Parasympathetic inhibition of sympathetic effects on sinus rate in anesthetized dogs

1996 ◽  
Vol 271 (1) ◽  
pp. H44-H50 ◽  
Author(s):  
Y. Furukawa ◽  
Y. Hoyano ◽  
S. Chiba
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Pulmonary Veins ◽  
Fatty Tissue ◽  
Sympathetic Stimulation ◽  
Vagus Stimulation ◽  
Sympathetic Nerve Stimulation ◽  
Chronotropic Response ◽  
Sinus Rate ◽  
Isoproterenol Infusion

The intracardiac parasympathetic neural elements that control sinus rate are found in the fatty tissue overlying the atrial junctions of the right pulmonary veins of mammalian hearts. We refer to these nerves as the sinus rate-related parasympathetic nerves (SRRPN). Thus, to elucidate the role of SRRPN, we studied the effects of cervical vagus stimulation on the positive chronotropic responses to cardiac sympathetic nerve stimulation and isoproterenol infusion before and after the SRRPN were removed in the open-chest anesthetized dog heart. Before SRRPN denervation, cervical vagus stimulation suppressed the sinus rate and the positive chronotropic response to sympathetic nerve stimulation or isoproterenol infusion. After SRRPN denervation, cervical vagus stimulation hardly decreased the sinus rate. On the other hand, even after SRRPN denervation, cervical vagus stimulation suppressed the rate increased by sympathetic stimulation. Cervical vagus stimulation also attenuated the sinus rate increased by isoproterenol. The inhibition by vagus stimulation of the chronotropic response to sympathetic stimulation was greater than that of the response to isoproterenol. The attenuation by cervical vagus stimulation was abolished by atropine. These results suggest that 1) a small number of vagus nerves to the sinoatrial nodal area different from the SRRPN decrease the sinus rate increased by adrenergic interventions and 2) the same activation that causes relatively small effects on sinus rate is capable of causing much larger changes in sinus rate during increased sympathetic tone or in the case of beta-adrenoceptor agonist treatment in the heart in situ.

Responses of atrium and ventricle to sustained sympathetic nerve stimulation

1991 ◽  
Vol 261 (6) ◽  
pp. H1889-H1894
Author(s):  
M. Furuyama ◽  
T. Haneda ◽  
J. Ikeda ◽  
T. Hiramoto ◽  
T. Sakuma ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Stellate Ganglion ◽  
Left Ventricular ◽  
Right Atrial ◽  
Control Group ◽  
Inotropic Response ◽  
Sympathetic Nerve Stimulation ◽  
Chronotropic Response ◽  
Control Value

To determine whether chronotropic and atrial inotropic responses to sympathetic nerve stimulation are maintained longer than ventricular inotropic response, the present study was performed with control and acute reserpinized dogs. We stimulated the right stellate ganglion of both groups supramaximally for 60 min and compared right atrial responses (chronotropism and inotropism) with left ventricular (LV) dP/dtmax. In the control group, heart rate (HR) immediately increased and was only slightly attenuated with 60 min of stimulation, and right atrial (RA) inotropic response was less attenuated than was LV response (7% in HR, 33% in RA dP/dtmax, 50% in LV dP/dtmax, P less than 0.01, from the peak value of each response). RA and LV norepinephrine (NE) content was decreased by the stimulation but remained higher than the LV control value. In the reserpinized group, NE content in the RA was low before the stimulation and was further decreased by the stimulation. In this group, HR response was attenuated (27% in HR, P less than 0.01) as was LV dP/dtmax, and the difference in contractile responsiveness between atrium and ventricle disappeared (58% in RA dP/dtmax vs. 61% in LV dP/dtmax, NS). The results indicate that the chronotropic response was only slightly attenuated and that the atrial contractile response was attenuated less than the ventricular response, with sustained sympathetic nerve stimulation in the normal heart. This can be ascribed to the much higher NE content in the RA than that in the LV.

Response of arteriolar network of skeletal muscle to sympathetic nerve stimulation

1988 ◽  
Vol 254 (5) ◽  
pp. H919-H928 ◽  
Author(s):  
M. A. Boegehold ◽  
P. C. Johnson
Keyword(s):  
Skeletal Muscle ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Vascular Tone ◽  
Volume Flow ◽  
Sartorius Muscle ◽  
Sympathetic Stimulation ◽  
Sympathetic Nerve Stimulation ◽  
Calculated Volume ◽  
Arteriolar Diameter

The influence of vessel location on arteriolar responses to sympathetic nerve stimulation was systematically studied in a skeletal muscle arteriolar network under normal and altered tissue O2 levels. The exteriorized cat sartorius muscle was exposed to 0, 5, and 10% ambient O2 during sympathetic chain stimulation at 8 pulses/s. Under 0% O2, stimulation initially caused a 25-45% constriction that was faster and more pronounced in distal arterioles. Ninety-one percent of vessels showed a secondary dilation (sympathetic escape), which was largest in distal arterioles. Escape had little effect on calculated volume flow, which, after a large initial fall, showed a modest secondary increase. Under 5 and 10% O2, resting arteriolar diameter was reduced by 12 and 17%, respectively, and escape was reduced by 60 and 73%. Escape was not attenuated in proximal arterioles preconstricted with vasopressin, suggesting that O2 did not attenuate escape through increased vascular tone. Therefore, the arteriolar response to sympathetic stimulation depends largely on location within the network and is modulated to varying degrees by metabolic influences.

Adrenergic responses in canine cutaneous vasculature during acute hemorrhagic hypotension

1975 ◽  
Vol 228 (3) ◽  
pp. 752-755 ◽  
Author(s):  
JC Liao ◽  
BG Zimmerman ◽  
FH Van Bergen
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
High Dose ◽  
Sodium Pentobarbital ◽  
Sympathetic Stimulation ◽  
Sympathetic Nerve Stimulation ◽  
Acute Hemorrhage ◽  
Renin Level

The purpose of this study was to determine the effect of acute hemorrhage on vascular responses to sympathetic nerve stimulation and norepinephrine. The experiments were carried out with sodium pentobarbital anesthesia. The preparation employed was the dog's hindpaw perfused at constant blood flow. Changes in vascular resistance in the paw were indicated by changes in perfusion pressure. Changes in perfusion pressure elicited by sympathetic nerve stimulation and intra-arterially administered norepinephrine were determined before and after hemorrhage of 15 ml/kg in normal and acutely nephrectomized animals. The response to sympathetic stimulation was increased by about 50% in normal but not in nephrectomized dogs, whereas the response to a low dose of norepinephrine (0.5-1 mug) was not significantly changed in either group of animals. In additional experiments in which the plasma renin level was measured, the potentiation of responses to sympathetic stimulation and a high dose of norepinephrine (2 mug) occurred at the time that the renin level was increased by hemorrhage. These results indicate that the level of circulating angiotensin attained after hemorrhage may facilitate vasoconstrictor responses to adrenergic stimuli.

Interactive Effects of Verapamil and Sympathetic Nerve Stimulation on the Sinus and AV Nodes in the Canine Hearts.

1992 ◽  
Vol 33 (1) ◽  
pp. 83-93 ◽  
Author(s):  
Katsusuke YANO ◽  
Masanobu HIRATA ◽  
Takao MITSUOKA ◽  
Yoriaki MATSUMOTO ◽  
Tetsuya HIRATA ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Interactive Effects ◽  
Sympathetic Nerve Stimulation
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