Lack of effect of peripheral nervous blockade on nocturnal fluctuations in lower-leg subcutaneous blood flow in man

Author:

Sindrup J. H.12,Petersen L. J.1,Kastrup J.3,Wroblewski H.3,Kristensen J. K.4

Affiliation:

1. Department of Clinical Physiology/Nuclear Medicine, University of Copenhagen, Bispebjerg Hospital, Copenhagen, Denmark

2. Department of Dermatology A, University of Copenhagen, Bispebjerg Hospital, Copenhagen, Denmark

3. Department of Cardiology B, University of Copenhagen, Rigshospitalet, Copenhagen, Denmark

4. Department of Dermatology, University of Copenhagen, Hvidovre Hospital, Hvidovre, Denmark

Abstract

1. The local subcutaneous adipose tissue blood flow was measured simultaneously in the right and left lower legs of 10 normal human subjects under outpatient nocturnal conditions. The 133Xe-wash-out technique, portable CdTe(Cl) detectors and a portable data-storage unit were used for the measurement of blood flow. 2. The purpose of the study was to unveil the possible role of centrally controlled nerve fibres to the measurement area as mediators of a previously described nocturnal subcutaneous hyperaemia of 2 h duration. Therefore, before the sleeping period, a local nervous blockade was applied immediately proximal to the isotope depot on the right lower leg by the injection of approximately 15 ml of bupivacaine (5 mg/ml) subcutaneously. 3. Control experiments revealed blockade of the baroreceptor vasoconstrictor reflex activity 4 h after application of the local nervous blockade in three subjects examined. 4. Identical nocturnal isotope-wash-out curves were recorded from the two legs. Subcutaneous blood flow was found to increase significantly (P <0.0001) after approximately 1 h of sleep and the hyperaemia persisted for 2 h. 5. A significant positive correlation was detected between the latency periods from going to bed until the onset of the hyperaemia in the right and left lower legs (P <0.001, r = 0.95). 6. No significant difference could be detected between the relative blood flow increase during the hyperaemic phase in the right and left lower legs (P = 0.83). 7. It is concluded that the present data seem to rule out a central nervous factor(s) as the eliciting mechanism of the nocturnal subcutaneous hyperaemia. A circulating humoral factor(s) might be involved, although modification by local metabolic factors cannot be excluded. The possible physiological significance of the nocturnal hyperaemia is discussed.

Publisher

Portland Press Ltd.

Subject

General Medicine

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