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. 1978 Aug;281:325–338. doi: 10.1113/jphysiol.1978.sp012425

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

P Hjemdahl, A Sollevi
PMCID: PMC1282700  PMID: 702388

Abstract

1. The circulatory and metabolic effects of temperature reduction were studied in autoperfused canine subcutaneous adipose tissue in situ. 2. Cooling the adipose tissue sufficiently to reduce venous effluent temperature by 5--6 degrees C decreased blood flow from an average of 6.4--4.1 ml. min-1 . 100g-1. 3. Vasoconstrictor responses to sympathetic nerve stimulation (4 HZ) and injected noradrenaline (5 n-mole) were potentiated by cooling while vasodilator components of the vascular responses, such as autoregulatory escape and post-stimulatory hyperaemia, were virtually abolished by this treatment. 4. Oxygen uptake was reduced by cooling without signs of tissue hypoxia. This reduced oxygen demand may partly cause the decrease in adipose tissue blood flow. 5. Cooling inhibited glycerol mobilization from the adipose tissue during sympathetic nerve stimulation. Post-stimulatory lipolysis was, however, not inhibited. In vitro studies with 'perifused' rat fat cells suggest that this may be due to impaired inactivation of the lipolytic process, rather than to changes in transmitter removal, following stimulation at low temperature. 6. 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. 7. It is concluded that cooling increases the sensitivity to vasoconstrictor stimuli and that inhibition of metabolic vasodilator mechanisms play a role for this effect. The stimultaneous 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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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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