山梨医科大学雑誌　第10巻3号　099-110(1995)

Cardiac Sympathetic and Vagal Activities during Suprapontine Brain
and Midbrain Ischemic Pressor Responses in Rabbits

Hisasi TERAJIMA and Toru TAKEUCHI

Abstract: The role of the midbrain and suprapontine brain structures in controlling the heart was studied in anesthetized and baroreceptor-denervated rabbits. Graded suprapontine brain ischemia (SI) and midbrain ischemia (MI) were evoked by the following methods. After stopping blood flow at the rostral end of the basilar artery as well as blood flow through the left common carotid artery, blood flow in the right common carotid artery was surgically equalized with that in the right internal carotid blood flow (ICF). Thus, the right common carotid artery was the sole route of blood supply to the suprapontine brain. This artery was then compressed in a stepwise manner with an actuator connected to a servo-controller so as to regulate blood flow to six reduced levels: 0, 1, 2, 3, 4, and 6 ml/min. Cardiac sympathetic nerve activity and mean arterial pressure (MAP) began to increase (+254±76% in SI, +257±56%, in MI) significantly at ICF below 3 ml/min, while Heart rate (HR) and cardiac vagus nerve activity respectively started to increase and decrease (-16±3% in SI, -21±3% in MI) significantly at ICF values below 2 ml/min. MAP, HR and total peripheral resistance (TPR) started to increase significantly at ICF below 3 ml/min, and cardiac output (CO) began to decrease significantly at ICF below 2 ml/min. There was no significant difference between any paired values of any variable during SI and MI. Bilateral blockade of the stellate ganglia (SGB) induced large and significant decreases in MAP, HR and CO and evoked disappearance of the significant increase in HR that accompanied the decrease in ICF described above. Additional vagus sectioning (VS) elicited no further significant change in any variables. In conclusion, sympathoexcitation elicited by SI and MI significantly increased HR. However, changes in variables other than the baseline during SI and MI were only slightly influenced by SGB and VS. A decrease in CO elicited with pressor responses induced by SI and MI was thought to be due to an increase in afterload to the heart.

Key words: Cardiac sympathetic nerve; cardiac parasympathetic nerve; midbrain ischemia; heart rate; cardiac output




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