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Myocardial beta-adrenoceptors in experimental hypertension
J Mol Cell Cardiol 23 (Supplement IV) (1991)
82 MYOCARDIAL
HYPERTROPHY IN EXPERIMENTAL HYPERTENSION. M. Galinier *, J.M. Senard, P. Valet, J.L. Montastruc, J.P. Bounhoure*, P. Montastruc. Department of Pharmacology, INSERM U 317 ; *Department of Cardiology, CHU Rangueil, Toulouse, France. The aim of the present study was to investigate the trophies factors involved in the mechanisms of myocardial structural changes during experimental hypertension induced by sinoaortic denervation in dogs. Mean arterial blood pressure (MABP, mmHg), plasma norepinephrine (NE) and epinephrine (E) concentrations (HPLC, pg/ml), cardiac hypertrophy (Rratio : heart weight/body weight) and left ventricular thickness (LVT, mm) were studied in three groups of 4 animals : A) normotensive controls, B) one month hypertensive dogs and C) 18 months hypertensive dogs. (* : p < 0.05). MABP NE E R LVT A 98k8 461ti4 85*45 6.7ti.2 13.2fl.l B 153+10* 861fl85* 191+23* 7.7ko.1* 16.2fl.5* C 148k9* 426&l 32 llMl6 7.8M.2* 18.lti.8* Sinoaortic denervation induces a sustained arterial hypertension associated with a transient rise in plasma catecholamines. Cardiac hypertrophy appears early during the hyperadrenergy state and persist despite catecholamine normalization. Thus the sympathectic nervous system contribures greatly to the early development of myocardial hypertrophy.
83 MYOCARDIAL
BETA-ADRENOCEPTORS IN EXPERIMENTAL HYPERTENSION. M. Galinier’ , J.M. Senard, P. Valet, J.L. Montastruc, J.P. Bounhoure*, P. Montastruc. Department of Pharmacology,, INSERM U 317 ; *Department of Cardiology, CHU Rangueil, Toulouse, France. The aim of the present study was to determine the evolution of myocardial beta-adrenoceptors (BA) duringexperimentalhypertensioninducedbysinoaorticdenervationindogs. BA densityof4cardisc cavities (Iodocyanopindolol binding, fmol/mg prot), plasmanorepinephrine (NE) and epinephrine (E) concentrations (HPLC, pg/ml) and cardiac hypertrophy (R ratio : heart weight/body weight) were studied in three groups of 4 animals : A) normotensive controls, B) one month hypertensive dogs and C) 18 months hypertensive dogs. (* : p< 0.05). RA LA RV NE R 6.7M.2 A 2% 43f3 22s 3741; 46194 85!45 B 7.7&O. 1* 13?2* 20+2* 1OZ!2* 10+3* 861+185* 191f23* 426+132 1 lof16 7.8f102" C 31s 42ti 21s 373 Hypertensive dogs show early cardiac hypertrophy which persists despite catecholamine normalization. BA number decreases only during the hyperadrenergy state whatever rhe cavities studied. We tollelude that BA down-regulation is the result of an increase in plasma catecholamines but is independant of cardiac hypertrophy.
84
CONTINIJOUS MEASUREMENT OF CORONARY SINUS OXYGEN SATURATION DURING SUSTAINED VENTRICULAR TACHYCARDIA Y. Gallais, J-F. Baron, A. Riahi, J. Tonet, R. Frank, G. Fontaine, Jean Rostand Hospital, Ivry, France. The aim of the present study was to assess the effects of VT on myocardial oxygen consumption (MVO2). Fourteen patients with dilated cardiomyopathy (EF: 0.33 + 0.09 X) suffering from life-threatening arrhythmias underwent ful uration. During sustained VT for electrophysiological mapping, mean arterial pressure 9 MAP), filling pressure (PCWP), cardiac output (CI1 and coronary sinus oxygen saturation !ScsOZ - oxymetry TO catheter) were monitored. Coronary sinus lactate (lactate oxydase - PAP) and hemodynamic measurements betore VT were compared with those during VT (mean duration 18.4 + For a heart rate of 162 + 16 beat/min, with a 12.1 min) just before fulquration. ;t;ti;tical significance ,p
82 MYOCARDIAL
HYPERTROPHY IN EXPERIMENTAL HYPERTENSION. M. Galinier *, J.M. Senard, P. Valet, J.L. Montastruc, J.P. Bounhoure*, P. Montastruc. Department of Pharmacology, INSERM U 317 ; *Department of Cardiology, CHU Rangueil, Toulouse, France. The aim of the present study was to investigate the trophies factors involved in the mechanisms of myocardial structural changes during experimental hypertension induced by sinoaortic denervation in dogs. Mean arterial blood pressure (MABP, mmHg), plasma norepinephrine (NE) and epinephrine (E) concentrations (HPLC, pg/ml), cardiac hypertrophy (Rratio : heart weight/body weight) and left ventricular thickness (LVT, mm) were studied in three groups of 4 animals : A) normotensive controls, B) one month hypertensive dogs and C) 18 months hypertensive dogs. (* : p < 0.05). MABP NE E R LVT A 98k8 461ti4 85*45 6.7ti.2 13.2fl.l B 153+10* 861fl85* 191+23* 7.7ko.1* 16.2fl.5* C 148k9* 426&l 32 llMl6 7.8M.2* 18.lti.8* Sinoaortic denervation induces a sustained arterial hypertension associated with a transient rise in plasma catecholamines. Cardiac hypertrophy appears early during the hyperadrenergy state and persist despite catecholamine normalization. Thus the sympathectic nervous system contribures greatly to the early development of myocardial hypertrophy.
83 MYOCARDIAL
BETA-ADRENOCEPTORS IN EXPERIMENTAL HYPERTENSION. M. Galinier’ , J.M. Senard, P. Valet, J.L. Montastruc, J.P. Bounhoure*, P. Montastruc. Department of Pharmacology,, INSERM U 317 ; *Department of Cardiology, CHU Rangueil, Toulouse, France. The aim of the present study was to determine the evolution of myocardial beta-adrenoceptors (BA) duringexperimentalhypertensioninducedbysinoaorticdenervationindogs. BA densityof4cardisc cavities (Iodocyanopindolol binding, fmol/mg prot), plasmanorepinephrine (NE) and epinephrine (E) concentrations (HPLC, pg/ml) and cardiac hypertrophy (R ratio : heart weight/body weight) were studied in three groups of 4 animals : A) normotensive controls, B) one month hypertensive dogs and C) 18 months hypertensive dogs. (* : p< 0.05). RA LA RV NE R 6.7M.2 A 2% 43f3 22s 3741; 46194 85!45 B 7.7&O. 1* 13?2* 20+2* 1OZ!2* 10+3* 861+185* 191f23* 426+132 1 lof16 7.8f102" C 31s 42ti 21s 373 Hypertensive dogs show early cardiac hypertrophy which persists despite catecholamine normalization. BA number decreases only during the hyperadrenergy state whatever rhe cavities studied. We tollelude that BA down-regulation is the result of an increase in plasma catecholamines but is independant of cardiac hypertrophy.
84
CONTINIJOUS MEASUREMENT OF CORONARY SINUS OXYGEN SATURATION DURING SUSTAINED VENTRICULAR TACHYCARDIA Y. Gallais, J-F. Baron, A. Riahi, J. Tonet, R. Frank, G. Fontaine, Jean Rostand Hospital, Ivry, France. The aim of the present study was to assess the effects of VT on myocardial oxygen consumption (MVO2). Fourteen patients with dilated cardiomyopathy (EF: 0.33 + 0.09 X) suffering from life-threatening arrhythmias underwent ful uration. During sustained VT for electrophysiological mapping, mean arterial pressure 9 MAP), filling pressure (PCWP), cardiac output (CI1 and coronary sinus oxygen saturation !ScsOZ - oxymetry TO catheter) were monitored. Coronary sinus lactate (lactate oxydase - PAP) and hemodynamic measurements betore VT were compared with those during VT (mean duration 18.4 + For a heart rate of 162 + 16 beat/min, with a 12.1 min) just before fulquration. ;t;ti;tical significance ,p