A correlation between multiple unit activity in the hypothalamus and electrocardiographic changes during a subarachnoid hemorrhage.

A sudden onset and short latency of cardiovascular responses that may follow a subarachnoid hemorrhage (SAH) in the vicinity of the circle of Willis implicate neural mechanisms. To investigate this, multi unit activity (MUA) was recorded from the posterolateral hypothalamus and electrocardiogram was recorded from lead II before and during SAH in rats. A temporal correlation between MUA, heart rate and rhythm changes was observed. Following SAH, transient depression of MUA (approximately 5 s or less) did not affect heart rate; a more sustained suppression preceded bradycardia and arrhythmias. Bradycardia, premature atrial contractions and premature ventricular contractions occurred under two conditions: when MUA was suppressed; and during bursts in MUA when interburst phases were suppressed. Further evidence that bradycardia may be the result of suppression of brain potentials was obtained by failure of bilateral vagotomy, atropine and isoproterenol to reverse bradycardia generated after SAH under the ventral aspect of the brain in the vicinity of circle of Willis. However, bilateral vagotomy reversed bradycardia after SAH in the cisterna magna indicating an activation of central parasympathetic neurons. The results indicate that different neural mechanisms underlie bradycardia generated from the above mentioned two sites, namely, ventral brain and cisterna magna.