title: In vitro buffering capacity of cardiac and skeletal muscle tissue in normotensive and hypertensive rats. Assessment using PCO2 equilibration of homogenates.
abstract: Experiments were performed to assess the in vitro buffering capacity (physicochemical buffering) of cardiac and skeletal muscle tissue in normotensive and hypertensive rats using the techniques of PCO2 equilibration of tissue homogenates. We have previously shown (Oldershaw PJ, Cameron IR. Int J Cardiol 1988;18:131-141 and Int J Cardiol 1988;18:143-149) that the ability of myocardial cells to regulate intracellular pH is improved in association with left ventricular hypertrophy (induced by experimental hypertension) and this study purports to investigate the role of physicochemical buffering in this improved control. Rats were made hypertensive using the technique of sub-diaphragmatic aortic constriction and left for 1 or 4 weeks at which time samples of left ventricular and skeletal muscle tissue were taken for analysis; sham-operated animals were used as controls. The tissue was homogenised and in vitro buffering capacity assessed using PCO2 equilibration. The slope of the log PCO2-pH plot was calculated for each tissue and taken as a measure of buffering capacity. In control animals, in vitro buffering was greater in skeletal than cardiac muscle (slopes 1.89 +/- 0.5 cf. 1.64 +/- 0.06 P less than 0.05). In association with hypertension of 1 or 4 weeks duration the buffering capacity of left ventricular tissue increased to 2.00 +/- 0.08 (P less than 0.01) at 1 week and to 2.05 +/- 0.06 (P less than 0.01) at 4 weeks. There was no comparable change in the buffering capacity of skeletal muscle tissue. At least part of the observed in vivo changes in intracellular pH control may therefore be explicable on the basis of improved intracellular physicochemical buffering.
authors.affiliation: Cardiac Department, Brompton Hospital, London, U.K.
authors.forename: P J
authors.initials: PJ
authors.lastname: Oldershaw
authors.forename: I R
authors.initials: IR
authors.lastname: Cameron
mesh_terms: D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D002312:Cardiomyopathy, Hypertrophic / Q000209:etiology / Q000503:physiopathology; D006321:Heart / Q000503:physiopathology; D006863:Hydrogen-Ion Concentration; D006973:Hypertension / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D066298:In Vitro Techniques; D009132:Muscles / Q000378:metabolism* / Q000503:physiopathology; D009200:Myocardial Contraction; D009206:Myocardium / Q000032:analysis / Q000378:metabolism*; D011506:Proteins / Q000032:analysis; D051381:Rats
chemical_list: D011506:Proteins; D002245:Carbon Dioxide