SYMPATHETIC SECRETORY RESPONSE TO HYPERCAPNIC ACIDOSIS IN SWINE

We studied the effect of graded acute hypercapnic acidosis (HA) on sympathetic neural activation in 15 juvenile farm swine in vivo. In seven animals with acute HA, plasma norepinephrine (NE) concentration increased progressively from 189 ± 34 to 483 ± 80 pg/ml (P < 0.04) as arterial CO2 partial pressure (Pa(CO2)) increased in steps from 40 to 80 Torr (pH 7.17 ± 0.01). Plasma epinephrine (EPI) concentration increased from 30 ± 15 to 125 ± 66 pg/ml (P = NS) over the same change in Pa(CO2). At Pa(CO2) of 110 Torr, plasma NE increased 3.4-fold above maximal basal concentrations; plasma EPI was 1.8-fold greater than basal under the same conditions. With HA, systemic vascular resistance (SVR) decreased from 1,748 ± 110 to 1,392 ± 145 dyn·s·cm-5 (P < 0.0002), cardiac output (CO) increased from 3.4 ± 0.3 to 4.3 ± 0.3 l/min (P < 0.01), and heart rate (HR) increased from 117 ± 11 to 154 ± 17 beats/min (P < 0.03). To demonstrate that catecholamine secretion was related directly to acidosis caused by an increase in Pa(CO2), HCO3- was infused in eight other swine to buffer extracellular acute HA (pH 7.37 ± 0.01 at Pa(CO2) of 80 Torr). Buffering attenuated the increase in plasma NE, which remained within the normal range at Pa(CO2) of 80 Torr. The decrease in SVR and increases in CO and HR also were also attenuated by HCO3- buffering of HA. We demonstrate the effects of graded acute HA on endogenous secretion of catecholamine and on the associated hemodynamic responses in swine. The sympathetic response to acute HA is mediated directly by a graded decrease in pH caused by an increase in Pa(CO2). Sympathetic secretion even with high levels of hypercapnia may not elicit significant homeostatic bronchodilatory activity.