Augmented catecholamine uptake by the heart during hemorrhage in the conscious dog

Changes in arterial and coronary sinus concentrations of norepinephrine (NE) and epinephrine (E) in response to hemorrhage were examined in conscious dogs. Hemorrhage (45 ± 3.2 ml/kg) decreased mean arterial pressure by 47 ± 6%, left ventricular (LV) dP/dt by 38 ± 6%, and mean left circumflex coronary blood flow by 47 ± 6%, while heart rate increased by 44 ± 13%. Increases in concentrations of arterial NE (5,050 ± 1,080 from 190 ± 20 pg/ml) and E (12,700 ± 3,280 from 110 ± 20 pg/ml) were far greater than increases in coronary sinus NE (1,700 ± 780 from 270 ± 50 pg/ml) and E (4,300 ± 2,590 from 90 ± 10 pg/ml). Net release of NE from the heart at rest was converted to a fractional extraction of 66 ± 9% after hemorrhage. Fractional extraction of E increased from 16 ± 6% at rest to 73 ± 8% after hemorrhage. In cardiac-denervated dogs, hemorrhage (46 ± 2.8 ml/kg) decreased mean arterial pressure by 39 ± 15%, LV dP/dt by 36 ± 10%, and mean left circumflex coronary blood flow by 36 ± 13%, while heart rate increased by 24 ± 10%. Hemorrhage increased arterial NE (1,740 ± 150 from 210 ± 30 pg/ml) and E (3,050 ± 880 from 140 ± 20 pg/ml) more than it increased coronary sinus NE (460 ± 50 from 150 ± 30 pg/ml) and E (660 ± 160 from 90 ± 20 pg/ml) but significantly less (P < 0.05) than observed in intact dogs. These experiments indicate that hemorrhage, unlike exercise and sympathetic nerve stimulation, does not induce net overflow of NE from the heart. Furthermore, cardiac nerves do not play a major role in either hemodynamic or uptake of catecholamines from the circulation during hemorrhage. However, afferent cardiac nerves may be important in mediating hemorrhage-induced increases in circulating catecholamines.