TRH‐Induced blood flow and mean arterial pressure changes in the rabbit are not dependent on the anaesthetic used

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Abstract
1 The effects of thyrotropin releasing hormone (TRH) on regional cerebral blood flow were studied in rabbits anaesthetized with pentobarbitone or ketamine. The blood flow was determined with the labelled microsphere method before and after the i.v. administration of either 50 μg kg−1 or 2 mg kg−1 TRH. 2 In order to measure the cerebral O2 consumption the arteriovenous difference in oxygen saturation in the brain (CAVOD) was measured before and after the administration of 2 mg kg−1 TRH. 3 In animals under pentobarbitone anaesthesia 50 μg kg−1 TRH elicited an increase in mean arterial blood pressure (MAP) of about 1 kPa and 2 mg kg−1 TRH elevated the MAP by about 2 kPa. With ketamine as the anaesthetic the corresponding values were 0.5 kPa and 7 kPa, respectively. TRH induced significant vasoconstriction in several peripheral tissues. 4 The total cerebral blood flow (CBFtot) increased from 54 ± 4 to 78 ± 5 g min−1 100 g−1 after the administration of 50 μg kg−1 TRH in pentobarbitone-anaesthetized animals. An even greater effect was elicited by 2 mg kg−1 TRH, from 48 ± 6 to 113 ± 19 g min−1 100 g−1. In ketamine-anaesthetized rabbits, 50 μg kg−1 TRH tended to enhance the CBFtot and 2 mg kg−1 increased it from 71 ± 6 to 141 ± 19 g min−1 100g−1. 5 In animals anaesthetized with pentobarbitone, the CAVOD decreased from 47.3 ± 1.7% to 35.1 ± 2.2% at 3 min after TRH delivery, and then gradually increased to the control level. In animals under ketamine anaesthesia the CAVOD decreased from 63.3 ± 2.0% to 45.2 ± 7.4% after the administration of 2 mg kg−1 TRH. 6 It is concluded that TRH elicits cerebral vasodilatation in excess of that required by the change in cerebral metabolism which may have taken place. The pattern of responses was similar to that produced in rabbits under urethane anaesthesia.