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The difficulty of defining the three so-called components of « an-esthesia » is emphasized: hypnosis, absence of movement, and adequacy of anti-nociception (intraoperative « analgesia »). Data obtained from anesthetized animals or humans delineate the activation of cardiac and vasomotor sympathetic reflex (somato-sympathetic reflex) and the cardiac parasympathetic deactivation observed following somatic stimuli. Sympathetic activation and parasympathetic deactivation are used as monitors to address the adequacy of intraoperative anti-nociception. Finally, intraoperative nociception through the administration of nonopioid analgesics vs. opioid analgesics is considered to achieve minimal postoperative side effects., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

The information carried by heart period (HP) given systolic arterial pressure (SAP) changes was assessed to characterize spontaneous baroreflex (i.e. the relation linking SAP variability to HP variability): the larger the information carried by HP given SAP changes, the greater the unpredictability of HP given SAP variations, the smaller the strength of the causal coupling from SAP series to HP series. It was typified according to two parameters: i) the information carried by HP given SAP changes within the same heart cycle (i.e. 0-step-ahead information) describing immediate effects of SAP variations on HP; ii) the rate of increase of the information carried by HP given SAP changes as a function of the temporal distance, k, between the conditioning SAP pattern and future HP value (i.e. the rate of increase of k-step-ahead information with k) describing short-term effects of SAP modifications on HP. Both parameters were found under vagal control. Indeed, i) 0-step-ahead information suggested that HP and SAP variabilities were significantly coupled from SAP to HP at baseline and after the reduction of the inhibitory effect of sympathetic control on vagal influences performed through the administration of propranolol or clonidine; and ii) during vagal blockade induced by atropine or combined vagal and sympathetic blockade induced by the administration of propranolol after atropine k-step-ahead information reached a level incompatible with coupled HP and SAP dynamics regardless of k. In addition, it was found that the 0-step-ahead information at baseline and after propranolol and the rate of increase of k-step-ahead information with k at baseline could be exclusively explained in terms of linear HP-SAP interactions. Conversely, the same parameters after clonidine suggested the raise of nonlinear mechanisms probably unveiled by the central sympathetic blockade. Comparison with more traditional parameters describing the HP-SAP variability relation such as baroreflex sensitivity and squared HP-SAP coherence confirmed the complementary value of the proposed information domain analysis., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Alpha-2 adrenergic agonists ("alpha-2 agonists") present multiple pharmacodynamic effects: rousable sedation, decreased incidence of delirium in the setting of critical care, preservation of respiratory drive, decreased whole body oxygen consumption, decreased systemic and pulmonary arterial impedance, improved left ventricular systolic and diastolic function, preserved vascular reactivity to exogenous catecholamines, preserved vasomotor baroreflex with lowered set point, preserved kidney function, decreased protein catabolism. These pharmacodynamic effects explain the interest for these drugs in the critical care setting. However, their exact role for sedation in critically ill-patients remains open for further studies. Given the few double-blind randomized multicentric trials available, the present non exhaustive analysis of the literature aims at presenting the utilization of alpha-2 agonists as potential first-line sedative agents, in the critical care setting. Suggestions regarding the use of alpha-2 agonists as sedatives are detailed., (Copyright © 2012 Société française d’anesthésie et de réanimation (Sfar). Published by Elsevier SAS. All rights reserved.)

Background: Association of low cardiac vagal activity and poor outcome is demonstrated in the cardiology setting. This has not been addressed in the postoperative setting. Cardiac vagal motoneurones (CVMs) in the brain stem generate sinus arrhythmia. They may reduce blood pressure (BP) variability ('pressure lability'). An alpha-2 agonist, clonidine, was administered to assess whether cardiac vagal activity could be recruited from a very low baseline activity, increase the sensitivity of the cardiac baroreflex and sinus arrhythmia, and reduce the pressure lability., Methods: In ventilated anaesthetized rats, single-unit activity from antidromically identified CVMs was recorded. Given complex interactions within the cardiac ganglion, a peripherally acting beta-blocker, atenolol, was administered before clonidine., Results: Atenolol 2 mg kg(-1) i.v. did not change systolic BP (SBP), CVM firing rate and slope of the cardiac baroreflex analysed at CVM (SBP-CVM unit activity relationship) level, or at the heart level (SBP-RR interval relationship) but evoked a significant bradycardia. In the presence of atenolol 2 mg kg(-1) h(-1), clonidine 10-100 microg kg(-1) i.v. evoked a significant reduction in SBP, a large increase of CVM firing rate from a very low base line [0.16 (sd 0.28) to 1.37 (1.21) spikes s(-1), n=7 cells], and increased the slope of the cardiac baroreflex analysed at the CVM level or at the heart level. sds of SBP were reduced, and that of RR interval was increased., Conclusions: Following peripheral beta-blockade, clonidine activated CVMs from a very low baseline, increased the slope of the cardiac baroreflex and sinus arrhythmia, and reduced pressure lability.

Pharmacologically-induced hypertension engages few aminergic ventrolateral medullary cells. To further address this issue, reflex hypertension evoked by acute sino-aortic deafferentation was chosen as a model. Adrenergic rostral ventrolateral neurons were recorded with a continuous, catechol-specific tool, i.e. in vivo voltammetry. Controlled hypotension led to the expected increase in catechol signal in sham rats (n = 4) but not in deafferented (vagi, superior laryngeal and glossopharyngeal nerves) rats (n = 5). Thus, the central responsiveness to known stimuli remained intact in this preparation following acute sino-aortic deafferentation. However, acute sino-aortic deafferentation itself induced no increase in catechol signal (n = 4 or 5 respectively). No increase in catechol signal was, observed when deafferentation was performed a) under hyperoxic conditions (O2 = 100%, n = 5) b) by extensive deafferentation involving also the cervical sympathetic trunk under halothane (n = 5) c) upon restrictive deafferentation leaving the vagi intact under pentobarbital (n = 5) d) in decerebrate animals (n = 4). Adrenergic rostral ventrolateral medullary barosensitive bulbospinal neurons may be primarily involved during hypotension.

After completion of abdominal aortic graft, 29 patients received an i.v. infusion of placebo (n = 16) or clonidine 7 micrograms kg-1 (n = 13) over 120 min in a double-blind study. Cardiovascular variables were measured and plasma samples obtained up to 5 h after arrival in the recovery room, for assay of noradrenaline, adrenaline, vasopressin and renin concentrations. Noradrenaline, adrenaline and vasopressin concentrations decreased in the clonidine group throughout recovery (P less than 0.001, 0.05 and 0.05, respectively, vs placebo). Heart rate was less in the clonidine group (P less than 0.01). There was no significant difference in mean arterial pressure between groups. Stroke volume was larger (P less than 0.01) and there were fewer episodes of hypertension (P less than 0.05) and tachycardia in the clonidine group. In addition, a reduction in the number of circulatory interventions (P less than 0.05) and episodes of shivering was noted in the clonidine group. Mean (SD) postoperative volume requirements were larger in the clonidine group (total postoperative input: clonidine 1462 (604) ml; placebo 1064 (348) ml (P less than 0.05]. These data are consistent with the observation that clonidine modifies endocrine and circulatory status after major surgery.