Influence of adipose tissue blood flow on the lipolytic response to circulating noradrenaline at normal and reduced pH.
Hypercapnic acidosis (pH 7.0) inhibits the lipolytic response of canine subcutaneous adipose tissue to i.v. infused noradrenaline (NA) by 80 per cent or more. The response to sympathetic nerve stimulation, on the other hand, is only reduced by 10-40 per cent during acidosis. The fate of intravenously infused 3H-labelled NA (0.35 ug X kg-1 X min-1 for 30 min) was not significantly altered by acidosis. The rate of disappearance of unmetabolized NA from the arterial plasma after an infusion was the same at pH 7.4 and 7.0 and the calculated increase in circulating NA during infusions was 4 ng/ml at both pH:s. I.v. infusion of Na increases adipose tissue blood flow, an effect which is attenuated by acidosis. There was a significant correlation (p less than 0.001) between adipose tissue blood flow and the lipolytic response at normal pH. Preventing the NA-induced increase in blood flow by constant flow perfusion reduced the lipolytic response at normal pH. The degree of inhibition by acidosis of the lipolytic response to i.v. NA was significantly reduced (from 79 to 56 per cent, p less than 0.05) when the adipose tissue was perfused at constant flow. These data suggest that adipose tissue blood flow is important in determining the lipolytic response to i.v. NA, probably by influencing the delivery of NA to the tissue. The marked inhibition by acidosis of lipolysis due to i.v. infused NA therefore appears to be the combined effect of a direct antilipolytic effect of acidosis and a decreased delivery of NA to the adipose tissue due to the attenuated blood flow response.
Influence of adipose tissue blood flow on the lipolytic response to circulating noradrenaline at normal and reduced pH. Hypercapnic acidosis (pH 7.0) inhibits the lipolytic response of canine subcutaneous adipose tissue to i.v. infused noradrenaline (NA) by 80 per cent or more. The response to sympathetic nerve stimulation, on the other hand, is only reduced by 10-40 per cent during acidosis. The fate of intravenously infused 3H-labelled NA (0.35 ug X kg-1 X min-1 for 30 min) was not significantly altered by acidosis. The rate of disappearance of unmetabolized NA from the arterial plasma after an infusion was the same at pH 7.4 and 7.0 and the calculated increase in circulating NA during infusions was 4 ng/ml at both pH:s. I.v. infusion of Na increases adipose tissue blood flow, an effect which is attenuated by acidosis. There was a significant correlation (p less than 0.001) between adipose tissue blood flow and the lipolytic response at normal pH. Preventing the NA-induced increase in blood flow by constant flow perfusion reduced the lipolytic response at normal pH. The degree of inhibition by acidosis of the lipolytic response to i.v. NA was significantly reduced (from 79 to 56 per cent, p less than 0.05) when the adipose tissue was perfused at constant flow. These data suggest that adipose tissue blood flow is important in determining the lipolytic response to i.v. NA, probably by influencing the delivery of NA to the tissue. The marked inhibition by acidosis of lipolysis due to i.v. infused NA therefore appears to be the combined effect of a direct antilipolytic effect of acidosis and a decreased delivery of NA to the adipose tissue due to the attenuated blood flow response.