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Cutaneous blood flow in the pigeon Columba livia: its possible relevance to cutaneous water evaporation
1 Department of Cell and Animal Biology, Institute of Life Sciences,
Hadassah School of Dental Medicine, The Hebrew University of Jerusalem,
Jerusalem, Israel
2 Division of Physiology, Hadassah School of Dental Medicine, The Hebrew
University of Jerusalem, Jerusalem, Israel
Deceased (8 March, 2000).
* Author for correspondence at present address: Israel Naval Medical Institute, POB 8040, Haifa 31080, Israel (e-mail: yehuda-a{at}maoz.org.il)
Accepted 20 May 2002
The heat-acclimated rock pigeon is thought to use cutaneous water evaporation (CWE) as the `preferred' route for heat dissipation, and this mechanism is controlled by adrenergic signaling. In the present study, we tested the hypothesis that adjustments in skin blood flow are a crucial component of this adaptation. Skin blood flow was measured by laser Doppler flowmetry and by ultrasonic flowmetry in heat-acclimated (HAc) and non-acclimated (NAc) pigeons. Skin blood flow, CWE and rectal and skin temperatures were measured under heat exposure (Ta=50°C) or following propranolol (1.3 mg kg-1) or clonidine (80 µg kg-1) administration. Using laser Doppler flowmetry, we found a significant increase (1.3-fold) in skin blood flow in the dorsal skin of HAc pigeons following propanolol administration. In contrast, a significant decrease (0.7-fold) was observed in NAc birds. Injection of clonidine resulted in a significant decrease in skin blood flow in both HAc and NAc pigeons (0.4- and 0.5-fold, respectively). Heat exposure increased blood perfusion in both groups (2.5- and 1.8-fold, respectively). Using ultrasonic flowmetry, we showed that both propanolol and clonidine increase the arterial blood flow (Qa) in HAc pigeons, while venous blood flow (Qv) decreases. In contrast, no significant changes were found in NAc pigeons. As shown by the effect of clonidine, augmentation of skin blood flow is not a prerequisite for CWE, but normally coincides with a greater difference in arterial—venous pressure. Possible regulatory mechanisms are discussed.
Key words: Adrenergic receptor, clonidine, heat acclimation, propranolol, thermoregulation, pigeon, Columba livia
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