Administration Of Vasopressin Research Articles

Effects of tibial and humerus intraosseous and intravenous vasopressin in porcine cardiac arrest model.

Compare maximum concentration (Cmax), time to maximum concentration (Tmax), mean serum concentration of vasopressin, return of spontaneous circulation (ROSC), time to ROSC, and odds of survival relative to vasopressin administration by tibial intraosseous (TIO), humerus intraosseous (HIO), and intravenous (IV) routes in a hypovolemic cardiac arrest model. Prospective, between subjects, randomized experimental design. TriService Research Facility. Yorkshire-cross swine (n = 40). Swine were anesthetized, exsanguinated to a Class III hemorrhage, and placed into cardiac arrest. After 2 minutes, cardiopulmonary resuscitation was initiated. After an additional 2 minutes, a dose of 40 units of vasopressin was administered by TIO, HIO, or the IV routes. Blood samples were collected over 4 minutes and analyzed by high-performance liquid chromatography tandem mass spectrometry. ROSC, time to ROSC, Cmax, Tmax, mean concentrations over time, and odds ratio. There was no significant difference in rate of ROSC or time to ROSC between the TIO, HIO, and IV groups (p > 0.05). The Cmax was significantly higher in the IV group compared to the TIO group (p = 0.015), but no significant difference between the TIO versus HIO or HIO versus IV groups (p > 0.05). The Tmax was significantly shorter for the HIO compared to the TIO group (p = 0.034), but no significant differences between the IV group compared to the TIO or HIO groups (p > 0.05). The odds of survival were higher in the HIO group compared to all other groups. The TIO and HIO provide rapid and reliable access to administer life-saving medications during cardiac arrest.

The effects of sternal and intravenous vasopressin administration on pharmacokinetics.

Purposes of this study were to compare intravenous (IV) and sternal intraosseous (SIO) administration of vasopressin relative to concentration maximum (Cmax), time to maximum concentration (Tmax), and mean concentration in a cardiac arrest model. Prospective, between subjects, randomized experimental design. Vivarium. Yorkshire-cross swine (N = 16) INTERVENTION: Swine were anesthetized, placed into cardiac arrest, and after 2 minutes, cardiopulmonary resuscitation was initiated. After additional 2 minutes, 40 units of vasopressin was administered either by SIO or IV route. Blood samples were collected over 4 minutes. Cmax and means were analyzed using high-performance liquid chromatography tandem mass spectrometry. Cmax, Tmax, and mean plasma concentrations. There were no significant differences in the SIO and IV groups in Cmax (p = 0.96) or Tmax (p = 0.27). The IV and SIO group had a mean Cmax of 68,151 ± SD 21,534 and 69,034 ± SD 40,169 pg/mL, respectively. The IV and SIO vasopressin groups had a mean Tmax of 105 ± SD 39 and 80 ± SD 41 seconds, respectively. A multivariate analyses of variance indicated that there were no statistically significant differences in pretest data, Cmax, and Tmax; a repeated analyses of variance indicated that there were no significant differences between the groups relative to mean concentrations of serum vasopressin over time (p > 0.05). When a patient is in cardiac arrest, it is essential to establish rapid and reliable access to blood vessels so that life-saving drugs can be administered and the SIO provides such a route.

Vasopressin as Therapy During Nonocclusive Mesenteric Ischemia

Vasopressin is used as an adjunct to norepinephrine to support blood pressure in vasodilatory shock after cardiopulmonary bypass (CPB). In this study, we report our observation of vasopressin treatment in 11 patients with nonocclusive mesenteric ischemia (NOMI). In an observational cohort study, 78 patients were studied after having been treated for NOMI with intraarterial iloprost infusion after elective cardiac operation. All patients received norepinephrine as vasopressor for marked vasodilation. In 11 patients mean arterial pressure could not be maintained with norepinephrine alone (≤0.4 μg · kg(-1) · min(-1)), and vasopressin was given in addition to norepinephrine as a rescue therapy. The 11 patients (Vaso) and the remaining 67 patients (Nor) were analyzed for clinical improvement after initiation of NOMI treatment, on the following days 1 and 2, and for hospital survival. Intestinal perfusion was controlled by mesenteric angiography. Before initiation of NOMI treatment Vaso patients had significantly higher doses of norepinephrine than the Nor patients (Vaso, 0.65 ± 0.20 μg · kg(-1) · min(-1); Nor, 0.20 ± 0.13 μg · kg(-1) · min(-1); p < 0.001), and their diagnostic score of the angiography was higher (Vaso, 5.4 ± 1.1 points; Nor, 3.5 ± 2.1 points; p= 0.004). After 2 days of NOMI treatment, Vaso patients had improved intestinal perfusion in the control angiography (Vaso, 3.8 ± 1.5 points) and significantly lower doses of norepinephrine than the Nor patients (Vaso, 0.28 ± 0.12 μg · kg(-1) · min(-1); Nor, 0.53 ± 0.34 μg · kg(-1) · min(-1); p= 0.002). All patients survived in the Vaso group; in the Nor group, 17 of 67 patients died in the hospital. Vasopressin administration during NOMI treatment after CPB seems to improve small intestine perfusion and appears be to associated with improved hospital survival.

Temporal trends in the utilization of vasopressors in intensive care units: an epidemiologic study

BackgroundThe choice of vasopressor use in the intensive care unit (ICU) depends primarily on provider preference. This study aims to describe the rate of vasopressor utilization and the trends of each vasoactive agent usage in the ICU over the span of 7 years in a tertiary referral center.MethodsAll adult ICU admissions, including medical, cardiac, and surgical ICUs from January 1st, 2007 through December 31st, 2013 were included in this study. Vasopressor use was defined as the continuous intravenous administration of epinephrine, norepinephrine, phenylephrine, dopamine, or vasopressin within a given ICU day. The vasopressor utilization index (VUI) was defined as the proportion of ICU days on each vasoactive agent divided by the total ICU days with vasopressor usage.ResultsDuring the study period, 72,005 ICU admissions and 272,271 ICU days were screened. Vasopressors were used in 19,575 ICU admissions (27 %) and 59,811 ICU days (22 %). Vasopressin was used in 24,496 (41 %), epinephrine in 23,229 (39 %), norepinephrine in 20,648 (34 %), dopamine in 9449 (16 %), and phenylephrine in 7508 (13 %) ICU days. The VUInorepinephrine increased from 0.24 in 2007 to 0.46 in 2013 and VUIphenylephrine decreased from 0.20 in 2007 to 0.08 in 2013 (p < 0.001 both). For epinephrine, dopamine, and vasopressin VUI did not change over the course of study.ConclusionVasopressors were used in about one fourth of ICU admissions and about one-fifth of ICU days. Although vasopressin is the most commonly used vasopressor, the use of norepinephrine found to have an increasing trajectory.Electronic supplementary materialThe online version of this article (doi:10.1186/s40360-016-0063-z) contains supplementary material, which is available to authorized users.

Intraoperative anaphylaxis to latex possibly facilitated by the administration of oxytocin and vasopressin

Intraoperative anaphylaxis to latex possibly facilitated by the administration of oxytocin and vasopressin

Risk Factors Involved in Central-to-Radial Arterial Pressure Gradient During Cardiac Surgery.

A central-to-radial arterial pressure gradient may occur after cardiopulmonary bypass (CPB), which, in some patients, may last for a prolonged time after CPB. Whenever there is a pressure gradient, the radial artery pressure measure may underestimate a more centrally measured systemic pressure, which may result in a misguided therapeutic strategy. It is clinically important to identify the risk factors that may predict the appearance of a central-to-radial pressure gradient, because more central sites of measurements might then be considered to monitor systemic arterial pressure in high-risk patients. The objective of this study was to assess preoperative and intraoperative risk factors for central-to-radial pressure gradient. Seventy-three patients undergoing cardiac surgery using CPB were included in this prospective observational study. A significant central-to-radial arterial pressure gradient was defined as a difference of 25 mm Hg in systolic pressure or 10 mm Hg in mean arterial pressure for a minimum of 5 minutes. Preoperative data included demographics, presence of comorbidities, and medications. Intraoperative data included type of surgery, CPB and aortic clamping time, use of inotropic drugs, and vasodilators or vasopressors agents. The diameter of the radial and femoral artery was measured before the induction of anesthesia using B-mode ultrasonography. Thirty-three patients developed a central-to-radial arterial pressure gradient (45%). Patients with a significant pressure gradient had a smaller weight (71.0 ± 16.9 vs 79.3 ± 17.3 kg, P = 0.041), a smaller height (162.0 ± 9.6 vs 166.3 ± 8.6 cm, P = 0.047), a smaller radial artery diameter (0.24 ± 0.03 vs 0.29 ± 0.05 cm, P < 0.001), and were at a higher risk as determined by the Parsonnet score (30.3 ± 24.9 vs 17.0 ± 10.9, P = 0.007). In addition, a longer aortic clamping time (85.8 ± 51.0 vs 64.2 ± 29.3 minutes, P = 0.036), mitral and complex surgery (P = 0.007 and P = 0.017, respectively), and administration of vasopressin (P = 0.039) were identified as potential independent predictors of a central-to-radial pressure gradient. By using multivariate logistic regression analysis, the following independent risk factors were identified: Parsonnet score (odds ratio [OR], 1.076; 95% confidence interval [CI], 1.027-1.127, P = 0.002), aortic clamping time >90 minutes (OR, 8.521; 95% CI, 1.917-37.870, P = 0.005), and patient height (OR, 0.933, 95% CI, 0.876-0.993, P = 0.029). The relative risk (RR) estimates remained statistically significant for the Parsonnet score and the aortic clamping time ≥90 minutes (RR, 1.010; 95% CI, 1.003-1.018, P = 0.009 and RR, 2.253; 95% CI, 1.475-3.443, P < 0.001 respectively) while showing a trend for patient height (RR, 0.974; 95% CI, 0.948-1.001, P = 0.058). Central-to-radial gradients are common in cardiac surgery. The threshold for using a central site for blood pressure monitoring should be low in small, high-risk patients undergoing longer surgical interventions to avoid inappropriate administration of vasopressors and/or inotropic agents.

Vasopressin increases human risky cooperative behavior

The history of humankind is an epic of cooperation, which is ubiquitous across societies and increasing in scale. Much human cooperation occurs where it is risky to cooperate for mutual benefit because successful cooperation depends on a sufficient level of cooperation by others. Here we show that arginine vasopressin (AVP), a neuropeptide that mediates complex mammalian social behaviors such as pair bonding, social recognition and aggression causally increases humans' willingness to engage in risky, mutually beneficial cooperation. In two double-blind experiments, male participants received either AVP or placebo intranasally and made decisions with financial consequences in the "Stag hunt" cooperation game. AVP increases humans' willingness to cooperate. That increase is not due to an increase in the general willingness to bear risks or to altruistically help others. Using functional brain imaging, we show that, when subjects make the risky Stag choice, AVP down-regulates the BOLD signal in the left dorsolateral prefrontal cortex (dlPFC), a risk-integration region, and increases the left dlPFC functional connectivity with the ventral pallidum, an AVP receptor-rich region previously associated with AVP-mediated social reward processing in mammals. These findings show a previously unidentified causal role for AVP in social approach behavior in humans, as established by animal research.

Does vasopressin improve the mortality of septic shock patients treated with high-dose NA.

Aim of Study:In Surviving Sepsis Campaign Guidelines 2012, noradrenalin (NA) is recommended as a first choice vasopressor. Although vasopressin (VP) is recommended for the treatment of NA-resistant septic shock, the optimal parameters for its administration remain unclear.Materials and Methods:We conducted a retrospective study to evaluate the clinical outcomes of the administration of VP to adult septic shock patients who were undergoing high-dose NA (≥0.25 μg/kg/min) therapy in our Intensive Care Unit between January 2010 and December 2013. We defined high-dose NA as a dose of >0.25 μg/kg/min, based on the definition of low-dose NA as a dose of 5–14 μg/min because the average body weight of the patients in this study was 53.0 kg.Results:Among 29 patients who required the administration of high-dose NA, 18 patients received VP. Although the patient background physiological conditions and NA dose did not differ between the two groups, the survival rate of the VP-treated patients was significantly lower (33%) than that of the patients who were managed with a high-dose of NA-alone (82%) (P = 0.014). The lactate clearance did not change after the administration of VP, whereas it improved when in NA treatment alone.Conclusion:The results suggest that the administration of VP did not improve the mortality among septic shock patients when administered in addition to high-dose NA.

Assessment of the Anti-anginal Effect of Tetramethylpyrazine Using Vasopressin-Induced Angina Model Rats.

Intravenous tetramethylpyrazine has been widely used in China as a complementary and/or alternative medicine to treat patients with ischemic heart disease. We assessed the anti-anginal effect of tetramethylpyrazine (10 mg/kg, intravenously (i.v.), n=6) in comparison with that of its vehicle, saline (1 mL/kg, i.v., n=6), using vasopressin-induced angina model rats. First, Donryu rats were anesthetized with pentobarbital sodium (60 mg/kg, intraperitoneally (i.p.)), and the surface lead I electrocardiogram was continuously monitored. Administration of vasopressin (0.5 IU/kg, i.v.) to the rats depressed the S-wave level of the electrocardiogram, indicating the onset of subendocardial ischemia. However, pretreatment with tetramethylpyrazine suppressed the vasopressin-induced depression of the S-wave level, which was not observed following pretreatment with its vehicle alone (saline), suggesting that tetramethylpyrazine ameliorated the vasopressin-induced subendocardial ischemia in vivo. These results may provide experimental evidence for the empirically known clinical efficacy of tetramethylpyrazine against ischemic heart disease, and could provide clues to better understanding its in vivo mechanism of action.

The feasibility of vasopressin administration via laryngeal mask airway using a porcine model

Background. In pre-hospital situations, delay in resuscitation might carry extra risks for patients, so resuscitative measures should be rapid, easy-to use, and effective. A laryngeal mask airway (LMA) is a quickly placed supraglottic airway that may be used as a route for drug administration. Vasopressin is a vasopressor and might be absorbed well via the mucosa of the airways and alveoli. We conducted this animal study to verify the feasibility of administering vasopressin via a LMA.Methods. Twenty-four Yorkshire pigs were anesthetized and randomly divided into four groups. The pigs in Groups Placebo and tracheal tube (TT) were intubated with a cuffed tracheal tube, and those in Groups LMA and laryngeal mask airway and a catheter (LMAC) underwent a size 4 LMA insertion. In the LMAC group, an aerosolized catheter was placed into the trachea through a LMA to deliver the drug. All pigs were able to breathe spontaneously without the assistance of a ventilator. The placebo group received 5 ml of distilled water via a tracheal tube. The other groups received 1 U/kg vasopressin, which was diluted to a total volume of 5 ml with distilled water via the varied routes. The heart rates and arterial pressures were recorded before and after drug administration.Results. The mean arterial pressure (MAP) and diastolic arterial pressure (DAP) increased significantly and maintained a plateau from 3 to 7 min in Group TT and 2 to 29 min in Group LMAC. Group LMA and Group Placebo demonstrated only one occasional elevation in MAP and no changes in DAP. Furthermore, the heart rate decreased significantly from 2 to 29 min in Group LMAC.Conclusions. In this porcine model, vasopressin administered via an aerosolized catheter and ventilated with a LMA demonstrated a positive and prolonged pressor effect. The results suggest that an aerosolized catheter placed through a LMA, may be a practical alternative route for vasopressin administration, and that the effective duration of vasopressin is long enough to cover the period of pre-hospital management.

Assessment of Blood Loss in Abdominal Myomectomy by Intramyometrial Vasopressin Administration Versus Conventional Tourniquet Application.

Myomectomy is an invasive surgical procedure. It can be associated with intraoperative and postoperative complications like excessive haemorrhage. There are various methods to control haemorrhage like pharmacological and as well as mechanical methods. This study was taken to compare intraoperative blood loss following abdominal myomectomy after receiving intramyometrial vasopressin or tourniquet application and to estimate postoperative reduction in haemoglobin & haematocrit values. The study was a randomised single blinded parallel group study. Total 48 patients were included in this study according to inclusion and exclusion criteria. All patients were divided into two groups i.e. 'T' and 'V' group, 24 in each group. 'T' group received conventional tourniquet application and 'V' group received intramyometrial vasopressin administration. The analyses in this study were both sided and p<0.05 was considered significant statistically. The Software used were Statistica version 6 (Tulsa, Oklahoma: Stat Soft Inc., 2001) and Graph Pad Prism version 5 (San Diego, California: Graph Pad Software Inc., 2007). The blood loss in the tourniquet group was significantly higher (p=<0.001). Postoperative haemoglobin and haematocrit were lower in tourniquet group than vasopressin group. There was significant fall in haemoglobin and haematocrit in postoperative period in both group (p=<0.001) but it was more in tourniquet group. Total five patients (three in tourniquet group and two in vasopressin group) had received one unit whole blood transfusion. Intramyometrial vasopressin injection during myomectomy operation more effectively decreases the blood loss, need for blood transfusion and it causes less reduction in haemoglobin and haematocrit. Thereby it seems to be an effective method without having any risk of ischemic damage to the uterus.

Vasopressin After the Fontan Operation.

Prolonged pleural effusion following Fontan operation is common and increases morbidity and hospital length of stay. Vasopressin (VP), a neurohypophysial hormone, has numerous effects on the cardiovascular system. The most notable is increased peripheral vascular resistance, but it may also reduce capillary leakage by tightening endothelial intercellular junctions and reducing capillary hydrostatic pressure We reviewed our experience with the perioperative administration of VP following Fontan operation. We retrospectively reviewed the records of 62 consecutive patients who underwent Fontan operation from January 2004 to June 2014. In January 2010, VP was introduced as part of the standard perioperative management of patients undergoing Fontan operation at our center. For this retrospective observational study, patients were grouped according to the use (VP; N = 40) or nonuse (non-VP; N = 22) of VP (0.3-0.5 mU/kg/min) in the perioperative period. The primary end point analyzed was chest tube output. Secondary end points analyzed included fluid balance and length of hospital stay, with groups compared using Mann-Whitney U test. There was no hospital mortality. Median total chest tube output was 22 mL/kg in the VP group and 68 mL/kg in the non-VP group (P < .001). The median total duration of chest tube indwelling time was five days in the VP group and was 11 days in the non-VP group (P < .001). Median fluid balance on first postoperative day was 13 and 38 mL/kg, respectively (P < .001). Median hospital stay for VP and non-VP groups was 9 and 16 days, respectively (P = .002). The more recent group of patients undergoing Fontan operations, all of whom received VP perioperatively, had less chest tube output and shorter duration of chest tube drainage after the Fontan operation relative to the earlier patient group whose perioperative management did not include VP. They also experienced less positive fluid balance in the early postoperative period and shorter hospital length of stay than the patients from the earlier era.

Effect of vasopressin on Na+–K+–2Cl− cotransporter (NKCC) and the signaling mechanisms on the murine late distal colon

It has been demonstrated that the antidiuretic hormone vasopressin is able to regulate the expression of Na–K–Cl cotransporters (NKCC1 and NKCC2) in the kidney. The present study investigated the effects of long- and short-term administration of vasopressin on NKCC and the possible signaling mechanism of vasopressin in the mouse distal colon using the siRNA, real-time PCR, western blotting and Ussing chambers method. The results showed the presence of NKCC2 expression in the colon, which was verified with a siRNA technique. The mRNA and protein expression level of NKCC2 significantly increased by about 40% and 90% respectively in response to restricting water intake to 1ml/day/20g for 7 days. In contrast, the NKCC1 expression level was unchanged in the colon. To determine the short-term activation of NKCC2 by vasopressin in vitro, we found that the administration of vasopressin caused a 3-fold increase in mouse colon NKCC2 phosphorylation, which was detected with phosphospecific antibody R5. In addition, the Ussing chamber results showed that NKCC2, cAMP and Ca2+ signaling pathway may be involved in the vasopressin-induced response. Further, adenylate cyclase inhibitor MDL-12330A and PKA inhibitor H89 and Ca2+ chelator BAPTA-AM reversed the vasopressin induced NKCC2 phosphorylation level increase by about 35%, 28% and 42% respectively suggesting vasopressin stimulate NKCC2 phosphorylation increase mediated by cAMP-PKA and Ca2+ signaling in the colon. Collectively, these data suggest that the expression and phosphorylation of NKCC2 are increased in the colon by vasopressin stimulation, in association with enhanced activity of the vasopressin/cAMP and Ca2+ pathways.

Effects of tibial intraosseous and IV administration of vasopressin on kinetics and survivability in cardiac arrest

PurposePurposes of this study were to compare tibial intraosseous (TIO) and intravenous (IV) administration of vasopressin relative to return of spontaneous circulation (ROSC) and time to ROSC in an adult swine cardiac arrest model. In addition, the purposes were to compare the concentration maximum (Cmax), time to maximum concentration (Tmax), and odds of ROSC. MethodsThis was a between-subjects, prospective experimental study. Yorkshire swine (N = 21) were randomly assigned to 1 of 3 groups: TIO, IV, or control groups. The swine were anesthetized and instrumented, and then cardiac arrest was induced and sustained for 2 minutes. Cardiopulmonary resuscitation was initiated and continued for 2 minutes. Vasopressin was then administered via the TIO or IV route. Blood samples were collected for 4 minutes to determine the Cmax and Tmax of vasopressin. Concentration maximum and Tmax were calculated by use of liquid chromatography with mass spectrometry. ResultsThere was no difference in ROSC between the TIO and IV groups (P = .63). The Cmax of vasopressin was significantly higher in the IV group compared to the TIO group (P = .017). However, there was no significant difference in ROSC, time to ROSC, or Tmax between groups (P > .05). All subjects had ROSC in both the IV and TIO groups, and none had ROSC in the control group. There was 225 times greater chance of survival for both the IV and TIO groups compared to the control group. ConclusionThe data support that the TIO is an effective route for vasopressin in a cardiac arrest model.

The role of hormone replacement therapy in the intensive care management of deceased organ donors: a primer for nurses.

Donation after brain death remains the primary contributor to the supply of organs available for transplantation in the United States. After brain death, both a surge of catecholamines and a dysregulation of the neurohormonal axis may result in hypotension, decreased organ perfusion, and reduced viability of organs to be transplanted. Hormone replacement therapy is widely used to maintain organ perfusion and has been shown to increase the number of organs procured. This article reviews the literature and mechanisms supporting the use of hormone replacement therapy in brain-dead organ donors and provides clinicians with information regarding the administration, monitoring, and preparation of thyroid hormone, arginine vasopressin, and corticosteroids.

Resuscitation Using Liposomal Vasopressin in an Animal Model of Uncontrolled Hemorrhagic Shock.

BackgroundCurrent research suggests that administration of vasopressin to patients with uncontrolled hemorrhagic shock (UHS) can avoid the detrimental effects associated with aggressive fluid resuscitation. However, vasopressin has a short half-life of 10~35 minutes in in vivo use and precludes its use in the pre-hospital setting. To increase the half-life of vasopressin, we proposed to synthesize liposome-encapsulated vasopressin and test it in a rat model of UHS.MethodsThe film hydration method was used to prepare liposomal vasopressin consisting of: Dipalmitoylphosphatidylcholine, cholesterol, and dipalmitoyl phosphatidylethanolamine (20:20:1 mole ratio). 42 rats were subjected to UHS and randomly received 5 different treatments (vasopressin, liposomal vasopressin, lactate ringer (LR), liposome only and sham). Outcome of UHS were measured using 4 common prognostic tests: mean arterial pressure (MAP), serum lactate level, inflammatory profile and pulmonary edema.ResultsThe dynamic light scattering results confirmed that we had prepared a successful liposomal vasopressin complex. Comparing the serum vasopressin concentration of liposomal vasopressin and vasopressin treated animals by ELISA, we found that the concentration of vasopressin for the liposomal vasopressin treated group is higher at 60 minutes. However, there was no significant difference between the MAP profile of rats treated with vasopressin and liposomal vasopressin in UHS. We also observed that animals treated with liposomal vasopressin performed indifferently to vasopressin treated rats in serum lactate level, inflammatory profile and edema profile. For most of our assays, the liposome only control behaves similarly to LR resuscitation in UHS rats.ConclusionWe have synthesized a liposomal vasopressin complex that can prolong the serum concentration of vasopressin in a rat model of UHS. Although UHS rats treated with either liposomal vasopressin or vasopressin showed no statistical differences, it would be worthwhile to repeat the experiments with different liposomal compositions.

Intraoperative administration of vasopressin during coronary artery bypass surgery is associated with acute postoperative kidney injury

BackgroundSevere vasodilatation is commonly seen upon weaning from cardiopulmonary bypass (CPB). We examined the effects of vasopressin (arginine vasopressin [AVP]) on acute kidney injury (AKI) in postoperative period. MethodsThe records of 483 patients undergoing coronary bypass surgery on CPB from 2004 to 2008 were retrospectively reviewed. Demographic, anthropometric, comorbid condition, and perioperative clinical/laboratory data were collected along with postoperative complications. Patients were grouped based on the perioperative use of AVP, and AKI was used as the primary end point. Univariate and multivariate logistic regression analyses were used, followed by propensity score matching for AKI. Null hypothesis was rejected at P < .05. ResultsPostoperative AKI occurred in 14.5% of patients. Arginine vasopressin was administered to 280 patients during the perioperative period. The prevalence of AKI in AVP was 20%, whereas it was 6.1% in controls (P < .0001). Arginine vasopressin was an independent factor that predicted the occurrence of AKI (odds ratio, 3.60; 95% confidence interval, 1.22-10.62; P = .02). However, after propensity score matching, the association between AKI and AVP was lost (P = .073). ConclusionAcute kidney injury is a common complication after cardiac surgery, and vasopressin use increases its incidence; however, this effect may rely on several clinical factors, and its true effect should be examined by large randomized trials.

Vasopressin induces endolymphatic hydrops in mouse inner ear, as evaluated with repeated 9.4 T MRI

From histopathological specimens, endolymphatic hydrops has been demonstrated in association with inner ear disorders. Recent studies have observed findings suggestive of hydrops using MRI in humans. Previous studies suggest that vasopressin may play a critical role in endolymph homeostasis and may be involved in the development of Ménière's disease. In this study we evaluate the effect of vasopressin administration in vivo in longitudinal studies using two mouse strains. High resolution MRI at 9.4 T in combination with intraperitoneally delivered Gadolinium contrast, was performed before and after chronic subcutaneous administration of vasopressin via mini-osmotic pumps in the same mouse. A development of endolymphatic hydrops over time could be demonstrated in C57BL6 mice (5 mice, 2 and 4 weeks of administration) as well as in CBA/J mice (4 mice, 2 weeks of administration; 6 mice, 3 and 4 weeks of administration). In most C57BL6 mice hydrops developed first after more than 2 weeks while CBA/J mice had an earlier response. These results may suggest an in vivo model for studying endolymphatic hydrops and corroborates the future use of MRI as a tool in the diagnosis and treatment of inner ear diseases, such as Ménière's disease. MRI may also be developed as a critical tool in evaluating inner ear homeostasis in genetically modified mice, to augment the understanding of human disease.This article is part of a Special Issue entitled <IEB Kyoto>.

Vasopressin decreases pulmonary-to-systemic vascular resistance ratio in a porcine model of severe hemorrhagic shock.

Vasopressors are gaining renewed interest as treatment adjuncts in hemorrhagic shock. The ideal vasoconstrictor will increase systemic blood pressure without increasing pulmonary vascular resistance (PVR), which hinders pulmonary perfusion and exacerbates hypoxemia. However, the selectivity of pressors for pulmonary versus systemic vasoconstriction during hemorrhage has not been characterized. The purpose of this study was to test the hypothesis that vasopressin (VP) has distinct effects on pulmonary versus systemic hemodynamics, unlike the catecholamine vasopressors norepinephrine (NE) and phenylephrine (PE). Anesthetized and ventilated pigs were assigned to resuscitation with saline only (n = 7) or saline with VP (n = 6), NE (n = 6), or PE (n = 6). Animals were hemorrhaged to a target volume of 30 mL/kg and a mean arterial pressure of 35 mmHg. One hour after the start of hemorrhage, animals were resuscitated with saline up to one shed blood volume, followed by either additional saline or a vasopressor. Hemodynamics and oxygenation were measured hourly for 4 h after the start of hemorrhage. Vasopressin increased systemic vascular resistance (SVR) while sparing the pulmonary vasculature, leading to a 45% decrease in the PVR/SVR ratio compared with treatment with PE. Conversely, NE induced pulmonary hypertension and led to an increased PVR/SVR ratio associated with decreased oxygen saturation. Phenylephrine and crystalloid had no significant effect on the PVR/SVR ratio. Sparing of pulmonary vasoconstriction occurs only with VP, not with administration of crystalloid or catecholamine pressors. The ability of VP to maintain blood oxygenation indicates that VP may prevent hypoxemia in the management of hemorrhagic shock.

Improved neurologic outcomes after cardiac arrest with combined administration of vasopressin, steroids, and epinephrine compared to epinephrine alone.

Is a vasopressin, steroid, and epinephrine (VSE) protocol for in-hospital cardiac arrest resuscitation associated with better survival to hospital discharge with favourable neurologic outcome compared to epinephrine alone? Article chosen Mentzelopoulos S, Malachias S, Konstantopoulos D, et al. Vasopressin, steroids, and epinephrine and neurologically favorable survival after in-hospital cardiac arrest: a randomized clinical trial. JAMA 2013;310:270-9. To determine if a VSE protocol during cardiopulmonary resuscitation with hydrocortisone administration in patients with postresuscitative shock at 4 hours after return of spontaneous circulation would improve survival to hospital discharge with favourable neurologic outcome.