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AJP - Heart and Circulatory Physiology, Vol 264, Issue 5 1355-H1359, Copyright © 1993 by American Physiological Society
ARTICLES |
W. F. Taylor and V. S. Bishop
Department of Physiology, University of Texas Health Science Center, San Antonio 78284-7756.
We have shown previously that an increase in ear blood flow velocity (EBF) in the conscious, chronically instrumented rabbit during whole body heating (WBH) involves active neurogenic vasodilation that is abolished by local nerve block. This study was designed to test the potential role of nitric oxide (NO) in rabbit ear neurogenic vasodilation during hyperthermia. Rabbits were instrumented for the measurement of arterial pressure, heart rate, and EBF (Doppler ultrasound). A catheter was also placed in the left lingual artery for administration of drugs to the left ear. WBH was achieved by circulating warm water through a rubber pad placed around the rabbit. Internal temperature was measured with a rectal thermocouple. During WBH, bolus injections of N omega-nitro-L-arginine (L-NNA), a false substrate for the formation of NO, were given via the lingual artery (10(-5) M, 4-5 ml total) to determine whether NO was involved in the increase in EBF. During WBH, left ear vascular conductance (EVC) increased from 0.07 +/- 0.03 to 5.87 +/- 0.73 kHz/100 mmHg and right EVC from 0.20 +/- 0.13 to 4.49 +/- 1.73 kHz/100 mmHg. When EVC was maximum, L-NNA was administered into the left lingual artery. EVC began to decrease after a latency of 23 min. At 56 +/- 8 min, left and right EVC had decreased to 0.18 +/- 0.10 and 0.23 +/- 0.11 kHz/100 mmHg, respectively (P < 0.05). Subsequent infusions of L-arginine, the true substrate for NO formation, restored EVC. These results suggest that NO is involved in active vasodilation during heating in the rabbit ear.
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