![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
1 Department of Pharmacology, Harvard Medical School, Boston, Massachusetts
A method is described for the use of field stimulation to produce pronounced and reproducibly graded sympathomimetic and parasympathomimetic effects in preparations of isolated heart muscle without disturbing the rate or rhythm of contraction. In addition to causing the release of autonomic neurotransmitters, field stimuli can alter the strength of contraction of heart muscle by at least three other mechanisms. If they are recognized, the latter need not interfere greatly with the method. The parasympathomimetic component of the response to field stimulation is abolished by atropine. There is a definite cholinergic response in the cat papillary muscle, though it is much less prominent than in atrial muscle. Maximally effective amounts of norepinephrine are readily liberated by field stimulation; the effects of submaximal stimulation are enhanced by cocaine. The adrenergic component of the response to field stimulation is markedly reduced by propranolol, and is absent in the chronically denervated heart. It is reduced after the administration of reserpine, and in cats (but not guinea pigs) it may be eliminated entirely by pretreatment with reserpine. In guinea-pig atria, reserpine pretreatment reduces the sympathomimetic response to field stimulation and the inotropic action of tyramine to about the same extent. There are important differences between the effects of reserpine pretreatment on the inotropic and chronotropic actions of tyramine. With proper precautions, it is possible to drive preparations of isolated heart muscle electrically without producing appreciable sympathomimetic or parasympathomimetic effects. However, many methods of stimulation in common use are likely to cause the release of substantial amounts of the autonomic neurotransmitters.
Accepted on September 13, 1965
This article has been cited by other articles:
|
|
 |
|
  S. N. Mink, Z.-Q. Cheng, R. Bose, H. Jacobs, K. Kasian, D. E. Roberts, L. E. Santos-Martinez, and R. B. Light Lysozyme, a mediator of sepsis, impairs the cardiac neural adrenergic response by nonendothelial release of NO and inhibitory G protein signaling Am J Physiol Heart Circ Physiol, November 1, 2007; 293(5): H3140 - H3149. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Miyauchi, M. C. Fishbein, and H. S. Karagueuzian Electrical current-induced atrial and pulmonary vein action potential duration shortening and repetitive activity Am J Physiol Heart Circ Physiol, July 1, 2004; 287(1): H178 - H186. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. P. Walcott, S. B. Melnick, C. R. Killingsworth, W. M. Smith, and R. E. Ideker Effects of burst stimulation during ventricular fibrillation on cardiac function after defibrillation Am J Physiol Heart Circ Physiol, July 11, 2003; 285(2): H766 - H774. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z.-Q. Cheng, D. Bose, H. Jacobs, R Bruce Light, and S. N Mink Sepsis causes presynaptic histamine H3 and {alpha}2-adrenergic dysfunction in canine myocardium Cardiovasc Res, November 1, 2002; 56(2): 225 - 234. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. K. Gwathmey, C. S. Kim, R. J. Hajjar, F. Khan, T. G. DiSalvo, A. Matsumori, and M. R. Bristow Cellular and molecular remodeling in a heart failure model treated with the beta -blocker carteolol Am J Physiol Heart Circ Physiol, May 1, 1999; 276(5): H1678 - H1690. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X. Li, G. Eschun, D. Bose, H. Jacobs, J. J. Yang, R. B. Light, and S. N. Mink Histamine H3 activation depresses cardiac function in experimental sepsis J Appl Physiol, November 1, 1998; 85(5): 1693 - 1701. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. J. Goldberger, J. R. Smith, Y.-H. Kim, R. S. Damle, and A. H. Kadish Effect of Increased Drive-train Stimulus Intensity on Dispersion of Ventricular Refractoriness Circulation, August 15, 1995; 92(4): 875 - 880. [Abstract] [Full Text]
|
|
|
|
 |
|
 F. Crews and C. Smith Presynaptic alpha-receptor subsensitivity after long-term antidepressant treatment Science, October 20, 1978; 202(4365): 322 - 324. [Abstract] [PDF]
|
|
 |
 |
 |
|
 |
 |
 |
