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Biomedical subjects

K W Clarke

Publications and source records attributed to K W Clarke.

52 records · Page 3Linked to original sources
PubMed1986

Detomidine: a new sedative for horses.

Detomidine, given intravenously at doses of 5 to 30 (mean 13) micrograms/kg bodyweight (bwt), provided adequate sedation for a variety of clinical procedures in 93 per cent of administrations, and improved the ease of handling in the remaining animals. Side effects of ataxia and bradycardia were minimal at the lower dose rates. Higher doses were required for intramuscular use. In experimental trials 10 and 20 micrograms/kg bwt resulted in deep sedation and also significant hypertension and bradycardia of over 15 mins duration. Current literature on the use of detomidine in horses is reviewed.

Animals↗
PubMedDate not supplied

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

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.

Anesthetics, Inhalation↗
PubMedDate not supplied

Characterisation of the cardiovascular pharmacology of medetomidine in the horse and sheep.

Medetomidine was administered to sheep and horses at a dose rate of 5 microg kg(-1) (i.v.). Heart rate and blood pressure were recorded. Medetomidine induced bradycardia and a biphasic blood pressure response consisting of a transient hypertension followed by hypotension. Administration of prazosin (an alpha1 adrenoceptor antagonist; 100 microg kg(-1), i.v.) had no effect on the cardiovascular response to medetomidine (5 microg kg(-1), i.v.), but inhibited the cardiovascular response of methoxamine (an alpha1 adrenoceptor agonist; 75 microg kg(-1), i.v.). L-659,066 (an alpha2 adrenoceptor antagonist which does not cross the blood brain barrier; 264 microg kg(-1), i.v.) attenuated the medetomidine induced bradycardia, but had no effect on the cardiovascular response to methoxamine. L659,066 also reduced the medetomidine induced hypertension in sheep, but had less effect on the horse. It is concluded that both alpha1 and alpha2 adrenoceptors are important in the control of cardiovascular function in horses and sheep. Medetomidine appears to act on alpha2 adrenoceptors alone in the sheep. The cardiovascular effects of medetomidine in the horse are complex and may be influenced by central alpha2 adrenoceptor regulation or effects on other receptor subtypes as well as direct stimulation of peripheral alpha2 adrenoceptors.

Adrenergic alpha-Agonists↗