OBJECTIVES: Little is known about the effect of hypothermia on neural regulation. We investigated the effects of hypothermia during cardiopulmonary bypass (CPB) on control of renal (RSNA) and lumbar sympathetic nerve activity (LSNA), and plasma catecholamine levels. METHODS: We directly measured RSNA (n = 14) and LSNA (n = 6) during CPB in anesthetized rabbits. CPB was performed via cannulae in the aortic root for arterial perfusion and the right atrium for venous drainage. Systemic hypothermia was induced by core cooling. RSNA and LSNA were recorded at the nasopharyngeal temperature of 37, 30, 24, and 18 degrees C and after rewarming up to 37 degrees C while keeping mean arterial pressure at 70 mmHg by altering perfusion flow. Other variables such as blood gases or electrolytes were kept constant. RESULTS: RSNA at the temperature of 30, 24, and 18 degrees C significantly decreased by 91, 97, and 95% from control (37 degrees C), respectively. LSNA decreased by 18, 57, and 89% from control as well. The decreases in RSNA at 30 and 24 degrees C were greater than those in LSNA (P < 0.05). At 18 degrees C both RSNA and LSNA nearly disappeared. Circulatory arrest for 20 min during hypothermia at 18 degrees C caused no increase in RSNA while it increased LSNA. Plasma catecholamine levels at 18 degrees C were not different from those at 37 degrees C. Rewarming to 37 degrees C increased RSNA and LSNA by 321 and 92% from control (37 degrees C before cooling), respectively (P < 0.01). CONCLUSIONS: Hypothermia progressively decreased and rewarming markedly increased sympathetic nerve activity, but the effects of hypothermia on RSNA and LSNA were not uniform.
OBJECTIVES: Little is known about the effect of hypothermia on neural regulation. We investigated the effects of hypothermia during cardiopulmonary bypass (CPB) on control of renal (RSNA) and lumbar sympathetic nerve activity (LSNA), and plasma catecholamine levels. METHODS: We directly measured RSNA (n = 14) and LSNA (n = 6) during CPB in anesthetized rabbits. CPB was performed via cannulae in the aortic root for arterial perfusion and the right atrium for venous drainage. Systemic hypothermia was induced by core cooling. RSNA and LSNA were recorded at the nasopharyngeal temperature of 37, 30, 24, and 18 degrees C and after rewarming up to 37 degrees C while keeping mean arterial pressure at 70 mmHg by altering perfusion flow. Other variables such as blood gases or electrolytes were kept constant. RESULTS:RSNA at the temperature of 30, 24, and 18 degrees C significantly decreased by 91, 97, and 95% from control (37 degrees C), respectively. LSNA decreased by 18, 57, and 89% from control as well. The decreases in RSNA at 30 and 24 degrees C were greater than those in LSNA (P < 0.05). At 18 degrees C both RSNA and LSNA nearly disappeared. Circulatory arrest for 20 min during hypothermia at 18 degrees C caused no increase in RSNA while it increased LSNA. Plasma catecholamine levels at 18 degrees C were not different from those at 37 degrees C. Rewarming to 37 degrees C increased RSNA and LSNA by 321 and 92% from control (37 degrees C before cooling), respectively (P < 0.01). CONCLUSIONS:Hypothermia progressively decreased and rewarming markedly increased sympathetic nerve activity, but the effects of hypothermia on RSNA and LSNA were not uniform.