Tissue hypoxia and increased physiological tissue shunt caused by Beta-Adrenergic stimulation

To clarify the role of adrenergic stimulation on the systemic microcirculation, the tissue oxygen tension and tissue shunt were measured with a multicathode surface oxygen electrode. In 15 healthy mongrel dogs anesthetized and mechanically ventilated, the tissue oxygen tension of the gracilis muscle was measured before and during an infusion of isoproterenol, a beta-adrenergic agonist. During the infusion of isoproterenol, at dosages of 0.025, 0.1, and 0.4 µg/kg/min, respectively, the cardiac output increased from 134 ± 10 ml/kg/min (mean ± SE) to 167 ± 13, 197 ± 14, and 219 ± 15 ml/kg/min; the total oxygen delivery increased from 26.7 ± 1.9 ml/kg/min to 34.6 ± 2.4, 42.4 ± 2.8, and 49.8 ± 3.1 ml/kg/min; the tissue oxygen tension decreased from 35.4 ± 1.2 torr to 34.2 ± 1.5, 32.6 ± 1.7, and 28.0 ± 1.9 torr; the oxygen tension of the drainage vein increased from 47.0 ± 2.5 torr to 52.6 ± 3.2,56.9 ± 3.3, and 57.6 ± 3.0 torr, and the difference in oxygen tension between the drainage vein and the tissue increased from 11.6 ± 2.7 torr to 18.4 ± 3.1 24.3 ± 3.2, and 29.6 ± 2.8 torr, showing that the increase in oxygen delivery exceeded the consumption. All changes were statistically significant except for the tissue oxygen tension at 0.025 µg/kg/min of isoproterenol. The decrease in tissue oxygen tension cannot be explained by either a decrease in oxygen supply or by an increase in oxygen consumption. Using a derived equation, the physiological tissue arteriovenous shunt (Qts/Qt) increased from 41.5 ± 6.9%to55.0 ± 6.8,63.7 ± 6.1, and 73.0 ± 5.5% (p < 0.01) at the dosage of 0.025, 0.1, and 0.4 µg/kg/min of isoproterenol, respectively. These findings are consistent with previous studies which demonstrated that beta-adrenergic stimulation with isoproterenol increases the pulmonary arteriovenous shunt.