This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Masuda, T. Articles by Izumi, T. Search for Related Content PubMed PubMed Citation Articles by Masuda, T. Articles by Izumi, T. Related Collections Contractile function Animal models of human disease Myocardial cardiomyopathy disease Cerebral Aneurysm, AVM, & Subarachnoid hemorrhage

(Stroke. 2002;33:1671.)
© 2002 American Heart Association, Inc.

Original Contributions

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

Takashi Masuda, MD; Kiyotaka Sato, MD; Shin-ichiro Yamamoto, MD; Narihisa Matsuyama, MD; Takao Shimohama, MD; Atsuhiko Matsunaga, PhD; Shuichi Obuchi, PhD; Yoshitaka Shiba, MS; Shinobu Shimizu, MS Tohru Izumi, MD

From the Department of Rehabilitation (T.M., A.M., S.O., Y.S., S.S.), School of Allied Health Sciences, and Departments of Internal Medicine (K.S., N.M., T.S., T.I.) and Emergency and Critical Care Medicine (S.Y.), School of Medicine, Kitasato University, Sagamihara, Japan.

Correspondence to Takashi Masuda, MD, Department of Rehabilitation, School of Allied Health Sciences, Kitasato University, 1-15-1 Kitasato, Sagamihara, Kanagawa, 228-8555, Japan. E-mail tak9999{at}med.kitasato-u.ac.jp

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 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).

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.

Key Words: cardiovascular diseases • catecholamines • subarachnoid hemorrhage • sympathetic nervous system • ventricular dysfunction • dogs

This article has been cited by other articles:

				K. A. Bybee and A. Prasad Stress-Related Cardiomyopathy Syndromes Circulation, July 22, 2008; 118(4): 397 - 409. [Full Text] [PDF]

				S. Laowattana, S. L. Zeger, J.A.C. Lima, S. N. Goodman, I. S. Wittstein, and S. M. Oppenheimer Left insular stroke is associated with adverse cardiac outcome Neurology, February 28, 2006; 66(4): 477 - 483. [Abstract] [Full Text] [PDF]

				M. Mazighi, J.-P. Saint Maurice, A. Rogopoulos, and E. Houdart Extracranial vertebral and carotid dissection occurring in the course of subarachnoid hemorrhage Neurology, November 8, 2005; 65(9): 1471 - 1473. [Abstract] [Full Text] [PDF]

				W J Schuiling, P J W Dennesen, J T. J Tans, L M Kingma, A Algra, and G J E Rinkel Troponin I in predicting cardiac or pulmonary complications and outcome in subarachnoid haemorrhage J. Neurol. Neurosurg. Psychiatry, November 1, 2005; 76(11): 1565 - 1569. [Abstract] [Full Text] [PDF]

				M. Schillinger Editorial Comment--Brain Natriuretic Peptide and Early Cardiac Dysfunction After Subarachnoid Hemorrhage Stroke, July 1, 2005; 36(7): 1570 - 1571. [Full Text] [PDF]

				D. S. Ditor, M. V. Kamath, M. J. MacDonald, J. Bugaresti, N. McCartney, and A. L. Hicks Effects of body weight-supported treadmill training on heart rate variability and blood pressure variability in individuals with spinal cord injury J Appl Physiol, April 1, 2005; 98(4): 1519 - 1525. [Abstract] [Full Text] [PDF]

				S. Homma and C. Grahame-Clarke Editorial Comment--Myocardial Damage in Patients With Subarachnoid Hemorrhage Stroke, February 1, 2004; 35(2): 552 - 553. [Full Text] [PDF]

				K. B. Wallace, E. Hausner, E. Herman, G. D. Holt, J. T. Macgregor, A. L. Metz, E. Murphy, I.Y. Rosenblum, F. D. Sistare, and M. J. York Serum Troponins as Biomarkers of Drug-Induced Cardiac Toxicity Toxicol Pathol, January 1, 2004; 32(1): 106 - 121. [PDF]