PubMed Health⌕ Search

Biomedical subjects

L K Cullen

Publications and source records attributed to L K Cullen.

30 records · Page 2Linked to original sources
PubMed1987

Venoconstriction causes different effects in the hindquarters venous compartment of cats and dogs.

1. A study was made of venoconstrictor mechanisms in the hindquarters region of cats and dogs by the use of autoperfused hindquarter preparations, together with the measurement of vena cava blood flow (VCBF). 2. Noradrenaline, adrenaline and angiotensin II (AII) were all administered intraarterially and their ability to alter perfusion pressure and VCBF was examined. 3. All three drugs increased perfusion pressure in both cats and dogs as a result of increases in arterial resistance. At the same time, noradrenaline and adrenaline increased VCBF in cats, while AII had a variable effect. In contrast, all three drugs decreased VCBF in dogs. 4. These differences in the venoconstrictor responses obtained in cats and dogs may be explained by an action of the drugs at different loci within the venous compartment of the two species.

Angiotensin II↗
PubMed1986

The effect of clonidine on venous haemodynamics in cats and dogs.

Experiments were undertaken to investigate a possible action of clonidine on venous haemodynamics, using cats and dogs with autoperfused hindquarters. This provided an arterial input to the region independent of cardiac output. Venous capacitance in the hindquarters was indicated by blood flow in the abdominal vena cava, as measured by an electromagnetic flow probe around this vessel. It was found that in both cats and dogs, clonidine given intravenously (5 micrograms kg-1 i.v.) or into the cisterna magna (1 microgram kg-1 i.c.m.) reduced mean arterial pressure and heart rate, but did not decrease hindquarter perfusion pressure. With the exception of dogs given i.v. clonidine, this drug caused a decrease in inferior vena cava (IVC) blood flow and this closely paralleled the hypotensive effect. However, when clonidine was given i.v. to dogs, the decrease in IVC blood flow preceded the hypotension. At the doses used, the reduction in IVC blood flow was larger following i.v. than i.c.m. clonidine in both species, and in all cases, it remained below control levels for at least 30 min, in spite of the constant arterial input to the region. In cats, dose-response curves were constructed to noradrenaline and adrenaline given into the perfusion circuit (i.a.) before and after clonidine. Following i.v. and i.c.m. clonidine, there was a selective depression of the venoconstrictor actions of the catecholamines, but no change in the arterial pressor action. Radiographic and latex studies in the dog and cat respectively were performed in order to visualize collateral blood flow that could account for the persistent decreases in IVC blood flow. In both species, intraspinal collateral flows were demonstrated which returned blood to the heart after ligation of the inferior vena cava below the renal veins. However, it was not possible to demonstrate radiographically any changes produced by clonidine in the collateral flow because of technical difficulties. These results suggest that clonidine causes a selective reduction in sympathetic tone to the veins that is mediated at least partly by a central action, as well as an expansion of the collateral venous routes. This, together with the selective impairment of venoconstrictor responses to both noradrenaline and adrenaline, may account for the decrease in cardiac output that is most often reported following clonidine.

Animals↗
PubMed1982

Residual non-depolarising neuromuscular block assessed by train-of-four stimulation in the dog.

A technique is described for assessing the extent of residual neuromuscular block following non-depolarising agents in the dog. The ulnar nerve was electrically stimulated with a train-of-four impulses and the muscle responses recorded. Heights of the control and, following the administration of the muscle relaxant, the first, second and fourth twitch tensions (T1, T2 and T4) of the train were measured. There was a highly significant linear correlation between the ratio T1/control, used to determine the extent of neuromuscular block, and the other ratios T2/T1 and T4/T1. Both of the ratios T2/T1 and T4/T1 avoid the use of control heights.

Animals↗
PubMed1981

Anesthesia of small kangaroos.

Small kangaroos were anesthetized, using sodium thiopental IV for induction followed by endotracheal intubation and administration of a halothane and oxygen mixture. Endotracheal intubation in these small kangaroos was difficult, primarily because the long oral cavity prevented adequate visualization of the larynx. Intubation was facilitated by the use of a laryngoscope and a straight wire stylet inserted into the lumen of the endotracheal tube. Blood samples were collected from the median saphenous artery, and analysis showed that statistically significant increases in PO2 and PCO2 had occurred during anesthesia. Only minor variable changes in pH values were recorded. During anesthesia, decreased heart rate and increased mean respiratory rate were accompanied by rapid depression in cloacal temperature.

Anesthesia, Intravenous↗
PubMed1980

Recording of train-of-four evoked muscle responses from the nose and foreleg in the intact dog.

Evoked muscle responses to train-of-four electrical nerve stimuli were recorded from the nose and foreleg in the intact dog. Low and high doses of both suxamethonium and either pancuronium or gallamine were injected, and the recordings of muscle responses from each dog were examined. Recordings taken from the foreleg showed the presence of train-of-four fade until complete neuromuscular block was established. Simultaneous recordings from the nose showed the development of a train-of-four fade in early stages of neuromuscular block, but as the block increased, an unusual response developed where the twitch height became equal. This finding occurred following suxamethonium as well as non-depolarising relaxants.

Animals↗
PubMed1980

The nature of suxamethonium neuromuscular block in the dog assessed by train-of-four stimulation.

Evoked muscle responses from continuous train-of-four (frequency 2Hz) electrical nerve stimuli, with an interval of 10 sec between each train, were recorded in the intact anaesthetised dog receiving multiple doses of suxamethonium at 0.035 mg/kg. The train-of-four twitches showed a slight progressive fade from the first to the fourth and this fade increased as additional doses of the muscle relaxant were given. The train-of-four ratio was used to divide the suxamethonium neuromuscular block into phase 1 and phase 2 components. Dogs receiving one dose of suxamethonium at 0.3 mg/kg were developing the phase 2 block during the return of neuromuscular activity and after the third to fourth dose this block was fully established. Evidence of tachyphylaxis was present in the phase 1 block which persisted into the phase 2 component.

Animals↗
PubMed1980

The effect of neostigmine on suxamethonium induced neuromuscular block in the dog.

The effects of neostigmine on suxamethonium induced neuromuscular block were investigated in the intact, anaesthetised dog using the train-of-four twitch to record neuromuscular activity. Marked antagonism of the block was observed when the train-of-four ratio was 0.38 and less. To avoid potentiating the block, the use of neostigmine is not recommended without first determining the state of neuromuscular activity with a peripheral nerve stimulator using train-of-four stimulation.

Animals↗
PubMedDate not supplied

Cardiovascular responses to amitraz in the presence of autonomic antagonists and agonists.

Blood pressure and heart rate were recorded continuously in methoxyflurane anaesthetized dogs. Amitraz (i.v.) caused a dose-dependent rise in blood pressure with a fall in heart rate at lower doses. Pressor responses to amitraz were reduced by phentolamine and slightly enhanced by atropine and hexamethonium, while bradycardia was reduced by phentolamine, atropine and hexamethonium. Amitraz reduced the responses to acetylcholine and enhanced pressor responses to tyramine, while reducing bradycardia. Pressor responses to DMPP were reduced, but there was little effect on responses to noradrenaline, isoprenaline or histamine. It is possible that amitraz exerts its cardiovascular effects by stimulation of alpha 2-adrenoceptors and has some similarities to clonidine and xylazine in action.

Animals↗