Vascular and metabolic responses to adrenergic stimulation in isolated canine subcutaneous adipose tissue at normal and reduced temperature.

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Abstract
The circulatory and metabolic effects of temperature reduction were studied in autoperfused canine subcutaneous adipose tissue in situ. Cooling the adipose tissue sufficiently to reduce venous effluent temperature by 5-6.degree. C decreased blood flow from an average of 6.4-4.1 ml .cntdot. min-1 .cntdot. 100 g-1. Vasoconstrictor responses to sympathetic nerve stimulation (4 Hz) and injected noradrenaline [norepinephrine] (5 n mole) were potentiated by cooling while vasodilator components of the vascular responses, such as autoregulatory escape and post-stimulatory hyperemia, were virtually abolished by this treatment. Oxygen uptake was reduced by cooling without signs of tissue hypoxia. This reduced O2 demand may partly cause the decrease in adipose tissue blood flow. Cooling inhibited glycerol mobilization from the adipose tissue during sympathetic nerve stimulation. Post-stimulatory lipolysis was not inhibited. In vitro studies with perifused rat fat cells suggest this may be due to impaired inactivation of the lipolytic process, rather than to changes in transmitter removal, following stimulation at low temperature. Cooling inhibited the mobilization of fatty acids more than that of glycerol, suggesting increased re-esterification of fatty acids within the tissue at low temperature. Cooling apparently increases the sensitivity to vasoconstrictor stimuli and inhibition of metabolic vasodilator mechanisms play a role for this effect. The simultaneous inhibition of activating and inactivating mechanisms could explain the unchanged vascular and lipolytic responses to brief stimuli. Some possible implications of the present findings for the physiology of adipose tissue during cooling are discussed.

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