Influence of anaesthesia on the cardiovascular effects of rilmenidine and clonidine in spontaneously hypertensive rats (original) (raw)
Related papers
Journal of Biotechnology Research Center
To examine the hypothesis of a role for α2-adrenoceptors in mediating the mechanism of urethane hypotensive effect whether it's peripheral or central, Wistar rats were anesthetized with urethane or (for comparison) with halothane, to study the influence of urethane that govern the mechanism of central and peripheral α2-adrenoceptors action, on basal BP & HR, and the rise in blood pressure (BP) to the stimulation of caudal pressor area (CPA), when these receptors were either centrally activated by bilateral rostral ventrolateral medulla (RVLM) microinjection of clonidine (30nM), and blockade with any of the clonidine antagonists, yohimbine (500pmol/50nl), and idazoxane (270nM) or yohimbine+idazoxane, or when peripherally activated (of urethane anesthetized rats) by i.v. clonidine (100nmol/kg), which also blockade with idazoxane or yohimbine+idazoxane. The results indicated presence of no anesthetic differences in a partial involvement of α2-receptors-RVLM, vs. a complete involve...
Studies of Anaesthesia in Relation to Hypertension V: Adrenergic Beta-Receptor Blockade
BJA: British Journal of Anaesthesia, 1973
The effects of intravenous practolol 0.4 mg/kg were studied in 12 hypertensive patients during halothane/nitrous oxide anaesthesia. Practolol decreased heart rate (HR) and cardiac output (Q) from the elevated levels following atropine administration during anaesthesia, but values of arterial pressure (AP), HR and Q after the combination of atropine and practolol were not significantly different from those during anaesthesia prior to blockade. The effects of a similar anaesthetic sequence were studied in a further 11 treated hypertensive patients given practolol by mouth 1.5 mg/kg/6 hours for at least 48 hours preoperatively in addition to current anti-hypertensive therapy. By comparison with treated hypertensive patients previously studied, those pretreated with practolol had similar AP awake, but higher AP throughout anaesthesia with either spontaneous or artificial ventilation. Cardiac output was higher and systemic vascular resistance was lower both before and during anaesthesia. Both the present groups of patients showed significantly attenuated responses of tachycardia and hypertension following laryngoscopy and intubation compared with previous studies. The incidence of dysrhythmia and e.c.g. evidence of myocardial ischaemia was significantly lower (4%) in beta-blocked patients compared with those who had not received practolol (38%).
Canadian Journal of Anaesthesia-journal Canadien D Anesthesie, 2000
Purpose: To investigate the effects of chronic ACE inhibition on cardiac neural function following induction of general anesthesia in patients with underlying coronary artery disease. Method: In a prospective case-control study, heart rate variability (HRV) and baroreflex control were compared preoperatively and 30 min after anesthesia induction in patients receiving, or not, ACEI (n=16, control group and n=16, ACEI group). All patients had normal cardiac function and anesthesia consisted of a fixed dose regimen of fentanyl and midazolam. Anesthesia-related hypotension was defined by systolic blood pressure0.15 to 0.6 Hz). Baroreflex sensitivity was estimated after blood pressure changes induced by injections of phenylephrine (PHE) and nitroglycerin (NTG). Results: The HRV parameters and baroreflex sensitivity were not different between groups, during the awake and anesthesia periods. Anesthesia produced similar reduction in total HRV in the Control and ACEI groups (−93±28% vs −89±32%,) and in baroreflex sensitivity during NTG (−64±21% vs −54±17%) or PHE tests (−74±25% vs −72±22%). Anesthesia-related hypotension occurred in nine patients in the ACEI group (vs two controls). Although the hypertensive response to phenylephrine was greater after anesthesia in both groups, the sensitivity to phenyle-phrine was attenuated in those patients experiencing hypotension in the ACEI group. Conclusions: Chronic preoperative treatment with ACEIs does not influence cardiac autonomic regulation and anesthetic- induced hypotensive episodes are mainly attributed to decreased-adrenergic vasoconstrictive response. Objectif: Rechercher les effets d’une inhibition chronique de l’ECA sur la fonction neurale cardiaque à la suite de l’induction d’une anesthésie générale chez des patients qui présentent une cardiopathie ischémique sous-jacente. Méthode: Lors d’une étude prospective cas-témoins, la variabilité de la fréquence cardiaque (VFC) et le contrôle baroréflexe ont été comparés avant l’opération et 30 min après l’induction de l’anesthésie chez des patients qui reçoivent, ou non, un IECA (groupe témoin: n=16, groupe IECA: n=16). Tous les patients présentaient une fonction cardiaque normale et l’anesthésie comprenait un schéma posologique fixe de fentanyl et de midazolam. On a défini l’hypotension reliée à l’anesthésie comme la tension artérielle systolique0,15 à 0,6 Hz). La sensibilité baroréflexe a été évaluée après les changements de pression sanguine induits par les injections de phényléphrine (PHE) et de nitroglycérine (NTG). Résultats: Les paramètres de la VFC et la sensibilité baroréflexe n’ont pas présenté de différence intergroupe pendant les périodes d’éveil et d’anesthésie. L’anesthésie a produit une réduction similaire de la VFC totale dans les groupes témoin et IECA (−93±28 % vs −89±32%,), et de la sensibilité baroréflexe pendant les tests avec la NTG (−64±21 % vs −54±17 %) ou la PHE (−74±25 % vs −72±22 %). L’hypotension reliée à l’anesthésie est survenue chez neuf patients du groupe IECA (vs deux témoins). Bien que la réponse hypertensive à la phényléphrine ait été plus grande après l’anesthésie dans les deux groupes, la sensibilité à la phényléphrine a été atténuée chez les patients qui ont présenté de l’hypotension dans le groupe IECA. Conclusion: Le traitement préopératoire prolongé avec l’IECA n’influence pas la régulation autonomique cardiaque et l’hypotension induite par l’anesthésique est principalement causée par la diminution de la réponse vasoconstrictive α-adrénergique.
Frontiers in physiology, 2016
We investigated the effects of chronic subcutaneous treatment with centrally-acting antihypertensive agents moxonidine, rilmenidine, and clonidine on the baroreflex control of heart rate (HR) in conscious normotensive rabbits over 3 weeks. Infusions of phenylephrine and nitroprusside were performed at week 0 and at weeks 1 and 3 of treatment to determine mean arterial pressure (MAP)-HR baroreflex relationships. A second curve was performed after intravenous methscopolamine to determine the sympathetic baroreflex relationship. The vagal component of the reflex was determined by subtracting the sympathetic curve from the intact curve. Clonidine and moxonidine (both 1 mg/kg/day), and rilmenidine (5 mg/kg/day), reduced MAP by 13 ± 3, 15 ± 2, and 13 ± 2 mmHg, respectively, but had no effect on HR over the 3-week treatment period. Whilst all three antihypertensive agents shifted baroreflex curves to the left, parallel to the degree of hypotension, moxonidine and rilmenidine decreased the ...
Comparison of the Cardiac Effects of Β-Adrenoreceptor Agonists in Anaesthetised and Conscious Dogs
Autonomic and Autacoid Pharmacology, 2010
The cardiovascular effects of some P-adrenoreceptor agonists on heart rate, blood pressure and myocardial contractility. (maximum rate of change of left ventricular pressurehntegrated isometric tension) were measured in pentobarbltone-anaesthetised and conscious, instrumented greyhounds. 2 In anaesthetised dogs isoprenaline increased heart rate and myocardial contractility and reduced blood pressure. Prenalterol and RO 363, in equiactive inotropic doses, induced greater increases in heart rate than isoprenaline if blood pressure fell by less than 25 mmHg. Salbutamol had hypotensive activity at all doses and appeared to be a relatively selective inotrope. 3 None of the agonists caused blood pressure to fall in the conscious dogs. Prenalterol and RO 363 were more effective inotropic stimulants, producing smaller increases in heart rate and more pronounced increases in myocardlal contractility. Salbutamol, however, elicited greater increases in heart rate in the conscious animals and the inotropic selectivity demonstrated in the anaesthetised animals was lost. 4 The direct effects of the P-adrenoreceptor agonists, without modification by reflexes could be observed in the anaesthetised animals. The differences in the actions of the agonists in the conscious animals appear to be attributable to the state of the baroreceptor reflex control system and the relatively enhanced responsiveness of the heart. orally active stimulant of cardiac adrenergic f%-receptors. Am. HearrJ., 95,602-610. McPHERSON, G. A., MALTA, E. &RAPER,C. (1980). fladrenoceptor mediated actions of R0363 and (-)isoprenaline in anaesthetized cats, rats and rabbits. 3.
Acta Anaesthesiologica Scandinavica, 2008
Background: In the post-operative setting, pressure lability is increased in hypertensive patients. a-2 agonists were shown qualitatively to reduce this lability qualitatively. Here, upon immobilization combined with emergence from anesthesia in rats and clonidine administration, pressure lability was quantitatively assessed and related to baroreflex sensitivity. Methods: After local anesthesia of all incisions and surgical wounds and myorelaxation with metocurine, rats had halothane withdrawn for 60 min. Rats received (a) saline (n 5 8), (b) clonidine 30 mg/kg i.v (n 5 8) simultaneous to halothane discontinuation and (c) halothane readministration (n 5 8) 20 min after halothane discontinuation. Pressure lability was quantitatively assessed using occurrence/amplitude of peaks in systolic blood pressure (SBP) and cardiac baroreflex slope. Results: Clonidine was associated with partial blunting of hypertension, reduced standard deviation of SBP, reduced number and amplitude of peaks in systolic pressure. Clonidine was also associated with increased slope of the cardiac baroreflex upon early intervals of emergence, but not at later intervals. Conclusion: Clonidine reduces pressure lability upon immobilization stress combined to emergence from anesthesia, via parasympathetic activation and possibly sympathetic inhibition during early emergence as opposed to sympathetic inhibition during late emergence.
Journal of Pharmacological and Toxicological Methods, 1997
The antiischemic effect of drugs can be detected at a lower dose range if the cardiac workload is increased. A brief period of frequency-loading (ventricular overpacing = VOP) results in well-defined, reproducible changes in cardiac parameters in the conscious, chronically instrumented rabbit; however, rapid pacing frequently evoked ventricular tachycardia or even fatal ventricular fibrillation. Therefore, cardiac workload has been increased by i.v. administration of adrenoceptor agonists, such as isoproterenol (ISO), phenylephrine (PHE), and their combination, respectively. The doses applied (especially the combination of 2 &kg IS0 and 16 &kg PHE, giving optimal changes) were sufficient to produce a marked elevation of both the ST segment in the intracavital electrogram and the left ventricular end-diastolic pressure, without evoking cardiac arrhythmias. We compared the effect of this adrenergic "test" stimulus with that of VOP on hemodynamic and electrophysiological parameters of the heart, and furthermore, on the modification of responses to both "test" stimuli by oral administration of the coronary vasodilator: Isosorbide-.5-mononitrate (IS-5-N), given in a dose of 40 mg/kg. Both VOP-and ISO+PHE-induced changes were significantly attenuated by IS-5-N, and a temporal coincidence of the maximal effects was found as well. We reached the following conclusion: The combined administration of IS0 and PHE not evoking fatal arrhythmias in the dose range applied can replace the more risky VOP as a "test" workload in the estimation of antiischemic action.
Journal of Anesthesia, 2008
Purpose. Circulatory instability is often observed upon emergence from general anesthesia. The increased blood pressure (BP) lability has been associated with poor clinical outcome. However, its underlying mechanisms are not fully understood. Thus, we investigated a possible role of the sympathetic nervous system (SNS) and cardiac barorefl ex in the increased pressure lability observed upon emergence from general anesthesia. Methods. Male rats (n = 16) were allocated to two groups, i.e., (1) a control group (n = 8) and (2) an α-methylparatyrosine (α-MPT; an inhibitor of tyrosine hydroxylase)-treated group (n = 8). In the α-MPT-treated group, in order to deplete catecholamines both in the central nervous system and in the SNS, α-MPT (300 mg·kg −1 ) was injected intraperitoneally (i.p.), administered twice, 4 and 2 h before halothane discontinuation (total dose, 600 mg·kg −1 i.p.). In the control group, saline was administered at identical time-points. Systolic BP (SBP) lability was evaluated on a beat-by-beat basis, using the coeffi cient of variation of SBP, and the occurrence of slow and rapid rises in SBP and their amplitude, while the cardiac barorefl ex slope was calculated using the "sequences" method. Results. In the control group, heart rate, SBP, and the three indices of BP lability (i.e., the 3 indices of BP lability are: coeffi cient of variation of SBP, number of slow and rapid rises in pressure, amplitude of slow and rapid rises in pressure) all increased upon emergence from anesthesia (P < 0.05). Such increases were all blunted in the α-MPT-treated group, with the increases in the three indices of BP lability almost entirely suppressed (P < 0.05). The cardiac barorefl ex slope was similarly decreased in both groups (P < 0.05). Conclusion. The postanesthetic increase in pressure lability seems largely a consequence of increased sympathetic activity, irrespective of any change in cardiac barorefl ex sensitivity.