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Global brain ischemia in anesthetized rabbits induces a pressor response, bradycardia, apnea, and a reduction in cardiac output. The bradycardia is virtually abolished by bilateral aortic denervation (ADN). To elucidate hemodynamic responses in the venous system and the role of bradycardia in these responses during brain ischemia, central venous pressure (CVP), femoral venous pressure (FVP), and circulation time (CT) of a dye in large veins were simultaneously measured before and after ADN. Cardiopulmonary blood volume (CPBV) and circulating blood volume (CBV) were also measured using a dye-dilution technique in separate experiments. Before brain ischemia, the value of CVP, FVP, mean arterial pressure (MAP), and heart rate (HR) were 0.2 +/- 1.2 cmH2O, 8.9 +/- 1.9 cmH2O, 76 +/- 16 mmHg, and 274 +/- 35 beats/min, respectively (n = 8, mean +/- SD). During brain ischemia, CVP, FVP, and MAP significantly increased to 5.8 +/- 2.6 cmH2O, 11.1 +/- 2.4 cmH2O, and 159 +/- 10 mmHg, respectively. HR decreased to 113 +/- 54 beats/min. After ADN, the changes of CVP, FVP, and HR evoked by brain ischemia were significantly suppressed to 2.4 +/- 1.6 cmH2O, 9.8 +/- 2.1 cmH2O, and 210 +/- 61 beats/min, respectively; however, the increase in MAP was not affected. During brain ischemia, CVP correlated negatively with HR, and positively with CT. CPBV tended to decrease and CBV significantly increased by 3.7 +/- 2.5 ml/kg from that before brain ischemia. It seems that the increased amount in CBV evoked by brain ischemia mainly exists in large veins. From these results we conclude that bradycardia is a major determinant of the blood volume in the cardiopulmonary system and prevents its overflow into pulmonary circulation during global brain ischemia in the rabbit when afterload to the left ventricle is extremely increased.

Hemodynamic Responses of the Venous System during Global Brain Ischemia Related to the Reflex Bradycardia in the Rabbit.