Sympathetic Nervous Activity and Myocardial Damage Immediately After Subarachnoid Hemorrhage in a Unique Animal Model

Abstract

Background and Purpose-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. Methods-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. Results-Noradrenaline (pg/mL), adrenaline (pg/mL), and MHPG (ng/mL) increased abruptly from 120Ϯ70, 130Ϯ70, and 1.3Ϯ0.5 before SAH to 1700Ϯ1200, 5600Ϯ3500, and 3.2Ϯ1.2 at 5 minutes after SAH, respectively. Aortic pressure, left ventricular wall motion, and cardiac output increased by 60%, 40%, and 30%, respectively (PϽ0.001) at 5 minutes and then decreased by 50%, 55%, and 40%, respectively (PϽ0.001) Ͼ60 minutes after SAH compared with baseline values. The peak value of CK-MB correlated positively with the peak values of noradrenaline and adrenaline (rϭ0.730 and rϭ0.611, respectively). The peak value of troponin T also correlated positively with the peak values of noradrenaline and adrenaline (rϭ0.828 and rϭ0.792, respectively). Conclusions-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.

Fundamental increase in pressure-dependent constriction of brain parenchymal arterioles from subarachnoid hemorrhage model rats due to membrane depolarization

“…Accordingly, the effects of SAH on parenchymal arteriolar constriction observed in the present study may be exacerbated by elevated blood pressures commonly observed in SAH (15,40). At this time, it is unclear how SAH causes enhanced pressure-dependent depolarization in parenchymal arterioles.…”

The Role of Norepinephrine and Estradiol in the Pathogenesis of Cardiac Wall Motion Abnormality Associated With Subarachnoid Hemorrhage

“…Second, plasma catecholamine released into the systemic circulation after SAH is rapidly degraded and plasma levels decrease over time. 30,32 We attempted to reduce such time-related variability by our strict inclusion criteria (ie, including only patients in whom TTE and blood sample collection had been conducted within 48 hours of SAH onset). Nevertheless, the possibility that the difference in the timing of sample collection may have influenced measurement results cannot be denied.…”

Subarachnoid Hemorrhage Complicated With Neurogenic Pulmonary Edema and Takotsubo-Like Cardiomyopathy

“…Both experimental and clinical studies show that destruction or mechanical compression of the dorsal and solitary tract nuclei, which suppress sympathetic activity, leads to acute change in pulmonary vascular permeability and subsequent NPE. 13,22,23,30) A lesion in the solitary tract nucleus also seems to alter the secretion of brain natriuretic peptide, which may also be involved in the pathogenesis of NPE. 6,7) These findings may explain why poor-grade patients with ruptured posterior circulation aneurysm were significantly more likely to sustain NPE compared with anterior circulation aneurysm, as previously reported.…”