The Effect of Sustained Stellate Ganglion Stimulation on Left Ventricular Contractility in the Dog

HITOSHI KANDA; TAKASHI HANEDA; JUN IKEDA; TETSUYA HIRAMOTO; MOTOYUKI FURUYAMA; TOSHIAKI SAKUMA; KUNIO SHIRATO; TAMOTSU TAKISHIMA

doi:10.1620/tjem.156.135

HITOSHI KANDA, TAKASHI HANEDA, JUN IKEDA, TETSUYA HIRAMOTO, MOTOYUKI FURUYAMA, TOSHIAKI SAKUMA, KUNIO SHIRATO, TAMOTSU TAKISHIMA

Author information

HITOSHI KANDA
The First Department of Internal Medicine, Tohoku University School of Medicine
TAKASHI HANEDA
The First Department of Internal Medicine, Tohoku University School of Medicine
JUN IKEDA
The First Department of Internal Medicine, Tohoku University School of Medicine
TETSUYA HIRAMOTO
The First Department of Internal Medicine, Tohoku University School of Medicine
MOTOYUKI FURUYAMA
The First Department of Internal Medicine, Tohoku University School of Medicine
TOSHIAKI SAKUMA
The First Department of Internal Medicine, Tohoku University School of Medicine
KUNIO SHIRATO
The First Department of Internal Medicine, Tohoku University School of Medicine
TAMOTSU TAKISHIMA
The First Department of Internal Medicine, Tohoku University School of Medicine

Keywords: stellate ganglion stimulation, left ventricular contractility, myocardial norepinephrine, plasma norepinephrine

JOURNAL FREE ACCESS

1988 Volume 156 Issue 2 Pages 135-148

DOI https://doi.org/10.1620/tjem.156.135

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Published: 1988 Received: May 31, 1988 Available on J-STAGE: August 31, 2006 Accepted: September 03, 1988 Advance online publication: - Revised: -
Correction information
Date of correction: August 31, 2006 Reason for correction: - Correction: ABSTRACT Details: Wrong : KANDA, H., HANEDA, T., IKEDA, J., HIRAMOTO, T., FURUYAMA, M., SAKUMA, T., SHIRATO, K. and TAKISHIMA, T. The Effect of Sustained stellate Ganglion Stimulation on Left Ventricular Contractility in the Dog. Tohoku J. exp. Med., 1988, 156 (2), 135-148 - Although a progressive reduction in left ventricular contractility during sustained left stellate ganglion stimulation has been well documented, there have been no reports on the contractile state after nerve stimulation. Left ventricular contractility after cessation of 60min of electrical (10V, 10 Hz, 1msec) left stellate ganglion stimulation has been assessed in open chest dogs. Before and 15min after stimulation, left ventricular contractility was evaluated by the end-systolic pressure-segment length relationship using ultrasonic crystals during a stepwise aortic constriction to increase left ventricular afterload. Res timulation of the left stellate ganglion was also performed 15min after cessation of the first stimulation. After sustained left stellate ganglion stimulation, the end-systolic points shifted to the right from the control and the slope of multiple pressure-segment length coordinates significantly decreased (102.5±16.1 to 76.5± 10.2mmHg/mm, mean+S.E., p<0.05, n=5), indicating a depression of left ventricular contractility. Increased left ventricular dP/dt max and norepinephrine level in the coronary sinus gradually returned to near base line during 60min of stimulation. These reduced responses lasted for at least 15min after cessation of stimulation. The myocardial norepinephrine content was reduced to 0.59±0.08 ( mean+S.E.) ng/mg wet tissue from 0.90±0.15 of the control level (p< 0.05). These data suggested that left ventricular contractility decreased after sustained cardiac sympathetic nerve stimulation, probably due to norepinephrine reduction in the myocardium.
Right : Although a progressive reduction in left ventricular contractility during sustained left stellate ganglion stimulation has been well documented, there have been no reports on the contractile state after nerve stimulation. Left ventricular contractility after cessation of 60 min of electrical (10 V, 10 Hz, 1 msec) left stellate ganglion stimulation has been assessed in open chest dogs. Before and 15 min after stimulation, left ventricular contractility was evaluated by the end-systolic pressure-segment length relationship using ultrasonic crystals during a stepwise aortic constriction to increase left ventricular afterload. Restimulation of the left stellate ganglion was also performed 15 min after cessation of the first stimulation. After sustained left stellate ganglion stimulation, the end-systolic points shifted to the right from the control and the slope of multiple pressure-segment length coordinates significantly decreased (102.5±16.1 to 76.5±10.2mmHg/mm, mean±S. E., p < 0.05, n=5), indicating a depression of left ventricular contractility. Increased left ventricular dP/dt max and norepinephrine level in the coronary sinus gradually returned to near base line during 60 min of stimulation. These reduced responses lasted for at least 15 min after cessation of stimulation. The myocardial norepinephrine content was reduced to 0.59±0.08 (mean±S. E.) ng/mg wet tissue from 0.90±0.15 of the control level (p < 0.05). These data suggested that left ventricular contractility decreased after sustained cardiac sympathetic nerve stimulation, probably due to norepinephrine reduction in the myocardium.

Date of correction: August 31, 2006 Reason for correction: - Correction: CITATION Details: Wrong : 1) Brown, J.W. (1979) Cholinergic inhibition of cathecholamine-stimulable cyclic AMP accumulation in marine atria. J. cyclic Nucleotide Res., 5, 423-433.
2) Cairoli, V.J., Reilly, J.F. & Robberts, J. (1962) Effect of reserpine pretreatment on the response of isolated papillary muscle to epinephrine. Brit. J. Pharmacol., 18, 588-594.
3) Chidsey, C.A., Sonnenblick, E.H., Morrow, A.G. & Braunwald, E. (1966) Norepinephrine stores and contractile force of papillary muscle from the failing heart. Circulation, 33, 43-51.
4) Covell, J.W., Chidsey, C.A. & Braunwald, E. (1966) Reduction of the cardiac response to postganglionic sympathetic nerve stimulation in experimental heart failure. Circulat. Res., 19, 51-56.
5) Crozatier, B., Caillet, D. & Bical, O. (1984) Left ventricular adaptation to sustained pressure overload in the conscious dog. Circulat. Res., 54, 21-29.
6) Dearnaley, D.P. & Geffin, L.B. (1966/7) Effect of nerve stimulation on the noradrenaline content of spleen. Proc. roy. Soc., 166, 303-315.
7) Dobson, J.G., Jr. (1978) Reduction by adenosine of the isoproterenol-induced increase in cyclic adenosine 3, 5-monophosphate formation and glycogen phosphorylase activity in rat heart muscle. Circulat. Res., 43, 785-792.
8) Felder, R.B. & Thames, M.D. (1981) The cardio-cardiac sympathetic reflex during coronary occlusion in anesthetized dogs. Circulat. Res., 48, 685-692.
9) Folkow, B., Haggendal, J. & Lisander, B. (1967) Extent of release and elimination of norepinephrine at peripheral adrenergic nerve terminals. Acta physiol. scand., Suppl., 307, 1-38.
10) Gordon, L.P., DeMaster, E.G. & Cohn, J.N. (1984) Regional differences in adrenergic function within the left ventricle. Amer. J. Physiol., 246, H824-H829.
11) Gross, S.S., Gou, Z.G., Levy, R., Bailey, W.H. & Chenouda, A.A. (1984) Release of histamine by sympathetic nerve stimulation in the guinea pig heart and modulation of adrenergic response: A physiological role for cardiac histamine? Circulat. Res., 54, 516-526.
12) Haneda, T., Miura, Y., Arai, T., Nakajima, T., Miura, T., Honda, T., Kobayashi, K., Sakuma, H., Adachi, M., Miyazawa, K., Yoshinaga, K. & Takishima, T. (1980) Norepinephrine levels in the coronary sinus in patients with cardiovascular disease at rest and during isometric handgrip exercise. Amer. Heart J., 100, 465-472.
13) Harrison, D.C., Chidsey, C.A., Goldman, R. & Braunwald, E. (1963) Relationships between the release and tissue depletion of norepinephrine from the heart by guanethidine and reserpine. Circulat. Res., 12, 256-263.
14) Ikeda, J., Haneda, T., Kanda, H., Hiramoto, T., Furuyama, M., Shirato, K. & Takishima, T. (1984) Does circulating norepinephrine affect the inotropic effect of the sympathetic nerve stimulation? Jap. Circulat. J., 48, 941. (Abstract)
15) Kanazawa, M., Shirato, K., Ishikawa, K., Nakajima, T., Haneda, T. & Takishima, T. (1983) The effect of pericardium on the end-systolic pressure segment length relationship in canine left ventricle in acute volume overload. Circulat. Res., 68, 1290-1298.
16) Lefkowitz, R.J. & Williams, L.T. (1978) Molecular mechanism of activation and desensitization of adenylate cyclase coupled beta-adrenergic receptors. Advanc. cyclic Nucleotide Res., 9, 1-17.
17) Levy, M.N. & Blattberg, B. (1976) Progressive reduction in norepinephrine overflow during cardiac sympathetic nerve stimulation in anesthetized dog. Cardiovasc. Res., 10, 549-555.
18) Miura, Y., Campese, V., DeQuattro, V. & Meijiner, D.J. (1977) Plasma cathe cholamine via an improved fluorometric assay: Comparison with an enzymatic method. J. Lab. clin. Med., 89, 421-427.
19) Monroe, R.J., LaFarge, C.G., Gamble, W.J., Rosenthal, A. & Honda, S. (1968) Left ventricular pressure-volume relation and performance as affected by sudden increase in developed pressure. Circulat. Res., 22, 333-344.
20) Pool, P.E., Covell, J.W., Levitt, M., Gibb, J. & Braunwald, E. (1967) Reduction on cardiac tyrosine hydroxylase activity in experimental congestive heart failure. Circulat. Res., 20, 349-353.
21) Spann, J.F., Sonnenblick, E.H., Cooper, T., Chidsey, C.A., Williams, V.L. & Braunwald, E. (1966) Cardiac norepinephrine stores and contractile state of heart muscle. Circulat. Res., 19, 317-325.
22) Suga, H. & Sagawa, K. (1974) Assesment of absolute volume from diameter of the intact canine left ventricular cavity. J. appl. Physiol., 36, 496-499.
23) Tsien, R.W. (1977) Cyclic AMP and contractile activity in heart. Advanc. cyclic Nucleotide Res., 8, 363-420.
24) Varoli, C., Brunori, C.A., Renzini, V. & Gorea, L. (1970) Improved procedure for formation of epinephrine and norepinephrine fluorophors by the trihydroxyindole reaction. Analyt. Biochem., 33, 159-167.
25) Yamaguchi, N., Champlain, J. & Nadeau, R. (1975) Correlation between the response of the heart to sympathetic stimulation and the release of endogenous cathecholamines into the coronary sinus of the dog. Circulat. Res., 36, 662-668.

Right : 1) Brown, J. W. (1979) Cholinergic inhibition of cathecholamine-stimulable cyclic AMP accumulation in murine atria. J. cyclic Nucleotide Res., 5, 423-433.
2) Cairoli, V. J., Reilly, J. F. & Robberts, J. (1962) Effect of reserpine pretreatment on the response of isolated papillary muscle to epinephrine. Brit. J. Pharmacol., 18, 588-594.
3) Chidsey, C. A., Sonnenblick, E. H., Morrow, A. G. & Braunwald, E. (1966) Norepinephrine stores and contractile force of papillary muscle from the failing heart. Circulation, 33, 43-51.
4) Covell, J. W., Chidsey, C. A. & Braunwald, E. (1966) Reduction of the cardiac response to postganglionic sympathetic nerve stimulation in experimental heart failure. Circulat. Res., 19, 51-56.
5) Crozatier, B., Caillet, D. & Bical, O. (1984) Left ventricular adaptation to sustained pressure overload in the conscious dog. Circulat. Res., 54, 21-29.
6) Dearnaley, D. P. & Geffin, L. B. (1966/7) Effect of nerve stimulation on the noradrenaline content of spleen. Proc. roy. Soc., 166, 303-315.
7) Dobson, J. G., Jr. (1978) Reduction by adenosine of the isoproterenol-induced increase in cyclic adenosine 3, 5-monophosphate formation and glycogen phosphorylase activity in rat heart muscle. Circulat. Res., 43, 785-792.
8) Felder, R. B. & Thames, M. D. (1981) The cardio-cardiac sympathetic reflex during coronary occlusion in anesthetized dogs. Circulat. Res., 48, 685-692.
9) Folkow, B., Haggendal, J. & Lisander, B. (1967) Extent of release and elimination of norepinephrine at peripheral adrenergic nerve terminals. Acta physiol. scand., Suppl., 307, 1-38.
10) Gordon, L. P., DeMaster, E. G. & Cohn, J. N. (1984) Regional differences in adrenergic function within the left ventricle. Amer. J. Physiol., 246, H824-H829.
11) Gross, S. S., Gou, Z. G., Levy, R., Bailey, W. H. & Chenouda, A. A. (1984) Release of histamine by sympathetic nerve stimulation in the guinea pig heart and modulation of adrenergic response : A physiological role for cardiac histamine ? Circulat. Res., 54, 516-526.
12) Haneda, T., Miura, Y., Arai, T., Nakajima, T., Miura, T., Honna, T., Kobayashi, K., Sakuma, H., Adachi, M., Miyazawa, K., Yoshinaga, K. & Takishima, T. (1980) Norepinephrine levels in the coronary sinus in patients with cardiovascular disease at rest and during isometric handgrip exercise. Amer. Heart J., 100, 465-472.
13) Harrison, D. C., Chidsey, C. A., Goldman, R. & Braunwald, E. (1963) Relationships between the release and tissue depletion of norepinephrine from the heart by guanethidine and reserpine. Circulat. Res., 12, 256-263.
14) Ikeda, J., Haneda, T., Kanda, H., Hiramoto, T., Furuyama, M., Shirato, K. & Takishima, T. (1984) Does circulating norepinephrine affect the inotropic effect of the sympathetic nerve stimulation? Jap. Circulat. J., 48, 941. (Abstract)
15) Kanazawa, M., Shirato, K., Ishikawa, K., Nakajima, T., Haneda, T. & Takishima, T. (1983) The effect of pericardium on the end-systolic pressure segment length relationship in canine left ventricle in acute volume overload. Circulat. Res., 68, 1290-1298.
16) Lefkowitz, R. J. & Williams, LT. (1978) Molecular mechanism of activation and desensitization of adenylate cyclase coupled beta-adrenergic receptors. Advanc. cyclic Nucleotide Res., 9, 1-17.
17) Levy, M. N. & Blattberg, B. (1976) Progressive reduction in norepinephrine overflow during cardiac sympathetic nerve stimulation in anesthetized dog. Cardiovasc. Res., 10, 549-555.
18) Miura, Y., Campese, V., DeQuattro, V. & Meijiner, D. J. (1977) Plasma cathecholamine via an improved fluorometric assay: Comparison with an enzymatic method. J. Lab. clin. Med., 89, 421-427.
19) Monroe, R. J., LaFarge, C. G., Gamble, W. J., Rosenthal, A. & Honda, S. (1968) Left ventricular pressure-volume relation and performance as affected by sudden increase in developed pressure. Circulat. Res., 22, 333-344.
20) Pool, P. E., Covell, J. W., Levitt, M., Gibb, J. & Braunwald, E. (1967) Reduction on cardiac tyrosine hydroxylase activity in experimental congestive heart failure. Circulat. Res., 20, 349-353.
21) Spann, J. F., Sonnenblick, E. H., Cooper, T., Chidsey, C. A., Williams, V. L. & Braunwald, E. (1966) Cardiac norepinephrine stores and contractile state of heart muscle. Circulat. Res., 19, 317-325.
22) Suga, H. & Sagawa, K. (1974) Assesment of absolute volume from diameter of the intact canine left ventricular cavity. J. appl. Physiol., 36, 496-499.
23) Tsien, R. W. (1977) Cyclic AMP and contractile activity in heart. Advanc. cyclic Nucleotide Res., 8, 363-420.
24) Varoli, C., Brunori, C. A., Renzini, V. & Gorea, L. (1970) Improved procedure for formation of epinephrine and norepinephrine fluorophors by the trihydroxyindole reaction. Analyt. Biochem., 33, 159-167.
25) Yamaguchi, N., Champlain, J. & Nadeau, R. (1975) Correlation between the response of the heart to sympathetic stimulation and the release of endogenous cathecholamines into the coronary sinus of the dog. Circulat. Res., 36, 662-668.

Date of correction: August 31, 2006 Reason for correction: - Correction: PDF FILE Details: -

Abstract

Although a progressive reduction in left ventricular contractility during sustained left stellate ganglion stimulation has been well documented, there have been no reports on the contractile state after nerve stimulation. Left ventricular contractility after cessation of 60 min of electrical (10 V, 10 Hz, 1 msec) left stellate ganglion stimulation has been assessed in open chest dogs. Before and 15 min after stimulation, left ventricular contractility was evaluated by the end-systolic pressure-segment length relationship using ultrasonic crystals during a stepwise aortic constriction to increase left ventricular afterload. Restimulation of the left stellate ganglion was also performed 15 min after cessation of the first stimulation. After sustained left stellate ganglion stimulation, the end-systolic points shifted to the right from the control and the slope of multiple pressure-segment length coordinates significantly decreased (102.5±16.1 to 76.5±10.2mmHg/mm, mean±S. E., p < 0.05, n=5), indicating a depression of left ventricular contractility. Increased left ventricular dP/dt max and norepinephrine level in the coronary sinus gradually returned to near base line during 60 min of stimulation. These reduced responses lasted for at least 15 min after cessation of stimulation. The myocardial norepinephrine content was reduced to 0.59±0.08 (mean±S. E.) ng/mg wet tissue from 0.90±0.15 of the control level (p < 0.05). These data suggested that left ventricular contractility decreased after sustained cardiac sympathetic nerve stimulation, probably due to norepinephrine reduction in the myocardium.

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