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D Kilpatrick

Publications and source records attributed to D Kilpatrick.

78 records · Page 5Linked to original sources
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The effects of nifedipine on the systemic and coronary vascular beds of the sheep: a potential method for induction of ischaemia.

Nifedipine has been reported to aggravate symptoms of ischaemic heart disease in some patients. To investigate the possible reasons for this, vascular resistance changes in the systemic and coronary beds of sheep were compared with and without coronary artery stenoses. In six anaesthetized sheep, the dose-response curve comparing vascular resistance to nifedipine dose showed greater sensitivity than that reported for either dogs or humans. The coronary vascular bed was more reactive than the systemic vascular bed but this difference did not reach a level of statistical significance. With fixed non-elastic proximal coronary artery stenoses, the relationship of both coronary flow and coronary resistance to a standard dose of nifedipine (5 micrograms/kg) was indirectly related to the degree of stenosis. With stenosis reducing flow at rest by 50% or more, nifedipine usually produced a reduction in coronary flow in the stenosed artery and associated ST elevation, consistent with severe ischaemia in the distribution of the coronary. This effect is related to the reduction in perfusion pressure.

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Coronary and peripheral vascular resistance in the anaesthetized diabetic sheep.

To determine whether vascular resistance was altered in diabetes, the vascular resistance in both the peripheral arterial bed and the circumflex coronary artery was compared in six normal and five diabetic adult sheep, under pentobarbitone anaesthesia. Diabetes induced by alloxan significantly increased blood glucose (15.6 mmol/l, s.e.m. = 2.8, vs 5.5 mmol/l, s.e.m. = 0.6; P greater than 0.001) compared with controls. Systolic blood pressure was lower in diabetics (92 mmHg, s.e.m. = 12, vs 123 mmHg, s.e.m. = 5; P less than 0.025) as was diastolic blood pressure (73 mmHg, s.e.m. = 15, vs 104 mmHg, s.e.m. = 4; P greater than 0.05). Basal peripheral resistance was lower in diabetics than controls (36.0 mmHg.min/l, s.e.m. = 7.9, vs 42.3 mmHg.min/l, s.e.m. = 2.8), but not significantly so. Methoxamine markedly increased peripheral vascular resistance in both groups, but did not change coronary vascular resistance, due to autoregulation. The dose-response curves of peripheral or coronary arteries to methoxamine showed no significant difference between diabetic and control sheep. Dose-response curves for isoprenaline and noradrenaline infusion suggested there may be altered beta-receptor sensitivity in diabetes. In conclusion, there are marked differences in the vascular beds of diabetic and normal sheep under basal conditions. In contrast to previous studies, alpha-adrenoceptors are not different in diabetics, but further studies in unanaesthetized animals are indicated, as beta-receptor sensitivity may be altered in diabetes.

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