Proceedings of The Physiological Society

Trinity College Dublin (2003) J Physiol 551P, C53


Baroreflex control of heart rate following autonomic blockade during acute hypothermia

R. Sabharwal, E.J. Johns and S. Egginton

Department of Physiology, University of Birmingham, Birmingham, UK and Department of Physiology, University College Cork, Cork, Ireland

We have shown that baroreflex control of renal sympathetic nerve activity (RSNA) was slightly reduced during acute hypothermia, but by contrast baroreflex control of heart rate (HR) was completely suppressed (Sabharwal et al. 2003). The aim of this study was to investigate the extent of sympathetic and vagal contributions towards baroreflex control of HR during acute hypothermia. This was done by generating baroreflex curves for HR at deep oesophageal core temperature (Tb) of 37 °C and on cooling to 25 °C in the presence of atropine (muscarinic cholinergic blocker) or propranolol (β-adrenergic blocker).

Male Wistar rats, 290-320 g, were anaesthetised with fluothane (2.5 % in O2) and α-chloralose/urethane (32/450 mg kg-1 I.V.). Mean arterial blood pressure (MABP) and HR were measured via a femoral artery. Tb was regulated by means of a thermostatted plate connected to a temperature control unit. HR baroreflex curves were generated using bolus doses of phenylephrine (10 µg) and sodium nitroprusside (10 µg) and the responses in HR to a change in MABP were recorded and fitted to logistic function curves (Kent et al. 1972). Responses were compared among control (n = 6) and animals treated I.V. with atropine methylnitrate (2 mg kg-1; n = 5) or propranolol (1 mg kg-1; n = 7). Rats were killed with an overdose of sodium pentabarbitone. Data (means ± S.E.M.) were analysed using ANOVA and significance taken at P < 0.05.

Basal levels of HR at Tb = 37 °C were 4 % higher (P < 0.01) and 18 % lower (P < 0.001) in rats treated with atropine and propranolol, respectively, compared with control (424 ± 1 beats min-1). MABP was 4 % lower (P < 0.01) in rats given propranolol compared with control (101 ± 1 mmHg) at Tb = 37 °C. In the presence of atropine, baroreflex-HR parameters (Kent et al. 1972) were: A1 = 27 ± 14 beats min-1, A2 = 0.06 ± 0.04 mmHg-1, A3 = 85 ± 1 mmHg and A4 = 442 ± 9 beats min-1 at Tb = 37 °C, while in the presence of propranolol A1 = 46 ± 6 beats min-1, A2 = 0.08 ± 0.18 mmHg-1, A3 = 106 ± 6 mmHg and A4 = 334 ± 16 beats min-1 at Tb = 37 °C. Atropine depressed the maximal gain by ~50 % (P < 0.05) compared to control values (Sabharwal et al. 2003) whereas it was unchanged with propranolol at Tb = 37 °C. Hypothermia decreased MABP (~10 %, P < 0.01) and HR (~35 %, P < 0.001) in all groups. Baroreflex-HR curves were markedly attenuated, in all groups of animals, at Tb = 25 °C with a decrease in maximal gain by ~85 % vs. control at Tb = 37 °C (-0.93 ± 0.2 beats min-1 mmHg-1; P < 0.001).

These results suggest that reduced levels of both sympathetic and vagal components contribute to the impairment of baroreflex control of HR during acute hypothermia.

Where applicable, experiments conform with Society ethical requirements