The cardiopulmonary effects of clenbuterol when administered to dorsally recumbent halothane-anaesthetised ponies--failure to increase arterial oxygenation

Abstract

Clenbuterol (0.8 microg kg(-1) intravenously) was investigated in ponies (small horses) anaesthetised with acepromazine, detomidine and thiopentone, then halothane in oxygen alone (hyperoxic group) or with nitrous oxide (hypoxic group). Following instrumentation, ponies were placed in dorsal recumbency for 60 minutes, clenbuterol (both groups) or a saline control (hyperoxic group) given, and cardiopulmonary parameters monitored for a further 60 minutes. In the hyperoxic group, clenbuterol administration resulted in a transitory (<five minutes) 15 per cent fall in arterial blood pressure and 78 per cent rise in intramuscular blood flow. Heart rate increased from a mean of 42 (SD 4) to 54 (12) beats per minute, the rise being significant for 15 minutes. Cardiac index increased from 2.1 (0.7) to 3.9 (0.7) litres m(-2) and remained significantly elevated for the remainder of the measurement period. Cardiovascular changes in the hypoxic group were similar. 30 minutes after clenbuterol administration, PaO2 had changed nonsignificantly from 32.3 (19.2) to 33.4 (17) kPa in the hyperoxic group and from 7.9 (1.8) to 8.6 (1.3) kPa in the hypoxic group. The study concludes that under these experimental conditions, clenbuterol does not cause significant improvement in arterial oxygenation, but its cardiovascular effects are minimal or advantageous.