Cardiovascular responses to graded doses of three catecholamines during lactic and hydrochloric acidosis in dogs

We have studied the cardiovascular effects of incremental dosesof three catecholamines in dogs subjected to lactic (LAC) andhydrochloric (HCl) acidosis. Fifty-four dogs were allocatedrandomly to one of three groups: control, LAC and HCl acidosis(n = 18 each group). In the acidotic models, 2 mol litre^–1of lactic acid (4 ml kg^–1 h^–1 or 2 mol litre^–1of HCl (1 ml kg^–1 h^–1) was infused i.v. until arterialpH was reduced to 7.00±0.1. Within each group, six dogsreceived one of three different drugs in logarithmically incrementaldoses: adrenaline 0.1, 0.2, 0.4, 0.8, 1.6, 3.2 µg kg^–1min^–1, noradrenaline 0.1, 0.2, 0.4, 0.8, 1.6, 3.2 µgkg^–1 min^–1 and dobutamine 5, 10, 20, 40, 80, 160µg kg^–1 min^–1 Cardiovascular variables weremonitored, with periodic measurements of plasma electrolyteand lactate concentrations. The pH reduction induced by HClor lactic acid was associated with a statistically significantincrease in mean pulmonary arterial pressure (MPAP), prominentespecially in the LAC group where MPAP increased from mean 18(SD 5) to 27 (6) mm Hg. In the acidotic models, the reductionin myocardial responsiveness to adrenaline or noradrenalinewas more prominent than that for the control for correspondingdoses of drugs. In the LAC group mean cardiac index decreasedsignificantly from 5.2 (1.8) to 2.2 (0.7) litre min^–1m^–2 after infusion of adrenaline 3.2 µg kg^–1min^–1 and decreased from 5.1 (1.1 to 2.4 (0.9) litre min^–1m^–1 after infusion of noradrenaline 3.2 µg kg^–1min^–1. In contrast, dobut amine showed dose-dependentincreases in cardiac index and heart rate in control, as wellas acidotic groups. The acute HCl acidosis induced greater hyperkalaemiathan the lactic acidosis. (Br. J. Anaesth. 1995; 74: 583–590)