TY - JOUR
T1 - Implications of altered inotropic effects of phenylephrine in pressure-overloaded cat ventricular muscle
AU - Gaide, Marion S.
AU - Wiggins, Jay R.
AU - Fitterman, William S.
AU - Cameron, John S.
AU - Myerburg, Robert J.
AU - Bassett, Arthur L.
PY - 1984
Y1 - 1984
N2 - The positive inotropic action of phenylephrine in cardiac muscle is mediated by α- and β-adrenoceptors. Data suggest the responsiveness of myocardium to inotropic agents is altered in cardiac disease. We evaluated the actions of phenylephrine on isometric contraction and K+-induced contracture in isolated cat right ventricular muscle from normal hearts and hearts with partial pulmonary artery ligation-induced pressure overload of 5-11 days in duration. Peak contractile force (P0) and rate of force development (dP/dt) were lower (p ≤ 0.005) in pressure-overloaded (0.59 ± 0.2 g/mm2 and 4.6 ± 1.7 g/s/mm2, respectively) than in normal (1.33 ± 0.2 g/mm2 and 10.5 ± 1.6 g/s/mm2, respectively) muscle. Phenylephrine (10-6, 5 x 10-6, and 10-5 M) significantly (P ≤ 0.01) increased P0 and dP/dt in normal but not in pressure-overloaded muscle. Phenylephrine (5 x 10-6 M) reduced peak K+-induced contracture force (P(c)) similarly in normal (-30 ± 8%) and pressure-overloaded (-36 ± 11%) muscles. β-Adrenergic blockade (nadolol, 10-4 M) reduced, but did not abolish, the 'relaxant' action of the drug on P(c) in both muscle groups. The lack of a positive inotropic effect of phenylephrine in pressure-overloaded muscle suggests a derangement in both α- and β-adrenoceptor function in this model of cardiac disease.
AB - The positive inotropic action of phenylephrine in cardiac muscle is mediated by α- and β-adrenoceptors. Data suggest the responsiveness of myocardium to inotropic agents is altered in cardiac disease. We evaluated the actions of phenylephrine on isometric contraction and K+-induced contracture in isolated cat right ventricular muscle from normal hearts and hearts with partial pulmonary artery ligation-induced pressure overload of 5-11 days in duration. Peak contractile force (P0) and rate of force development (dP/dt) were lower (p ≤ 0.005) in pressure-overloaded (0.59 ± 0.2 g/mm2 and 4.6 ± 1.7 g/s/mm2, respectively) than in normal (1.33 ± 0.2 g/mm2 and 10.5 ± 1.6 g/s/mm2, respectively) muscle. Phenylephrine (10-6, 5 x 10-6, and 10-5 M) significantly (P ≤ 0.01) increased P0 and dP/dt in normal but not in pressure-overloaded muscle. Phenylephrine (5 x 10-6 M) reduced peak K+-induced contracture force (P(c)) similarly in normal (-30 ± 8%) and pressure-overloaded (-36 ± 11%) muscles. β-Adrenergic blockade (nadolol, 10-4 M) reduced, but did not abolish, the 'relaxant' action of the drug on P(c) in both muscle groups. The lack of a positive inotropic effect of phenylephrine in pressure-overloaded muscle suggests a derangement in both α- and β-adrenoceptor function in this model of cardiac disease.
KW - Isolated ventricular muscle
KW - Isometric contraction
KW - K-induced contracture
KW - Phenylephrine
KW - Pressure-overloaded muscle
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U2 - 10.1097/00005344-198403000-00005
DO - 10.1097/00005344-198403000-00005
M3 - Article
C2 - 6200710
AN - SCOPUS:0021320730
VL - 6
SP - 238
EP - 243
JO - Journal of Cardiovascular Pharmacology
JF - Journal of Cardiovascular Pharmacology
SN - 0160-2446
IS - 2
ER -