Rabbit carotid sinus reflex under pentobarbital, urethan, and chloralose anesthesia

Ishikawa, Nobuyoshi; Kallman, Clayton H.; Sagawa, K

doi:10.1152/ajpheart.1984.246.5.h696

Cited by 27 publications

(25 citation statements)

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“…Urethane was used for basal anesthesia since it does not affect arterial baroreflex sensitivity and produces long-lasting anesthesia with minimal cardiovascular depression. 7 Brief but abrupt reductions of HR and MAP soon after remifentanil injection were observed in the neuraxis intact animals (vagus intact) but not in the barodenervated bilaterally vagotomized animals ( Figure 1). This means that remifentanil exerts central vagotonic action, leading to bradycardia and hypotension.…”

Section: Discussionmentioning

confidence: 93%

Suppressive effects of remifentanil on hemodynamics in baro-denervated rabbits

Shinohara

Aono

Unruh

et al. 2000

Can J Anesth/J Can Anesth

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Purpose: To elucidate mechanisms by which remifentanil, an ultra-short-acting µ-opioid receptor agonist, causes hypotension and bradycardia.Methods: Mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were measured and recorded after bolus injections of 1, 2 or 5 µg·kg -1 of remifentanil in neuraxis intact (n=6 for each dose) and baro-denervated rabbits (n=6 for each dose). Arterial baroreflex sensitivity was assessed by depressor tests. An additional six baro-denervated animals received remifentanil, 5 µg·kg -1 after pretreatment with naloxone, 40 µg·kg -1 .Results: All values were expressed in % change from baseline. In the neuraxis intact animals, MAP and HR were decreased briefly immediately after remifentanil injection. RSNA was increased dose-dependently: 137 ± 8% (mean ± SE), 170 ± 14% (P < 0.05) and 225 ± 29% (P < 0.05) after 1, 2 and 5 µg·kg -1 remifentanil, respectively. RSNA was increased even after MAP and HR had returned to baseline values. The depressor tests revealed that remifentanil did not attenuate arterial baroreflex sensitivity. In the baro-denervated animals, MAP and HR decreased gradually to 77 ± 3% (P < 0.05) and 94 ± 1% (P < 0.05), respectively 300 sec after 5 µg·kg -1 remifentanil. At that time, increased RSNA (159 ± 9%, P < 0.05) had returned to baseline. Pretreatment with naloxone in the baro-denervated animals abolished these changes. Conclusion:Remifentanil decreases HR and MAP by its central vagotonic effect and by stimulating peripheral µ-opioid receptors. These effects appear to be counteracted and masked by its central sympathotonic effect and by maintaining arterial baroreflex integrity.Objectif : Expliquer les mécanismes par lesquels le rémifentanil, un agoniste à action ultra brève du récepteur de µ-opioïde, provoque de l'hypotension et de la bradycardie.Méthode : La tension artérielle moyenne (TAM), la fréquence cardiaque (FC) et l'activité nerveuse sympathique rénale (ANSR) ont été mesurées et notées après l'injections de bolus de 1, 2 ou 5 µg·kg -1 de rémifentanil dans le névraxe de lapins intacts (n=6 pour chaque dose) et de lapins baroénervés (n=6 pour chaque dose). La sensibilité artérielle baroréflexe a été évaluée par des tests dépresseurs. Six animaux supplémentaires, baroénervés, ont reçu 5µg·kg -1 de rémifentanil après un prétraitement avec 40µg·kg -1 de naloxone.Résultats : Toutes les valeurs sont exprimées en % de changement par rapport aux mesures de base. Chez les animaux intacts, la TAM et la FC ont brièvement baissé immédiatement après l'injection de rémifentanil. L'ANSR s'est accrue d'une manière dépendante de la dose : 137 ± 8 % (moyenne ± écart type), 170 ± 14 % (P < 0,05) et 225 ± 29 % (P < 0,05) après 1, 2 et 5 µg·kg -1 de rémifentanil, respectivement. L'ANSR a augmenté même après que la TAM et la FC ont retrouvé les valeurs de base. Les tests dépresseurs ont révélé que le rémifentanil n'a pas atténué la sensibilité artérielle baroréflexe. Chez les lapins baroénervés, la TAM et la FC ont diminué graduellement jusqu'à...

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Section: Discussionmentioning

confidence: 93%

Suppressive effects of remifentanil on hemodynamics in baro-denervated rabbits

Shinohara

Aono

Unruh

et al. 2000

Can J Anesth/J Can Anesth

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“…27,28 Therefore, it seems difficult to infer the role of ghrelin in the NTS on cardiovascular and sympathetic regulation in conscious animals. However, because ICV administration of ghrelin suppressed the RSNA and decreased blood pressure in conscious rabbits, 8 ghrelin may act at the NTS to suppress sympathetic nerve activity and decrease arterial pressure even in conscious animals.…”

Section: Discussionmentioning

confidence: 99%

Ghrelin Acts at the Nucleus of the Solitary Tract to Decrease Arterial Pressure in Rats

et al. 2004

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Abstract-Ghrelin is an orexigenic peptide originally isolated from the stomach. Intracerebroventricular administration of ghrelin has been shown to elicit decreases in arterial pressure and renal sympathetic nerve activity in conscious rabbits. The aim of the present study was to determine the role of ghrelin in the brain stem in cardiovascular responses in rats. Unilateral microinjection of ghrelin into the nucleus of the solitary tract significantly decreased the mean arterial pressure and heart rate (Ϫ17.3Ϯ0.8 mm Hg and Ϫ13.6Ϯ3.5 bpm by 20 pmol). The microinjection of ghrelin into the nucleus of the solitary tract also suppressed the renal sympathetic nerve activity (Ϫ29.5Ϯ3.4%; PϽ0.0001). Pretreatment with intravenous injection of pentolinium (5 mg/kg), a ganglion-blocking agent, eliminated these cardiovascular responses induced by the microinjection of ghrelin (20 pmol) into the nucleus of the solitary tract; however, pretreatment with intravenous injection of atropine sulfate (0.1 mg/kg), an antagonist of muscarinic acetylcholine receptors, failed to prevent them. In contrast, unilateral microinjection of ghrelin into the area postrema, rostral, and caudal ventrolateral medulla caused no significant changes in the mean arterial pressure and heart rate. On the other hand, immunohistochemical study revealed that the receptor for ghrelin, the growth hormone secretagogue receptor, was expressed in the neuronal cells of the nucleus of the solitary tract and the dorsal motor nucleus of the vagus, but not in the cells of the area postrema. These results suggest that ghrelin acts at the nucleus of the solitary tract to suppress sympathetic activity and to decrease arterial pressure in rats. Key Words: blood pressure Ⅲ immunohistochemistry Ⅲ rats G hrelin, an acylated 28-residue peptide originally isolated from rat stomach, is an endogenous ligand for the growth hormone secretagogue (GHS) receptor. 1,2 Although ghrelin is likely to regulate pituitary growth hormone (GH) secretion, along with GH-releasing hormone and somatostatin, 2,3 intracerebroventricular (ICV) administration of ghrelin has been shown to generate a dose-dependent increase in food intake and body weight, 4,5 suggesting that ghrelin participates in the regulation of both food intake and GH secretion.It has been suggested that ghrelin may participate not only in feeding behavior but also in cardiovascular and sympathetic regulation. 6 -10 Ghrelin has a vasodilatory effect in humans, 6 and intravenous injection of human ghrelin has been shown to elicit a decrease in blood pressure without an increase in heart rate (HR) in healthy men. 7 We have recently reported that ICV administration of ghrelin suppresses the renal sympathetic nerve activity (RSNA) and decreases arterial pressure in conscious rabbits, suggesting that intravenous injection of ghrelin acts, at least in part, on the central nervous system to decrease arterial pressure and RSNA. 8 Moreover, ICV administration of ghrelin augments baroreflex control of RSNA and HR. 8 Our previous finding...

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“…To evaluate the sympathetic nervous system precisely, the present study was conducted on conscious rabbits with direct recording of renal sympathetic nerve activity (RSNA), because the sympathetic nervous system and baroreceptor reflex are greatly affected by anesthesia. 12,13 …”

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confidence: 99%

Central Ghrelin Modulates Sympathetic Activity in Conscious Rabbits

et al. 2002

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Abstract-Ghrelin is an orexigenic peptide originally isolated from the stomach. Intravenous administration of ghrelin has been shown to elicit a decrease in arterial pressure without a significant change in heart rate (HR), suggesting that ghrelin may act on the central nervous system to modulate sympathetic activity. The aim of the present study was to determine the central effects of ghrelin on cardiovascular and sympathetic responses in conscious rabbits. Key Words: baroreceptors Ⅲ blood pressure Ⅲ central nervous system Ⅲ ghrelin Ⅲ nervous system, sympathetic renal G hrelin, an acylated 28-residue peptide originally isolated from the rat stomach, is an endogenous ligand for the growth hormone (GH) secretagogue receptor. 1,2 Although ghrelin is likely to regulate pituitary GH secretion along with GH-releasing hormone and somatostatin, 2,3 GH secretagogue receptors have also been identified in hypothalamic neurons and in the brainstem. 4,5 Intracerebroventricular (ICV) administration of ghrelin has been shown to generate a dose-dependent increase in food intake and body weight, 6,7 suggesting that ghrelin participates in the regulation of food intake and GH secretion. Furthermore, ICV administration of ghrelin has been shown to increase plasma vasopressin level without a significant change in arterial pressure in conscious rats. 8 It has also been reported that intravenous injection of human ghrelin elicits a decrease in blood pressure without an increase in heart rate (HR) in healthy men. 9 In addition, plasma ghrelin concentration is increased in patients with cachexia associated with chronic heart failure. 10 These previous findings suggest that ghrelin may participate not only in feeding behavior but also in cardiovascular and sympathetic regulation. Although ghrelin has been reported to have a vasodilatory effect in humans, 11 the underlying mechanisms of depressor response induced by intravenous injection of ghrelin have not yet been determined. Because the depressor response was not accompanied by tachycardia, it is likely that mechanisms other than direct vasodilating effects, at least in part, are involved in this depressor response. To clarify the mechanisms for this depressor response, the effects of ghrelin on sympathetic activity and on the baroreceptor reflex should be determined. We hypothesized that intravenous administration of ghrelin acts at the central nervous system to modulate the sympathetic nervous system, resulting in a decrease in arterial pressure without tachycardia. Accordingly, in the present study, we focused on the central effect of ghrelin on sympathetic activity and baroreceptor reflex. To evaluate the sympathetic nervous system precisely, the present study was conducted on conscious rabbits with direct recording of renal sympathetic nerve activity (RSNA), because the sympathetic nervous system and baroreceptor reflex are greatly affected by anesthesia. 12,13

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Rabbit carotid sinus reflex under pentobarbital, urethan, and chloralose anesthesia

Cited by 27 publications

References 0 publications

Suppressive effects of remifentanil on hemodynamics in baro-denervated rabbits

Suppressive effects of remifentanil on hemodynamics in baro-denervated rabbits

Ghrelin Acts at the Nucleus of the Solitary Tract to Decrease Arterial Pressure in Rats

Central Ghrelin Modulates Sympathetic Activity in Conscious Rabbits

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