Sympathetic nervous activity and myocardial damage immediately after subarachnoid hemorrhage in a unique animal model

Obvious cardiac dysfunction, including ECG abnormalities and left ventricular asynergy, is known to develop after subarachnoid hemorrhage (SAH). To clarify the close relationship between myocardial damage and sympathetic nervous activity immediately after SAH, a novel experimental animal model was used.

SAH was provoked by perforation of the basilar artery with the use of a microcatheter inserted through the femoral artery in 18 beagle dogs. Hemodynamic changes were recorded, and plasma concentrations of noradrenaline, adrenaline, and 3-methoxy-4-hydroxy-phenylethylene glycol (MHPG) and serum levels of creatine kinase-MB (CK-MB) and troponin T were measured at 0, 5, 15, 30, 60, 120, and 180 minutes after SAH.

Noradrenaline (pg/mL), adrenaline (pg/mL), and MHPG (ng/mL) increased abruptly from 120+/-70, 130+/-70, and 1.3+/-0.5 before SAH to 1700+/-1200, 5600+/-3500, and 3.2+/-1.2 at 5 minutes after SAH, respectively. Aortic pressure, left ventricular wall motion, and cardiac output increased by 60%, 40%, and 30%, respectively (P<0.001) at 5 minutes and then decreased by 50%, 55%, and 40%, respectively (P<0.001) >60 minutes after SAH compared with baseline values. The peak value of CK-MB correlated positively with the peak values of noradrenaline and adrenaline (r=0.730 and r=0.611, respectively). The peak value of troponin T also correlated positively with the peak values of noradrenaline and adrenaline (r=0.828 and r=0.792, respectively).

These results suggest that the elevated activity of the sympathetic nervous system observed in the acute phase of SAH induced myocardial damage and contributed to the development of cardiac dysfunction.