Sevoflurane Alters Right Ventricular Performance But Not Pulmonary Vascular Resistance in Acutely Instrumented Anesthetized Pigs

Kerbaul, François; Bellezza, M.; Mekkaoui, Choukri; Feier, Horéa; Guidon, C.; Gouvernet, Joanny; Rolland, Pierre H.; Gouin, F.; Mesana, Thierry G.; Collart, Frédéric

doi:10.1053/j.jvca.2005.05.017

Cited by 21 publications

(9 citation statements)

References 17 publications

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“…Previous studies reported that isoflurane, sevoflurane and desflurane decrease RV contractility in a dose-related manner[ 12 , 32 ]. Our study showed that sevoflurane produced dose-dependent slight decreases of RV contractility (Ees, PRSW, and dP/dt max -EDV) in normal and PAH rats.…”

Section: Discussionmentioning

confidence: 99%

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Rats with Chronic, Stable Pulmonary Hypertension Tolerate Low Dose Sevoflurane Inhalation as Well as Normal Rats Do

et al. 2016

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BackgroundThe effects of low concentration of sevoflurane on right ventricular (RV) function and intracellular calcium in the setting of pulmonary arterial hypertension (PAH) have not been investigated clearly. We aim to study these effects and associated signaling pathways in rats with PAH.MethodsHemodynamics were assessed with or without sevoflurane inhalation in established PAH rats. We analysis the classic RV function parameters and RV-PA coupling efficiency using steady-state PV loop recordings. The protein levels of SERCA2, PLB and p-PLB expression was analyzed by western blot to assess their relevance in PAH.ResultsRats with PAH presented with RV hypertrophy and increased pulmonary arterial pressure. The values of Ea, R/L ratio, ESP, SW, PRSW, +dP/dtmax and the slope of the dP/dtmax-EDV relationship increased significantly in PAH rats (P<0.05). Sevoflurane induced a concentration-dependent decrease of systemic and pulmonary blood pressure, HR, RV contractility, and increased the R/L ratio in both groups. Sevoflurane reduced the expression of SERCA2 and increased the expression of PLB in both groups. Interestingly, sevoflurane only reduced the p-PLB/PLB ratio in PAH rats, not in normal rats.ConclusionsRats with chronic, stable pulmonary hypertension tolerate low concentrations of sevoflurane inhalation as well as normal rats do. It may be related to the modulation of the SERCA2-PLB signaling pathway.

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Section: Discussionmentioning

confidence: 99%

“…However, sevoflurane can produce dose-dependent decreases of both pulmonary and systemic pressures. [ 12 , 13 ]. Little is known about the effects of sevoflurane on RV function in patients with PAH.…”

Section: Introductionmentioning

confidence: 99%

Rats with Chronic, Stable Pulmonary Hypertension Tolerate Low Dose Sevoflurane Inhalation as Well as Normal Rats Do

et al. 2016

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“…Inhaled anaesthetics such as isoflurane and desflurane have a marked dose-dependent effect in reducing right ventricular contractility and some negative impact on right ventricular afterload; hence, they significantly impair right ventricle pulmonary artery coupling [46,47]. Sevoflurane causes significant depression of global right ventricular function associated with a qualitatively different effect on inflow and outflow tracts, without any modification of pulmonary vascular resistance [48]. The use of nitrous oxide should be restricted because it increases pulmonary vascular resistance [49].…”

Section: Principles Of Anaesthetic Managementmentioning

confidence: 99%

“…During induction of general anaesthesia, there is a period of susceptibility until the airway is secured and ventilation controlled. An adequate depth of anaesthesia should be ensured before attempting laryngoscopy and tracheal intubation, as sympathetic stimulation has deleterious Table 7 Effect of anaesthetic agents on right ventricular (RV) contractility and pulmonary vascular resistance [46][47][48][49][50][51][52][53][54][55][56][57].…”

Section: Airway and Ventilationmentioning

confidence: 99%

Pulmonary hypertension and its management in patients undergoing non‐cardiac surgery

2014

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SummaryPulmonary hypertension is a complex disorder of the pulmonary vasculature that leads to increased peri-operative morbidity and mortality. Non-cardiac surgery constitutes a significant risk in patients with pulmonary hypertension. The management of right ventricular failure is inherently challenging and fraught with life-threatening consequences. A thorough understanding of the pathophysiology, the severity of the disease and its treatment modalities is required to deliver optimal peri-operative care. This review provides an evidence-based overview of the definition, classification, pathophysiology, diagnosis and treatment of pulmonary hypertension and focuses on the peri-operative management and treatment of pulmonary hypertensive crises in a non-cardiac setting.

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“…Opioid drugs, benzodiazepines and propofol used for premedication and induction of GA in this study do not affect pulmonary vascular reactivity, and are not considered a significant initiator for V/Q mismatch (Gibbs and Johnson, 1978 ; Benumof et al, 1987 ; Reves et al, 2010 ). Sevoflurane and other modern inhaled anesthetic on the other hand have a moderate inhibitory effect on HPV (Marshall et al, 1984 ; Wang et al, 1998 ; Kerbaul et al, 2006 ) and may even cause a reduction in J VA . Because sevoflurane in this study was delivered in O 2 , some degree of atelectasis would theoretically be expected (Sylvester et al, 2012 ).…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Circulation Transvascular Fluid Fluxes Do Not Change during General Anesthesia in Dogs

et al. 2018

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General anesthesia (GA) can cause abnormal lung fluid redistribution. Pulmonary circulation transvascular fluid fluxes (JVA) are attributed to changes in hydrostatic forces and erythrocyte volume (EV) regulation. Despite the very low hydraulic conductance of pulmonary microvasculature it is possible that GA may affect hydrostatic forces through changes in pulmonary vascular resistance (PVR), and EV through alteration of erythrocyte transmembrane ion fluxes (ionJVA). Furosemide (Fur) was also used because of its potential to affect pulmonary hydrostatic forces and ionJVA. A hypothesis was tested that JVA, with or without furosemide treatment, will not change with time during GA. Twenty dogs that underwent castration/ovariectomy were randomly assigned to Fur (n = 10) (4 mg/kg IV) or placebo treated group (Con, n = 10). Baseline arterial (BL) and mixed venous blood were sampled during GA just before treatment with Fur or placebo and then at 15, 30 and 45 min post-treatment. Cardiac output (Q) and pulmonary artery pressure (PAP) were measured. JVA and ionJVA were calculated from changes in plasma protein, hemoglobin, hematocrit, plasma and whole blood ions, and Q. Variables were analyzed using random intercept mixed model (P < 0.05). Data are expressed as means ± SE. Furosemide caused a significant volume depletion as evident from changes in plasma protein and hematocrit (P < 0.001). However; Q, PAP, and JVA were not affected by time or Fur, whereas erythrocyte fluid flux was affected by Fur (P = 0.03). Furosemide also affected erythrocyte transmembrane K+ and Cl−, and transvascular Cl− metabolism (P ≤ 0.05). No other erythrocyte transmembrane or transvascular ion fluxes were affected by time of GA or Fur. Our hypothesis was verified as JVA was not affected by GA or ion metabolism changes due to Fur treatment. Furosemide and 45 min of GA did not cause significant hydrostatic changes based on Q and PAP. Inhibition of Na+/K+/2Cl− cotransport caused by Fur treatment, which can alter EV regulation and JVA, was offset by the Jacobs Stewart cycle. The results of this study indicate that the Jacobs Stewart cycle/erythrocyte Cl− metabolism can also act as a safety factor for the stability of lung fluid redistribution preserving optimal diffusion distance across the blood gas barrier.

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Sevoflurane Alters Right Ventricular Performance But Not Pulmonary Vascular Resistance in Acutely Instrumented Anesthetized Pigs

Cited by 21 publications

References 17 publications

Rats with Chronic, Stable Pulmonary Hypertension Tolerate Low Dose Sevoflurane Inhalation as Well as Normal Rats Do

Rats with Chronic, Stable Pulmonary Hypertension Tolerate Low Dose Sevoflurane Inhalation as Well as Normal Rats Do

Pulmonary hypertension and its management in patients undergoing non‐cardiac surgery

Pulmonary Circulation Transvascular Fluid Fluxes Do Not Change during General Anesthesia in Dogs

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