|
|
||||||||
AJP - Regulatory, Integrative and Comparative Physiology, Vol 262, Issue 4 579-R585, Copyright © 1992 by American Physiological Society
ARTICLES |
S. Koyama, F. Sawano, Y. Matsuda, Y. Saeki, T. Shibamoto, T. Hayashi Jr, Y. Matsubayashi and M. Kawamoto
Department of Physiology, Shinshu University School of Medicine, Nagano, Japan.
We performed simultaneous multifiber recordings of cardiac, renal (RNA), hepatic (HNA), adrenal, and splenic sympathetic nerve activities during 10 min of sustained hemorrhagic hypotension to a mean blood pressure of 50 mmHg. One minute after bleeding in dogs with intact baroreceptors, all measured nerve activities increased significantly, and a gradual decline toward prebleeding level followed. Only RNA showed a great inhibition below prebleeding level. In cervically vagotomized dogs, all nerve activities showed significantly higher levels than prebleeding control throughout the experiment. The initial increase in HNA observed at 1 min postbleeding in animals with intact baroreceptors was attenuated. HNA in the vagotomized group showed a gradual increase so that 5 min postbleeding, HNA reached a peak level that was maintained until the end of the experiment. Sympathoinhibition in RNA and decrease in heart rate during hemorrhagic hypotension were reversed to significant increases after vagotomy. In contrast, animals with denervation of the carotid sinus and aortic nerves showed initial increases in nerve activities followed by recovery to prebleeding control level within 2 min postbleeding. After complete denervation of systemic baroreceptors, rapid hemorrhage did not cause any significant change in sympathetic nerve activity in any nerve. These results indicate that early reflex response to hemorrhage in regional sympathetic nerves is unidirectional sympathoexcitation mediated by summative unloading of both arterial baroreceptors and cardiopulmonary receptors. When greater than 1 min passed after bleeding and sustained hypotension of 50 mmHg was established, a reflex mechanism through the vagal afferents participated to inhibit the unidirectional sympathoexcitation mediated by unloading of arterial baroreceptors, with different magnitude in different innervated organs.(ABSTRACT TRUNCATED AT 250 WORDS)
This article has been cited by other articles:
![]() |
H. Xu, G. D. Fink, and J. J. Galligan Nitric oxide-independent effects of tempol on sympathetic nerve activity and blood pressure in DOCA-salt rats Am J Physiol Heart Circ Physiol, September 1, 2002; 283(3): H885 - H892. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. F. Morrison Differential control of sympathetic outflow Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2001; 281(3): R683 - R698. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. C. Malpas and D. E. Burgess Renal SNA as the primary mediator of slow oscillations in blood pressure during hemorrhage Am J Physiol Heart Circ Physiol, September 1, 2000; 279(3): H1299 - H1306. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Kawase, T. Komatsu, K. Nishiwaki, T. Kimura, Y. Fujiwara, T. Takahashi, and Y. Shimada Heart rate variability during massive hemorrhage and progressive hemorrhagic shock in dogs Can J Anesth, August 1, 2000; 47(8): 807 - 814. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Hagiike, H. Maeta, H. Murakami, K. Okada, and H. Morita Mechanism of biphasic response of renal nerve activity during acute cardiac tamponade in conscious rabbits Am J Physiol Regulatory Integrative Comp Physiol, May 1, 1999; 276(5): R1232 - R1240. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Fukae, R. Tominaga, S. Tokunaga, Y. Kawachi, T. Imaizumi, and H. Yasui THE EFFECTS OF PULSATILE AND NONPULSATILE SYSTEMIC PERFUSION ON RENAL SYMPATHETIC NERVE ACTIVITY IN ANESTHETIZED DOGS J. Thorac. Cardiovasc. Surg., February 1, 1996; 111(2): 478 - 484. [Abstract] [Full Text] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |