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Relationship between heart rate and myocardial oxygen consumption during atrial pacing at different inotropic levels in the pig
J Mol Cell Cardiol 17 (Supplement 3) (1985) 1 3 3 R E L A T I O N S H I P BETWEEN HEART RATE AND MYOCARDIAL OXYGEN CONSUMPTION DURING ATRIAL PACING AT DIFFERENT INOTROPIC LEVELS IN THE PIG. F. R. Andersen, A. Ilebekk, F. Kill. University of Oslo, Institute for Experimental Medical Research, Ullevaal Hospital, Oslo, Norway. Myocardial oxygen consumption per beat (MVO2/beat) and L V d P / d t increase, both at control and low inotropy, when heart rate is augmented by atrial pacing and stroke work is kept unchanged. At high inotropy, however, MVO2/beat and LVdP/dt may have approached maximal values, so that pacing tachycardia may not induce f u r t h e r increments. To examine this hypothesis, we increased heart rate by 37 + 2 beats/min in 9 open-chest pigs at control, high and low inotropy. High inotropy-was induced by isoproterenol into the left coronary a r t e r y (0.9 /~g/min). Low inotropy was induced by i . v . propranolol (3 mg). Left ventricular systolic pressure, stroke volume and dimensions (measured with ultrasonic technique) were kept unchanged by blood infusion and adjustments of an aortic constriction. At low inotropy the control MVO2/beat of 2.69 + 0.30 /~nol/100 g rose by 17.4 + 2.8% (P<0.02) when heart rate was increased. At-control inotropy MVO2/beat rose by 7.1 + 1.4% (P<0.01) from 3.60 + 0.20 p mol/100 g, but at high inotropy the MVO2/beat-of 4.90 _+ 0. 52 /~ mol /100 g remained unchanged. Also L V d P / d t increased only at low and control inotropy. Thus, MVO2/beat and L V d P / d t do not increase f u r t h e r by pacing tachycardia at high inotropy.
134TIME-RELATIONS OF MYOCARDIAL POTASSIUM CHANGES AND INCREASED CONTRACTILITY DURING INTRACORONARY ISOPROTERENOL INFUSION TO THE P I G . A . l l e b e k k , O.A.Vengen, O.Ellingsen. U n i v e r s i t y of Oslo, I n s t i t u t e f o r Experimental Medical Research, No[way. During beta-adrenergic s t i m u l a t i o n of the myocardium a net K uptake has been observed, but the r e l a t i o n s h i p of t h i s uptake and the r i s e in c o n t r a c t i l i t y has not been e s t a b l i s h e d . We t h e r e f o r e recorded changes in c o n t r a c t i l i t y and myocardial K§ uptake during i n t r a c o r o n a r y i n f u s i o n ( i c ) of i s o p r o t e r e n o l ( i s o ) ( 0 . 6 - 0 . 8 pg/min) to 8 open-chest pigs. K c o n c e n t r a t i o n s w e r e monitored by PVC-valinomycin mini.electrodes in a r t e r i a l blood (a) in the l e f t atrium and in coronary sinus blood (os) in a shunt to the r i g h t atrium. L e f t v e n t r i c u l a r pressure (LVP) was measured by a m i c r o t i p pressure transducer and LVdP/dt used as the c o n t r a c t i l i t y parameter. During iso ic LVdP/dt rose by 60 (34~88) Z (median and 95Z c o n f . i n t e r v a ] ) o f i t s maximal increase w i t h i n 45 s, and by 78 (60-9?) Z w l t h i n 90 s. Simultaneously there was a small myocardial K+ l e s s . A net uptake began a f t e r 90 s. At steady s t a t e a-cs conc. d i f f e r e n c e s a f t e r 7 3/4 (4 I / 2 - 8 3/4) min of i c iso, the cumulative myocardial uptake was 69 (37-292) pmol/IOOg. The i n i t i a l myocardial K+ loss was not due to tachycardia and probably not to ischemia since there was no ST-segment e l e v a t i o n in 4 i n t r a m u r a l ECG recordings. Thus during beta-adrenergic s t i m u l a t i o n the main r i s e in myocardial c o n t r a c t i l i t y occurs simultaneously w i t h a myocardial K+ loss, and before myocardial K+ uptake.
1 3 5 E F F E C T OF ~-AGONIST AND ~-ANTAGONIST ON CARDIAC PERFORMANCE. M. Marzilli, *H.N. Sabbah, D. Levantesi and *P.D. Stein. Institute of Clinical Physiology, Pisa (Italy), and *Henry Ford Hospital, Detroit (USA). Left ventricular (LV), subendocardial (ENDO) and subepicardial (EPI) systolic pressures (SP) were measured simultaneously in 6 open-chest dogs under control conditions and following e.v. injection of isoproterenol (ISO) and propranolol (PRO). Both ISO and PRO decreased LVSP from 121~15 to 96~11 mmHg (P<.05) and from I06~7 to 85+--8 mmHg (P=NS), respectively. ISO increased ENDOSP from 161~20 to 232~22 mmHg (P<.01) and EPISP from 89~11 to 135~8 mmHg (P<.05); PRO decreased ENDOSP from ]60~14 to 99~9 mmHg (P<.01) and EPISP from 85A8 to 56~9 mmHg (P<.05). Conclusions: ~-adrenergic drugs ISO and PRO induced similar changes of intracavitary pressure but opposite changes of intramyocardial pressures.
134TIME-RELATIONS OF MYOCARDIAL POTASSIUM CHANGES AND INCREASED CONTRACTILITY DURING INTRACORONARY ISOPROTERENOL INFUSION TO THE P I G . A . l l e b e k k , O.A.Vengen, O.Ellingsen. U n i v e r s i t y of Oslo, I n s t i t u t e f o r Experimental Medical Research, No[way. During beta-adrenergic s t i m u l a t i o n of the myocardium a net K uptake has been observed, but the r e l a t i o n s h i p of t h i s uptake and the r i s e in c o n t r a c t i l i t y has not been e s t a b l i s h e d . We t h e r e f o r e recorded changes in c o n t r a c t i l i t y and myocardial K§ uptake during i n t r a c o r o n a r y i n f u s i o n ( i c ) of i s o p r o t e r e n o l ( i s o ) ( 0 . 6 - 0 . 8 pg/min) to 8 open-chest pigs. K c o n c e n t r a t i o n s w e r e monitored by PVC-valinomycin mini.electrodes in a r t e r i a l blood (a) in the l e f t atrium and in coronary sinus blood (os) in a shunt to the r i g h t atrium. L e f t v e n t r i c u l a r pressure (LVP) was measured by a m i c r o t i p pressure transducer and LVdP/dt used as the c o n t r a c t i l i t y parameter. During iso ic LVdP/dt rose by 60 (34~88) Z (median and 95Z c o n f . i n t e r v a ] ) o f i t s maximal increase w i t h i n 45 s, and by 78 (60-9?) Z w l t h i n 90 s. Simultaneously there was a small myocardial K+ l e s s . A net uptake began a f t e r 90 s. At steady s t a t e a-cs conc. d i f f e r e n c e s a f t e r 7 3/4 (4 I / 2 - 8 3/4) min of i c iso, the cumulative myocardial uptake was 69 (37-292) pmol/IOOg. The i n i t i a l myocardial K+ loss was not due to tachycardia and probably not to ischemia since there was no ST-segment e l e v a t i o n in 4 i n t r a m u r a l ECG recordings. Thus during beta-adrenergic s t i m u l a t i o n the main r i s e in myocardial c o n t r a c t i l i t y occurs simultaneously w i t h a myocardial K+ loss, and before myocardial K+ uptake.
1 3 5 E F F E C T OF ~-AGONIST AND ~-ANTAGONIST ON CARDIAC PERFORMANCE. M. Marzilli, *H.N. Sabbah, D. Levantesi and *P.D. Stein. Institute of Clinical Physiology, Pisa (Italy), and *Henry Ford Hospital, Detroit (USA). Left ventricular (LV), subendocardial (ENDO) and subepicardial (EPI) systolic pressures (SP) were measured simultaneously in 6 open-chest dogs under control conditions and following e.v. injection of isoproterenol (ISO) and propranolol (PRO). Both ISO and PRO decreased LVSP from 121~15 to 96~11 mmHg (P<.05) and from I06~7 to 85+--8 mmHg (P=NS), respectively. ISO increased ENDOSP from 161~20 to 232~22 mmHg (P<.01) and EPISP from 89~11 to 135~8 mmHg (P<.05); PRO decreased ENDOSP from ]60~14 to 99~9 mmHg (P<.01) and EPISP from 85A8 to 56~9 mmHg (P<.05). Conclusions: ~-adrenergic drugs ISO and PRO induced similar changes of intracavitary pressure but opposite changes of intramyocardial pressures.