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Myocardial tissue pH in respiratory acidosis and ischaemia
RESPIRATORY FUNCTION AND VASCULARISATION OF LEFT VENTRICULAR MYOCARDIUM FROM RATS WITH CHRONICAL ANEMIA. F. Cluzeaud, M. Laplace, G. Renault and J. Moravec, I.N.S.E.R.M. U2, HBpital L&on Bernard, 94450 Limeil-Brevannes France. Severe ferriprive anemia was induced in new-born rats by feeding a standard iron deficiency diet. Three months after the birth, hemoglobin content of the blood varied between 3 and 5g per cent, while that of control animals was about 159 per cent. At the same stage, considerable increase in absolute heart weight was regularly found in anemic animals ; the heart weight being indirectly related to blood hemoglobin. Most of the increment of heart weight was apparently related to cell multiplication since neither average cell volume nor the density of nuclei per unit of longitudinal section did change. Another significant modification of myocardial structure, as revealed by quantitative analysis, was an increase of total capacity of terminal bed resulting mostly from increased tortuosity of capillaries. During in vitro perfusions, an improved ability of anemic hearts to reoxidize an excess of NADH was found by means of optical monitoring of reduction degree of PdN. Both, cytochrome c content and relative volume It is concluded that increased respiratoof mitochondria were unchanged. ry activity of anemic myocardium as detected in situ is essentially related to improved oxygen supply to tissue. (Supported
by D.G.R.S.T.
BFM, Grant
no 74.7.0790).
MYOCARDIAL TISSUE pH IN RESPIRATORY ACIDOSIS AND ISCHAEMIA S. M. Cobbe, P.A. Poole-Wilson Cardiothoracic Institute, 2 Beaumont Street, London WlN ZDX, England. Tissue acidosis has been suggested as a mechanism for the early contractile failure in myocardial ischaemia. We have measured myocardial tissue pH (pHt) with a pH sensitive needle electrode in the isolated arterially perfused interventricular septum of the rabbit heart. The relationship between pH, and developed tension has been compared in ischaemia and respiratory acidosis. The septa were maintained at 32’C, and stimulated at 60 beats. min -1. The perfusate was a modified Krebssolution equilibrated with 95% 02 5% CO2 (control, pH 7.37) or 70% 02, 30% CO2 (respiratory acidosis, pH 6.58). pH, under control conditions was 7.20 + 0.02 (mean + SEM, n = 5) and stable over 120 min. pH, fell by 95% of the perfusate pH changein response to a respiratory acidosis and developed tension fell to 24 +3.9% of control. At the onset of ischaemia, pH, fell within 55, while tension didnot fall below control for 20s. pH, fell steadily during ischaemia, to 1 .41 + 0.09 units below control after 60 min. Tension fell to 9 + 1% within 15 min, with a small further decline. pHt and tension returned rapidly towards control on reperfusion. Tissue acidosis in ischaemia is rapid in onset and large in magnitude. Comparison of the pHItension relationship in ischaemia and respiratory acidosis suggests that acidosis accounts‘for most of the early decline of contractility in myocardial ischaemia,Supported by The British Heort Foundation.
by D.G.R.S.T.
BFM, Grant
no 74.7.0790).
MYOCARDIAL TISSUE pH IN RESPIRATORY ACIDOSIS AND ISCHAEMIA S. M. Cobbe, P.A. Poole-Wilson Cardiothoracic Institute, 2 Beaumont Street, London WlN ZDX, England. Tissue acidosis has been suggested as a mechanism for the early contractile failure in myocardial ischaemia. We have measured myocardial tissue pH (pHt) with a pH sensitive needle electrode in the isolated arterially perfused interventricular septum of the rabbit heart. The relationship between pH, and developed tension has been compared in ischaemia and respiratory acidosis. The septa were maintained at 32’C, and stimulated at 60 beats. min -1. The perfusate was a modified Krebssolution equilibrated with 95% 02 5% CO2 (control, pH 7.37) or 70% 02, 30% CO2 (respiratory acidosis, pH 6.58). pH, under control conditions was 7.20 + 0.02 (mean + SEM, n = 5) and stable over 120 min. pH, fell by 95% of the perfusate pH changein response to a respiratory acidosis and developed tension fell to 24 +3.9% of control. At the onset of ischaemia, pH, fell within 55, while tension didnot fall below control for 20s. pH, fell steadily during ischaemia, to 1 .41 + 0.09 units below control after 60 min. Tension fell to 9 + 1% within 15 min, with a small further decline. pHt and tension returned rapidly towards control on reperfusion. Tissue acidosis in ischaemia is rapid in onset and large in magnitude. Comparison of the pHItension relationship in ischaemia and respiratory acidosis suggests that acidosis accounts‘for most of the early decline of contractility in myocardial ischaemia,Supported by The British Heort Foundation.