supplied

Changes in the distribution of histochemically localized mercury in the CNS and in tissue levels of organic and inorganic mercury during the development of intoxication in methylmercury treated rats.

The development of neurotoxicity in rats after exposure to methylmercuric chloride was monitored using behavioural indices. At selected time points the cellular localization of mercury and the relative amounts of organic and inorganic mercury were determined in several regions of the CNS, and in some non-neural tissues. The CNS showed an affinity for organic mercury, the levels of inorganic mercury remaining low throughout symptomatic intoxication. Histopathological changes were not closely related to the regional tissue content of the organic or inorganic forms, nor to mercury localized histochemically at the cellular level. The stained deposits, which had focal cytoplasmic distribution, appeared in glial cells initially then in larger neurones as the intoxication progressed. These observations may represent changes in the mercury content of different cell types or reflect differences in the way that they handle a similar burden of mercury. A transitory accumulation of mercury in glial cells may be a factor contributing to the occurrence of a latent period and sequestration of mercury in cytoplasmic organelles may serve to protect some cell types from injury.

Animals↗