Comparison of the role of endothelin, vasopressin and angiotensin in arterial pressure regulation during sevoflurane anaesthesia in dogs

Picker, O.; Schwarte, L. A.; Hj, Roth; Greve, Jens; Scheeren, Thomas

doi:10.1093/bja/aeh025

Cited by 13 publications

(7 citation statements)

References 27 publications

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“…We tested the effects of the ammonia stimulus on the nasal mucosa of rats whose brain stems had been transected after initial sedation with the volatile anesthetic isoflurane. While volatile anesthetics themselves also can affect cardiovascular reflex activity (29,62,64,82,105), they are quickly eliminated from the body (see Nagasaki et al, 2001). The median HRs seen after submersion in awake voluntary diving rats in the present study were similar to those seen in rats whose brain stems were transected (present study; Ref.…”

Section: Voluntary Diving Versus Voluntary Swimmingsupporting

confidence: 75%

The rat: a laboratory model for studies of the diving response

Panneton

Gan

Juric

2010

Journal of Applied Physiology

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Underwater submersion in mammals induces apnea, parasympathetically mediated bradycardia, and sympathetically mediated peripheral vasoconstriction. These effects are collectively termed the diving response, potentially the most powerful autonomic reflex known. Although these physiological responses are directed by neurons in the brain, study of neural control of the diving response has been hampered since 1) it is difficult to study the brains of animals while they are underwater, 2) feral marine mammals are usually large and have brains of variable size, and 3) there are but few references on the brains of naturally diving species. Similar responses are elicited in anesthetized rodents after stimulation of their nasal mucosa, but this nasopharyngeal reflex has not been compared directly with natural diving behavior in the rat. In the present study, we compared hemodynamic responses elicited in awake rats during volitional underwater submersion with those of rats swimming on the water's surface, rats involuntarily submerged, and rats either anesthetized or decerebrate and stimulated nasally with ammonia vapors. We show that the hemodynamic changes to voluntary diving in the rat are similar to those of naturally diving marine mammals. We also show that the responses of voluntary diving rats are 1) significantly different from those seen during swimming, 2) generally similar to those elicited in trained rats involuntarily "dunked" underwater, and 3) generally different from those seen from dunking naive rats underwater. Nasal stimulation of anesthetized rats differed most from the hemodynamic variables of rats trained to dive voluntarily. We propose that the rat trained to dive underwater is an excellent laboratory model to study neural control of the mammalian diving response, and also suggest that some investigations may be done with nasal stimulation of decerebrate preparations to decipher such control.

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Section: Voluntary Diving Versus Voluntary Swimmingsupporting

confidence: 75%

The rat: a laboratory model for studies of the diving response

Panneton

Gan

Juric

2010

Journal of Applied Physiology

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“…Vasopressin is increased during epidural anesthesia to maintain blood pressure (Picker et al 2001). Additionally, it is increased during anesthesia with high doses (3 MAC) of sevoflurane (Picker et al 2004). With regard to our results, the role of vasopressin and its receptor seems to be of minor importance under physiological conditions with low vasopressin plasma levels, but it is necessary, e.g.…”

Section: Interpretation Of the Resultssupporting

confidence: 49%

Vasopressin V1A receptors mediate the increase in gastric mucosal oxygenation during hypercapnia

Vollmer

Schwartges

Naber

et al. 2013

Journal of Endocrinology

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Hypercapnia (HC) improves systemic oxygen delivery (DO 2 ) and microvascular hemoglobin oxygenation of the mucosa (mHbO 2 ). Simultaneously, HC increases plasma levels of vasopressin. Although vasopressin is generally regarded a potent vasoconstrictor particularly in the splanchnic region, its effects on splanchnic microcirculation during HC is unclear. The aim of this study was to evaluate the role of endogenous vasopressin on gastric mucosal oxygenation and hemodynamic variables during physiological (normocapnia) and hypercapnic conditions. Five dogs were repeatedly anesthetized to study the effect of vasopressin V 1A receptor blockade ([Pmp 1 ,Tyr(Me) 2 ]-Arg 8 -Vasopressin, 35 mg/kg) on hemodynamic variables and mHbO 2 during normocapnia or HC (end-tidal CO 2 70 mmHg). In a control group, animals were subjected to HC alone. mHbO 2 was measured by reflectance spectrophotometry, systemic DO 2 was calculated from intermittent blood gas analysis, and cardiac output was measured by transpulmonary thermodilution. Data are presented as meanGS.E.M. for nZ5 animals. During HC alone, DO 2 increased from 12G1 to 16G1 ml/kg per min and mHbO 2 from 70G4 to 80G2%. By contrast, additional vasopressin V 1A receptor blockade abolished the increase in mHbO 2 (80G2 vs 69G2%) without altering the increase in DO 2 (16G1 vs 19G 2 ml/kg per min). Vasopressin V 1A receptor blockade (VB) during normocapnia neither affected DO 2 (13G1 vs 14G1 ml/kg per min) nor mHbO 2 (75G3 vs 71G5%). Vasopressin V 1A receptor blockade abolished the increase in mHbO 2 during HC independent of DO 2 . Thus, in contrast to its generally vasoconstrictive properties, the vasopressin V 1A receptors seem to mediate the increase in gastric microcirculatory mucosal oxygenation induced by acute HC.

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“…In the present study, the dogs were anesthetized with 1.5 MAC Sevoflurane. Sevoflurane is known to raise AVP plasma levels in a MAC-dependent manner [46]. The increased AVP plasma concentrations may overlay effects of ultra-low dose exogenous vasopressin administration.…”

Section: Discussionmentioning

confidence: 99%

Exogenous vasopressin dose-dependently modulates gastric microcirculatory oxygenation in dogs via V1A receptor

et al. 2019

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BackgroundHypercapnia improves gastric microcirculatory oxygenation (μHbO2) and increases vasopressin plasma levels, whereas V1A receptor blockade abolishes the increase of μHbO2. The aim of this study was to evaluate the effect of exogenous vasopressin (AVP) in increasing doses on microcirculatory perfusion and oxygenation and systemic hemodynamic variables. Furthermore, we evaluated the role of the vasopressin V1A receptor in mediating the effects.MethodsIn repetitive experiments, six anesthetized dogs received a selective vasopressin V1A receptor inhibitor ([Pmp1, Tyr (Me)2]-Arg8-Vasopressin) or sodium chloride (control groups). Thereafter, a continuous infusion of AVP was started with dose escalation every 30 min (0.001 ng/kg/min–1 ng/kg/min). Microcirculatory variables of the oral and gastric mucosa were measured with reflectance spectrometry, laser Doppler flowmetry, and incident dark field imaging. Transpulmonary thermodilution was used to measure systemic hemodynamic variables. AVP plasma concentrations were measured during baseline conditions and 30 min after each dose escalation.ResultsDuring control conditions, gastric μHbO2 did not change during the course of experiments. Infusion of 0.001 ng/kg/min and 0.01 ng/kg/min AVP increased gastric μHbO2 to 87 ± 4% and 87 ± 6%, respectively, compared to baseline values (80 ± 7%), whereas application of 1 ng/kg/min AVP strongly reduced gastric μHbO2 (59 ± 16%). V1A receptor blockade prior to AVP treatment abolished these effects on μHbO2. AVP dose-dependently enhanced systemic vascular resistance (SVR) and decreased cardiac output (CO). After prior V1A receptor blockade, SVR was reduced and CO increased (0.1 ng/kg/min + 1 ng/kg/min AVP).ConclusionsExogenous AVP dose-dependently modulates gastric μHbO2, with an increased μHbO2 with ultra-low dose AVP. The effects of AVP on μHbO2 are abolished by V1A receptor inhibition. These effects are independent of a modulation of systemic hemodynamic variables.

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Comparison of the role of endothelin, vasopressin and angiotensin in arterial pressure regulation during sevoflurane anaesthesia in dogs

Abstract: At 1 MAC, angiotensin attenuated the decrease in arterial pressure during sevoflurane anaesthesia more than endothelin and vasopressin. However, at higher MAC only vasopressin was specifically activated to partly compensate for the arterial pressure decrease.

Cited by 13 publications

References 27 publications

The rat: a laboratory model for studies of the diving response

The rat: a laboratory model for studies of the diving response

Vasopressin V1A receptors mediate the increase in gastric mucosal oxygenation during hypercapnia

Exogenous vasopressin dose-dependently modulates gastric microcirculatory oxygenation in dogs via V1A receptor

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