Effect of catecholamine depletion on increased blood pressure lability upon emergence from halothane anesthesia in rats: the role of sympathetic nervous activity in postanesthetic circulatory instability

Cividjian, Andrei; Rentero, N.; Pequignot, J. M.; Quintin, Luc

doi:10.1007/s00540-007-0594-y

Cited by 6 publications

(4 citation statements)

References 32 publications

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“…Because all rats received the same dose of anesthetics according to their body weight (30 mg/kg pentobarbital sodium), the two accidents may not have been due to anesthetic overdose. We speculate that the death of these 2 rats might be related to the high BP, which is relevant to a high-sodium diet, as reported by Cividjian et al [16]. …”

Section: Methodsmentioning

confidence: 55%

High Sodium Intake Impairs Small Artery Vasoreactivity in vivo in Dahl Salt-Sensitive Rats

Wang

Chen

et al. 2019

J Vasc Res

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The effects of high sodium intake on the functionality of resistance arteries have been repeatedly studied in vitro, but no study has focused on salt-sensitive hypertension in vivo. We studied the in vivo reactivity of mesenteric small arteries (MSAs) to vasoactive agents in Dahl salt-sensitive (DS) rats with various sodium diets. Twenty-four male DS rats were randomized into 3 groups: LS (0.3% NaCl diet), NS (0.6% NaCl diet), and HS (8% NaCl diet). After a 12-week intervention, the diameter changes of the MSAs after noradrenaline (NA) and acetylcholine (ACh) exposure were detected by a microscope, and changes in blood perfusion through the MSAs were measured by full-field laser perfusion imaging. HS enhanced the constrictive response of the MSAs to NA and attenuated the relaxing response to ACh. Low sodium intake reduced the response of the MSAs to NA and promoted ACh-induced vasodilatation. HS also aggravated NA-induced blood perfusion reduction and impaired ACh-induced hyperperfusion of the MSAs. Pathologically, HS was associated with arteriolar structural damage and fibrosis of the MSAs. We conclude that sodium intake affects the responsiveness of the MSAs to vasoactive agents in DS rats and might play important roles in modulating blood pressure in hypertensive individuals.

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Section: Methodsmentioning

confidence: 55%

High Sodium Intake Impairs Small Artery Vasoreactivity in vivo in Dahl Salt-Sensitive Rats

Wang

Chen

et al. 2019

J Vasc Res

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“…In addition, it allows the estimation of gain of the relation from HP to SAP (i.e., the gain of the mechanical feedforward pathway) as well, thus completing the description of the closed-loop HP-SAP regulation during general anesthesia. This method could be a valuable tool to better understand differences among anesthesiological strategies (i.e., intravenous vs. volatile) (14), to compare different drugs within the same anesthesiological strategy (halothane vs. sevoflurane) (16), to contrast different modalities of mechanical ventilation (pressure controlled vs. pressure support mechanical ventilation) (9), to manage the increased arterial pressure lability observed upon the emergence from general anesthesia (15), and to improve perioperative risk models (4). Also, critical care medicine might take advantage for a more reliable continuous monitoring of BRS.…”

Section: Discussionmentioning

confidence: 99%

Model-based causal closed-loop approach to the estimate of baroreflex sensitivity during propofol anesthesia in patients undergoing coronary artery bypass graft

Porta¹,

Bari

Bassani

et al. 2013

Journal of Applied Physiology

128

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Cardiac baroreflex is a fundamental component of the cardiovascular control. The continuous assessment of baroreflex sensitivity (BRS) from spontaneous heart period (HP) and systolic arterial pressure (SAP) variations during general anesthesia provides relevant information about cardiovascular regulation in physiological conditions. Unfortunately, several difficulties including unknown HP-SAP causal relations, negligible SAP changes, small BRS values, and confounding influences due to mechanical ventilation prevent BRS monitoring from HP and SAP variabilities during general anesthesia. We applied a model-based causal closed-loop approach aiming at BRS assessment during propofol anesthesia in 34 patients undergoing coronary artery bypass graft (CABG) surgery. We found the following: 1) traditional time and frequency domain approaches (i.e., baroreflex sequence, cross-correlation, spectral, and transfer function techniques) exhibited irremediable methodological limitations preventing the assessment of the BRS decrease during propofol anesthesia; 2) Granger causality approach proved that the methodological caveats were linked to the decreased presence of bidirectional closed-loop HP-SAP interactions and to the increased incidence of the HP-SAP uncoupling; 3) our model-based closed-loop approach detected the significant BRS decrease during propofol anesthesia as a likely result of accounting for the influences of mechanical ventilation and causal HP-SAP interactions; and 4) the model-based closed-loop approach found also a diminished gain of the relation from HP to SAP linked to vasodilatation and reduced ventricular contractility during propofol anesthesia. The proposed model-based causal closed-loop approach is more effective than traditional approaches in monitoring cardiovascular control during propofol anesthesia and indicates an overall depression of the HP-SAP closed-loop regulation.

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“…Such a link was not observed in a previous report. 18 Thus, the present and previous data bring us three steps ahead in our understanding of beat-by-beat perioperative circulatory stability 4 33 in that an inhibitor of catecholamine synthesis, alpha-methylparatyrosine, suppresses pressure lability upon emergence in rats, 34 suggesting sympathetic vascular activity as a cause of pressure lability, and atenolol suppresses pressure lability, suggesting sympathetic cardiac activity as a cause of pressure lability. A mechanistic link, that is, CVM activation, exists between increased sinus arrhythmia and reduced pressure lability following clonidine, but not atenolol.…”

Section: Discussionmentioning

confidence: 68%

Recruitment of cardiac parasympathetic activity: effects of clonidine on cardiac vagal motoneurones, pressure lability, and cardiac baroreflex slope in rats

Toader

Cividjian

Quintin

2009

British Journal of Anaesthesia

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Effect of catecholamine depletion on increased blood pressure lability upon emergence from halothane anesthesia in rats: the role of sympathetic nervous activity in postanesthetic circulatory instability

Abstract: The postanesthetic increase in pressure lability seems largely a consequence of increased sympathetic activity, irrespective of any change in cardiac baroreflex sensitivity.

Cited by 6 publications

References 32 publications

High Sodium Intake Impairs Small Artery Vasoreactivity in vivo in Dahl Salt-Sensitive Rats

High Sodium Intake Impairs Small Artery Vasoreactivity in vivo in Dahl Salt-Sensitive Rats

Model-based causal closed-loop approach to the estimate of baroreflex sensitivity during propofol anesthesia in patients undergoing coronary artery bypass graft

Recruitment of cardiac parasympathetic activity: effects of clonidine on cardiac vagal motoneurones, pressure lability, and cardiac baroreflex slope in rats

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