Effects of epinephrine and vasopressin in a piglet model of prolonged ventricular fibrillation and cardiopulmonary resuscitation*

Voelckel, Wolfgang G.; Lurie, Keith G.; McKnite, Scott; Zielinski, Todd; Lindstrom, Paul; Peterson, Colleen; Wenzel, Volker; Lindner, Karl H.; Benditt, David G.

doi:10.1097/00003246-200205000-00001

Cited by 71 publications

(21 citation statements)

References 20 publications

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“…These results are consistent with our observation that cardiac contractility is diminished in hearts of animals with HF and elevated plasma AVP. By contrast, AVP has been shown to improve survival in swine after experimental cardiac arrest, presumably due to enhanced myocardial blood flow secondary to enhanced peripheral vasoconstriction 49-53 . Unfortunately, AVP has not consistently proven beneficial in humans in large clinical trials of patients who have sustained cardiogenic shock 54-57 .…”

Section: Discussionmentioning

confidence: 96%

β-Adrenergic Receptor–Mediated Cardiac Contractility Is Inhibited via Vasopressin Type 1A-Receptor–Dependent Signaling

Tilley¹,

Zhu²,

Myers³

et al. 2014

Circulation

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Background Enhanced arginine vasopressin (AVP) levels are associated with increased mortality during end-stage human heart failure (HF), and cardiac AVP type 1A receptor (V1AR) expression becomes increased. Additionally, mice with cardiac-restricted V1AR overexpression develop cardiomyopathy and decreased β-adrenergic receptor (βAR) responsiveness. This led us to hypothesize that V1AR signaling regulated βAR responsiveness and in doing so contributes to HF development. Methods and Results Transaortic constriction resulted in decreased cardiac function and βAR density and increased cardiac V1AR expression, effects reversed by a V1AR-selective antagonist. Molecularly, V1AR stimulation led to decreased βAR ligand affinity, as well as βAR-induced Ca2+ mobilization and cAMP generation in isolated adult cardiomyocytes, effects recapitulated via ex vivo Langendorff analysis. V1AR-mediated regulation of βAR responsiveness was demonstrated to occur in a previously unrecognized Gq protein-independent/GRK-dependent manner. Conclusions This newly discovered relationship between cardiac V1AR and βAR may be informative for the treatment of patients with acute decompensated HF and elevated AVP.

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Section: Discussionmentioning

confidence: 96%

β-Adrenergic Receptor–Mediated Cardiac Contractility Is Inhibited via Vasopressin Type 1A-Receptor–Dependent Signaling

Tilley¹,

Zhu²,

Myers³

et al. 2014

Circulation

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“…They found that coronary perfusion pressure, left ventricular myocardial blood flow, and ROSC rates were higher in the 45 and 90 mcg/kg groups compared to the two lower dose groups. Further studies established that the combination of epinephrine and vasopressin was superior in the swine model of ventricular fibrillation, 41, 42 pulseless electrical activity, 43 asphyxial cardiac arrest 44–46 and recently in the swine model of bupivacaine-induced cardiac arrest. 9 …”

Section: Discussionmentioning

confidence: 99%

Lipid Emulsion Combined with Epinephrine and Vasopressin Does Not Improve Survival in a Swine Model of Bupivacaine-induced Cardiac Arrest

Hicks

Salcido²,

Logue³

et al. 2009

Anesthesiology

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Background We sought to evaluate the efficacy of lipid emulsion in reversing bupivacaine-induced cardiovascular collapse when added to a resuscitation protocol that included the use of epinephrine and vasopressin. Methods Following induction of general anesthesia and instrumentation, 19 mixed-breed domestic swine had cardiovascular collapse induced by an intravenous bolus of 10 mg/kg bupivacaine. After 5 minutes of resuscitation including chest compressions, epinephrine (100 μg/kg) and vasopressin (1.5 u/kg), animals were randomized to receive either a bolus of 20% lipid emulsion (4 mL/kg) followed by a continuous infusion (0.5 mL· kg−1 ·min−1) or an equal volume of saline. Investigators were blinded to the treatment assignment. The primary end-point was return of spontaneous circulation (mean arterial pressure of ≥ 60 mmHg for ≥ 1 minute). Results Treatment groups were similar with respect to baseline measurements of weight, sex, hemodynamic and metabolic variables. The rates of return of spontaneous circulation were similar between groups, 3 of 10, in the lipid group, and 4 of 9, in the saline group (P = 0.65). Total serum bupivacaine concentrations were higher in the lipid group at the 10-minute time point, (mean ± SEM: 23.13 ± 5.37 ng/mL versus 15.33 ± 4.04 ng/mL, P = 0.004). More norepinephrine was required in the lipid group compared to the saline group to maintain a mean arterial pressure > 60 mmHg during the 60 minute survival period (mean ± SEM: 738.6 ± 94.4 vs. 487.3 ± 171.0 μg). Conclusions In this swine model, lipid emulsion did not improve rates of return of spontaneous circulation after bupivacaine-induced cardiovascular collapse.

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“…The latter observation may relate to redistribution in blood flow or an indirect effect of vasopressin on cerebral blood flow, although these observations are speculative. In a pediatric (porcine) model of VF arrest, vasopressin, alone or in combination with HDE, significantly improved total cerebral blood flow during CPR (28). The authors speculate that improvements in brain perfusion may relate to vasopressin-mediated nitric oxide release and cerebral vasodilation.…”

Section: Impact Of Vasopressin On Myocardial Performancementioning

confidence: 93%

Vasopressin improves survival compared with epinephrine in a neonatal piglet model of asphyxial cardiac arrest

et al. 2014

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Background: Epinephrine is a component of all resuscitation algorithms. Vasopressin is a pulmonary vasodilator and systemic vasopressor. We investigated the effect of epinephrine vs. vasopressin on survival and hemodynamics after neonatal porcine cardiac arrest (CA). Methods: A 4-min asphyxial CA was induced, after which cardiopulmonary resuscitation (CPR) was commenced. Animals were randomized to low-(LDE: 0.01 mg/kg) or high-dose epinephrine (HDE: 0.03 mg/kg), low-(LDV: 0.2 U/kg) or high-dose vasopressin (HDV: 0.4 U/kg), or control (saline). Clinical and echocardiography indexes were monitored. results: Sixty-nine animals were randomized. Survival was greater in HDV (n = 8 (89%); P < 0.05 ANOVA) vs. control (n = 7 (43%)) and LDE (n = 5 (36%)) but not vs. HDE (n = 7 (64%)) or LDV (n = 6 (75%)). Animals resuscitated with LDE required more shocks (2.5 (interquartile range: 2-6); P < 0.05) and higher doses of energy (15 J (interquartile range: 10-20); P < 0.05). Left ventricular output was comparable between groups, but a greater increase in superior vena caval flow was seen after HDV (P < 0.001 vs. control, LDE, and HDE). Plasma troponin was greatest in the HDE group (P < 0.05 vs. control and HDV). conclusion: Vasopressin results in improved survival, lower postresuscitation troponin, and less hemodynamic compromise after CA in newborn piglets. Vasopressin may be a candidate for testing in human neonates. t he need for active neonatal resuscitation is common with an incidence of 5-10%, although there is likely to be regional variability (1). Guidelines for drug use in neonatal resuscitation guidelines are based on extrapolations from adult literature. Pressors, almost invariably epinephrine, are recommended as core therapy during cardiopulmonary resuscitation (CPR) in order to enhance systemic perfusion (especially cerebral and coronary perfusion) by maintaining vascular tone while forward flow is generated by chest compressions. Epinephrine, although an integral part of every published protocol for neonatal resuscitation, may be associated with adverse effects (2-6); similar concerns exist in pediatric and adult cardiac arrest (CA). However, because of concerns associated with epinephrine (2,7), vasopressin was studied in the setting of asystolic CA. Vasopressin is an intense systemic vasoconstrictor, which may explain why it increases cerebral (and systemic) perfusion during experimental cardiac massage, as well as increasing cerebral oxygenation, neurological outcome, and resuscitation success following experimental .Vasopressin was first proposed as a resuscitation agent after endogenous vasopressin levels were found to be higher in successfully resuscitated patients compared with those who died (13). Evidence from a large, adult, multicenter, randomized controlled trial suggests it to be superior to epinephrine, when the nature of the CA was primary asystole (14). For the following reasons, vasopressin may be a good candidate for pressor support during CPR. First, CA in neonates is almost always due to asphy...

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Effects of epinephrine and vasopressin in a piglet model of prolonged ventricular fibrillation and cardiopulmonary resuscitation*

Cited by 71 publications

References 20 publications

β-Adrenergic Receptor–Mediated Cardiac Contractility Is Inhibited via Vasopressin Type 1A-Receptor–Dependent Signaling

β-Adrenergic Receptor–Mediated Cardiac Contractility Is Inhibited via Vasopressin Type 1A-Receptor–Dependent Signaling

Lipid Emulsion Combined with Epinephrine and Vasopressin Does Not Improve Survival in a Swine Model of Bupivacaine-induced Cardiac Arrest

Vasopressin improves survival compared with epinephrine in a neonatal piglet model of asphyxial cardiac arrest

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