The Effects of Intravenous Anaesthetics on the Cardiovascular System of the Rabbit

McGrath, J.C.; Mackenzie, John Edwin

doi:10.1111/j.1476-5381.1977.tb08405.x

Cited by 25 publications

(15 citation statements)

References 26 publications

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“…In order to take a static image of the rabbits, we used ketamine as an anesthetic agent in this study. McGrath and MacKenzie showed that ketamine can attenuate the effects of sympathetic nerve stimulation [17]. In this study, all animals showed a similar weight gain and received the same amount of ketamine for anesthesia.…”

Section: Cholesterol and Sympathetic Functionmentioning

confidence: 74%

Dietary Cholesterol Affects Sympathetic Nerve Function in Rabbit Hearts

Luo

Liu

et al. 2004

J Biomed Sci

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In order to assess the effect of hypercholesterolemia on cardiac sympathetic nerve function, New Zealand white rabbits were fed a normal diet (the control group) or one enriched with 0.5% cholesterol [the hypercholesterol (HC) group] for 3 months. Before and after the 3-month diet treatment, we performed serial imaging examinations and analyzed the uptake and washout ratio of ¹²³I-meta-iodobenzylguanidine (¹²³I-MIBG) from the myocardium by administration of ¹²³I-MIBG through an ear vein. At the end of the experiments, the rabbits were sacrificed, and right ventricular strips were taken from their hearts. The inotropic response of the right ventricular strips to isoproterenol (ISO) and norepinephrine (NE) were evaluated. The cardiac MIBG uptake of the HC group, which was evaluated using the heart to mediastinum ratio, was higher than that of the age-matched control group. However, the washout ratios of ¹²³I-MIBG did not differ statistically between the two groups. On pretreatment with cocaine, NE-enhanced contractility was greater in papillary muscles isolated from the HC group. The concentration-response curve to ISO was shifted to the right in the HC group, compared with that in the control group. In conclusion, hypercholesterolemia in rabbits resulted in an increase in sympathetic nerve density in the myocardium, a decrease in the inotropic response to ISO and an increase in the inotropic response to NE in cocaine-treated myocardium. Both the in vivo and in vitro studies demonstrated the functional significance of neural remodeling induced by hypercholesterolemia.

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Section: Cholesterol and Sympathetic Functionmentioning

confidence: 74%

Dietary Cholesterol Affects Sympathetic Nerve Function in Rabbit Hearts

Luo

Liu

et al. 2004

J Biomed Sci

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“…Further variation in results (and subsequent conclusions) arises from the differing effects of different anaesthetics in the peripheral vasculature (Clark & MacCannell, 1975;Miller & Wiegman, 1977), on cardiac function (Jandhyala & Buckley, 1977;McGrath & MacKenzie, 1977), on circulating catecholamines (Pettinger et al, 1975) or centrally (Bielicki & Kreiglstein, 1977;Sung, Frederickson & Holtzman, 1973).…”

Section: Anaesthesia and Central Cardiovascular Controlmentioning

confidence: 99%

The central noradrenergic control of blood pressure and heart rate

Elliott

1979

Clin Exp Pharmacol Physiol

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Investigation of the postulated central hypotensive actions of clonidine, methyldopa and P-adrenoreceptor blocking drugs has prompted intensive research into the neurophysiological basis of central cardiovascular control. Species differences and the general lack of specificity of the pharmacological tools available complicate such investigations. Although many studies implicate noradrenaline as a transmitter in central cardiovascular control, there have been conflicting reports regarding the role(s) of this putative neurotransmitter. The postulated roles of brain amines in experimental hypertension have been reviewed by Chalmers (1975).In this review evidence for the noradrenergic control of blood pressure and heart rate in the spinal cord, at the level of the medulla and from within the hypothalamus is discussed in the light of recent attempts to characterise central adrenoreceptors.Early electrical brain stimulation studies showed the most important areas able to modify cardiovascular function are located in the brain stem and hypothalamus (reviews by Korner, 1971 ;Smith, 1974). The area of the nucleus tractus solitarius in the medulla was found to be the site of one of the primary relays of the baroreceptor or carotid sinus afferent fibres (Crill & Reis, 1968). Baroreceptor activity has been found to project via polysynaptic pathways as far as the hypothalamus; furthermore, electrical stimulation of the hypothalamus has been shown to modify baroreceptor reflexes.The histochemical fluorescence technique developed by Falck et al.(1 962) and the more sensitive glyoxylic acid fluorescence method used by Lindvall & Bjorklund (1974) subsequently revealed a dense noradrenergic innervation of nuclei within the brain stem, spinal cord and hypothalamus. These nuclei include the intermedio-lateral nucleus of the spinal cord, the nucleus tractus solitarius, dorsal vagal nucleus, nucleus reticularis lateralis and locus coeruleus of the medulla, and nuclei of both the posterior and anterior hypothalamus. From the beginning of this decade therefore, it has been general opinion that the distribution of noradrenaline containing nerve endings in the mid brain and hind brain strongly suggests a transmitter role of noradrenaline in modulating central cardiovascular control (Bolme, Fuxe & Lidbrink, 1972). Control of blood pressure at the spinal levelA high density of noradrenalinecontaining neurones has been demonstrated in the intermedio-lateral columns where they appear to make intimate synaptic contact with sympathetic preganglionic neurones. a-Adrenoreceptors and glycine receptors appear to mediate inhibition of thoracico-lumbar preganglionic sympathetic neurones (Haeusler, 1976) while padrenoreceptors at this level may facilitate tachycardia and hypertension (Bhargava et al., 1978).

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“…Male New Zealand white rabbits (3-4 kg) were initially anaesthetized with Althesin injected via an ear vein and were pithed under halothane anaesthesia (McGrath & McKenzie, 1977), then artificially ventilated with 100% oxygen. Right and left carotid arteries were cannulated to monitor arterial blood pressure and for the addition of propranolol at 30 min intervals, respectively.…”

Section: Methodsmentioning

confidence: 99%

Difference in the potency of α₂‐adrenoceptor agonists and antagonists between the pithed rabbit and rat

Bulloch

Docherty

Flavahan

et al. 1987

British J Pharmacology

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1 The subtypes ofa-adrenoceptors which mediate pressor responses to sympathomimetic agonists or to nerve stimulation in pithed rabbits have been classified according to the effects of 'selective' antagonists and a comparison has been made, for the xt2-subtype, with corresponding responses in the rat.2 In the rabbit the dose-response curve for phenylephrine was shifted to the right in parallel by prazosin (1 mg kg-') and was unaffected by rauwolscine (1 mg kg '). The dose-response curve for noradrenaline was shifted to the right by prazosin (I mg kg -') and was shifted to a smaller extent by rauwolscine (1 mg kg -') or imiloxan (1Omg kg-'). After rauwolscine, prazosin produced a rightward shift larger than when given alone. After prazosin, rauwolscine produced a rightward shift larger than when given alone. 3 The responses to pressor nerve stimulation at low frequencies (< 1 Hz) could be reduced by prazosin, rauwolscine or imiloxan but those at a higher frequency could be reduced only by prazosin. 4 These results indicate that the responses to noradrenaline or to nerve stimulation are mediated by both a,-and a2-adrenoceptors. Low doses or frequencies have a proportionately greater component which is M2 5 Responses to noradrenaline after prazosin (1 mg kg -'), were sufficiently sensitive to rauwolscine to be considered as predominantly a2. A comparison was therefore made of such responses in the rat and rabbit. They were produced by a lower dose per unit body weight in the rat whereas this was less marked for the M2-adrenoceptor agonist guanabenz. In the rabbit they were more susceptible to blockade by rauwolscine but were less sensitive to Wy 26703 than in the rat. This demonstrates that the ;c2-adrenoceptors mediating pressor responses in vivo, like those in other tissues in vitro, are different in rat and rabbit, with regard to antagonists.

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The Effects of Intravenous Anaesthetics on the Cardiovascular System of the Rabbit

Cited by 25 publications

References 26 publications

Dietary Cholesterol Affects Sympathetic Nerve Function in Rabbit Hearts

Dietary Cholesterol Affects Sympathetic Nerve Function in Rabbit Hearts

The central noradrenergic control of blood pressure and heart rate

Difference in the potency of α₂‐adrenoceptor agonists and antagonists between the pithed rabbit and rat

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The Effects of Intravenous Anaesthetics on the Cardiovascular System of the Rabbit

Cited by 25 publications

References 26 publications

Dietary Cholesterol Affects Sympathetic Nerve Function in Rabbit Hearts

Dietary Cholesterol Affects Sympathetic Nerve Function in Rabbit Hearts

The central noradrenergic control of blood pressure and heart rate

Difference in the potency of α2‐adrenoceptor agonists and antagonists between the pithed rabbit and rat

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Difference in the potency of α₂‐adrenoceptor agonists and antagonists between the pithed rabbit and rat