Cardiovascular and renal function after burn injury in the rat

Philpot, Margaret Elizabeth (1981) Cardiovascular and renal function after burn injury in the rat. University of Southampton, Doctoral Thesis.

Abstract

The histological changes caused by burn injury in the rat were investigated. Cardiovascular responses to burn injury were measured in anaesthetised rats by the relatively new method of impedance cardiography. This method was validated by comparison with a well-established method, namely thermal dilution, and good agreement was found before and after burn injury. Burn injury caused immediate falls in cardiac output, stroke volume and the Heather Index (an index of cardiac contractility), a rise in total peripheral resistance but only small changes in heart rate and arterial blood pressure. The fall in cardiac output occurred before any measured increase in arterial haematocrit and also occurred in rats pretreated with the histamine I12-receptor antagonist, cimetidine, which has previously been shown to reduce oedema formation in the burn-injured rat and, in the present study, suppressed the rise in arterial haematocrit. Similar cardiovascular responses were observed in normal assay rats which received blood from burned rats. Transfer of blood from mock-burned rats, however, had no effect. Plasma renin activity increased significantly after burn injury. Nephrectomy, one hour before burn injury, protected the rats since the cardiovascular responses were much less marked and only transient. Adrenalectomy one hour before burn injury only slightly modified the cardiovascular responses. It is suggested that the immediate fall in cardiac output is due to reduced cardiac contractility (possibly induced by circulating toxins) and increased afterload (possibly due to sympathetic reflexes and circulating angiotensin) but not hypovolaemia. A conscious rat preparation, with cannulae implanted in the right jugularvein, left carotid artery and urinary bladder, was developed to investigate the changes in renal function in the early post-burn period and to study the effects of fluid replacement. Burn injury produced immediate falls in urine flow, sodium and potassium excretion, glomerular filtration rate, effective renal plasma flow and effective renal blood flow, and caused a gradual rise in haematocrit. Saline infusion was shown to be beneficial but reduced urine output did not always indicate reduced renal perfusion. These results are comparable to those observed in burned patients. It is suggested that to use the urine output alone, as an index of effective fluid therapy, may be inappropriate. In anaesthetised rats, burn injury did not produce any significant change in the extraction ratios of PAH and inulin, indicating that the clearances of these markers were giving accurate measures of effective renal plasma flow and GFR after burn injury.

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