Arginine vasopressin during sinus rhythm: effects on haemodynamic variables, left anterior descending coronary artery cross sectional area and cardiac index, before and after inhibition of NO-synthase, in pigs.

UNLABELLED: We have shown previously that arginine vasopressin (AVP) given during sinus rhythm increases mean arterial blood pressure (MAP) and left anterior descending (LAD) coronary artery cross sectional area. AVP was assumed to result in vasodilatation via activation of the endothelial nitric oxide system. The purpose of the present study was to assess the effects of AVP before and after NO-inhibition. Nine domestic pigs were instrumented for measurement of haemodynamic variables using micromanometer-tipped catheters, and measurement of LAD coronary artery cross sectional area employing intravascular ultrasound (IVUS). Haemodynamic variables, LAD coronary artery cross sectional area and cardiac output were measured at baseline, 90 s and 5, 15, and 30 min after AVP (0.4 U kg (-1) IV) before and after blockade of nitric oxide synthase with N(G)-nitro L-arginine methyl ester (L-NAME). Compared with baseline, AVP significantly increased MAP after 90 s (89+/-4 versus 160+/-5 mm Hg), increased LAD coronary artery cross sectional area (11.3+/-1 versus 11.8+/-1 mm(2)) and decreased cardiac index (138+/-6 versus 53+/-6 mL/min kg(-1)). After blockade of nitric oxide synthase, AVP significantly increased MAP after 90 s (135+/-4 versus 151+/-3 mm Hg), increased LAD coronary artery cross sectional area (8.7+/-1 versus 8.9+/-1 mm(2)), and significantly decreased cardiac index (95+/-6 versus 29+/-4 mL/min kg (-1)). IMPLICATIONS: During sinus rhythm, AVP increased MAP and LAD coronary artery cross sectional area, but decreased cardiac index.

Vasopressin improves survival in a porcine model of abdominal vascular injury.

INTRODUCTION: We sought to determine and compare the effects of vasopressin, fluid resuscitation and saline placebo on haemodynamic variables and short-term survival in an abdominal vascular injury model with uncontrolled haemorrhagic shock in pigs. METHODS: During general anaesthesia, a midline laparotomy was performed on 19 domestic pigs, followed by an incision (width about 5 cm and depth 0.5 cm) across the mesenterial shaft. When mean arterial blood pressure was below 20 mmHg, and heart rate had declined progressively, experimental therapy was initiated. At that point, animals were randomly assigned to receive vasopressin (0.4 U/kg; n = 7), fluid resuscitation (25 ml/kg lactated Ringer's and 25 ml/kg 3% gelatine solution; n = 7), or a single injection of saline placebo (n = 5). Vasopressin-treated animals were then given a continuous infusion of 0.08 U/kg per min vasopressin, whereas the remaining two groups received saline placebo at an equal rate of infusion. After 30 min of experimental therapy bleeding was controlled by surgical intervention, and further fluid resuscitation was performed. Thereafter, the animals were observed for an additional hour. RESULTS: After 68 +/- 19 min (mean +/- standard deviation) of uncontrolled bleeding, experimental therapy was initiated; at that time total blood loss and mean arterial blood pressure were similar between groups (not significant). Mean arterial blood pressure increased in both vasopressin-treated and fluid-resuscitated animals from about 15 mmHg to about 55 mmHg within 5 min, but afterward it decreased more rapidly in the fluid resuscitation group; mean arterial blood pressure in the placebo group never increased. Seven out of seven vasopressin-treated animals survived, whereas six out of seven fluid-resuscitated and five out of five placebo pigs died before surgical intervention was initiated (P < 0.0001). CONCLUSION: Vasopressin, but not fluid resuscitation or saline placebo, ensured short-term survival in this vascular injury model with uncontrolled haemorrhagic shock in sedated pigs.

An observational study of vasopressin infusion during uncontrolled haemorrhagic shock in a porcine trauma model: Effects on bowel function.

The effects of vasopressin on the gut in a porcine uncontrolled haemorrhagic shock model are described. In eight anaesthetised pigs, a liver laceration was performed; when haemorrhagic shock was decompensated, all animals received 0.4 IU/kg vasopressin, followed by 0.08 IU/kg min over 30 min, which maintained a mean arterial blood pressure >40 mmHg. Subsequent surgical intervention, infusion of whole blood and fluids resulted in a stable cardiocirculatory status. Three hours after stabilisation, all pigs developed non-bloody diarrhoea which converted into normal bowel movements within 24 h. All histological samples retained 7 days after the experiment revealed no histopathological changes. In conclusion, in this small observational study of uncontrolled porcine haemorrhagic shock, a resuscitation strategy that included high dose vasopressin was associated with transient diarrhoea and good long term survival.

Effects of face mask ventilation in apneic patients with a resuscitation ventilator in comparison with a bag-valve-mask.

Bag-valve-mask ventilation in an unprotected airway is often applied with a high flow rate or a short inflation time and, therefore, a high peak airway pressure, which may increase the risk of stomach inflation and subsequent pulmonary aspiration. Strategies to provide more patient safety may be a reduction in inspiratory flow and, therefore, peak airway pressure. The purpose of this study was to evaluate the effects of bag-valve-mask ventilation vs. a resuscitation ventilator on tidal volume, peak airway pressure, and peak inspiratory flow rate in apneic patients. In a crossover design, 40 adults were ventilated during induction of anesthesia with either a bag-valve-mask device with room air, or an oxygen-powered, flow-limited resuscitation ventilator. The study endpoints of expired tidal volume, minute volume, respiratory rate, peak airway pressure, delta airway pressure, peak inspiratory flow rate and inspiratory time fraction were measured using a pulmonary monitor. When compared with the resuscitation ventilator, the bag-valve-mask resulted in significantly higher (mean+/-SD) peak airway pressure (15.3+/-3 vs. 14.1+/-3 cm H2O, respectively; p=0.001) and delta airway pressure (14+/-3 vs. 12+/-3 cm H2O, respectively; p<0.001), but significantly lower oxygen saturation (95+/-3 vs. 98+/-1%, respectively; p<0.001). No patient in either group had clinically detectable stomach inflation. We conclude that the resuscitation ventilator is at least as effective as traditional bag-valve-mask or face mask resuscitation in this population of very controlled elective surgery patients.

Effects of decreasing peak flow rate on stomach inflation during bag-valve-mask ventilation.

Reducing inspiratory flow rate and peak airway pressure may be important in order to minimise the risk of stomach inflation when ventilating an unprotected airway with positive pressure ventilation. This study was designed to yield enough power to determine whether employing an inspiratory gas flow limiting bag-valve device (SMART BAG, O-Two Medical Technologies Inc., Ontario, Canada) would also decrease the likelihood of stomach inflation in an established bench model of a simulated unintubated respiratory arrest patient. The bench model consists of a training lung (lung compliance, 50 ml/cm H2O; airway resistance, 4 cm H2O/l/s) and a valve simulating lower oesophageal sphincter opening at a pressure of 19 cm H(2)O. One hundred and ninety-one emergency medicine physicians were requested to ventilate the manikin utilising a standard single-person technique for 1 min (respiratory rate, 12/min; Vt, 500 ml) with both a standard adult bag-valve-mask and the SMART BAG. The volunteers were blinded to the experimental design of the model until completion of the experimental protocol. The SMART BAG versus standard bag-valve-mask resulted in significantly (P < 0.001) lower (mean +/- S.D.) mean airway pressure (14 +/- 2 cm H2O versus 16 +/- 3 cm H2O), respiratory rates (13 +/- 3 breaths per min versus 14 +/- 4 breaths per min), incidence of stomach inflation (4.2% versus 38.7%) and median stomach inflation volumes (351 [range, 18-1211 ml] versus 1426 [20-5882 ml]); lung tidal volumes (538 +/- 97 ml versus 533 +/- 97 ml) were comparable. Inspiratory to expiratory ratios were significantly (P < 0.001) increased (1.7 +/- 0.5 versus 1.5 +/- 0.6). In conclusion, the SMART BAG reduced inspiratory flow, mean airway pressure and both the incidence and actual volume of stomach inflation compared with a standard bag-valve-mask device while maintaining delivered lung tidal volumes and increasing the inspiratory to expiratory ratio.

Developing a strategy to improve ventilation in an unprotected airway with a modified mouth-to-bag resuscitator in apneic patients.

The strategies to ensure safety during ventilation of an unprotected airway are limiting airway pressure and/or inspiratory flow. In this prospective, randomized study we assessed the effect of face mask ventilation with small tidal volumes in the modified mouth-to-bag resuscitator (maximal volume, 500 mL) versus a pediatric self-inflatable bag versus automatic pressure-controlled ventilation in 40 adult apneic patients during induction of anesthesia. The mouth-to-bag resuscitator requires the rescuer to blow up a balloon inside the self-inflating bag that subsequently displaces air which then flows into the patient's airway. Respiratory variables were measured with a pulmonary monitor (CP-100). Mouth-to-bag resuscitator and pressure-controlled ventilation resulted in significantly lower (mean +/- sd) peak airway pressure (8 +/- 2 and 8 +/- 1 cm H(2)O), peak inspiratory flow rate (0.7 +/- 0.1 and 0.7 +/- 0.1 L/s), and larger inspiratory time fraction (33% +/- 5% and 47% +/- 2%) in comparison to pediatric self-inflating bag ventilation (12 +/- 3 cm H(2)O; 1 +/- 0.2 L/s; 27% +/- 4%; all P < 0.001). The tidal volumes were similar between groups. No stomach inflation occurred in either group. We conclude that using a modified mouth-to-bag resuscitator or automatic pressure-controlled ventilation with similar small tidal volumes during face mask ventilation resulted in an approximately 25% reduction in peak airway pressure when compared with a standard pediatric self-inflating bag.

A strategy to optimise the performance of the mouth-to-bag resuscitator using small tidal volumes: effects on lung and gastric ventilation in a bench model of an unprotected airway.

When ventilating an unintubated patient with a standard adult self-inflating bag, high peak inspiratory flow rates may result in high peak airway pressures with subsequent stomach inflation. In a previous study we have tested a newly developed mouth-to-bag-resuscitator (max. volume, 1500 ml) that limits peak inspiratory flow, but the possible advantages were masked by excessive tidal volumes. The mouth-to-bag-resuscitator requires blowing up a balloon inside the self-inflating bag that subsequently displaces air, which then flows into the patient's airway. Due to this mechanism, gas flow and peak airway pressures are reduced during inspiration when compared with a standard bag-valve-mask-device. In addition, the device allows the rescuer to use two hands instead of one to seal the mask on the patient's face. The purpose of the present study was to assess the effects of the mouth-to-bag-resuscitator, which was modified to produce a maximum tidal volume of 500 ml, compared with a paediatric self-inflating bag (max. volume, 380 ml), and a standard adult self-inflating bag (max. volume, 1500 ml) in an established bench model simulating an unintubated patient with respiratory arrest. The bench model consisted of a face mask, manikin head, training lung (lung compliance, 100 ml/0.098 kPa (100ml/cm H2O); airway resistance, 0.39 kPa/(l s) (4 cm H2O/(l s)), and a valve simulating lower oesophageal sphincter pressure, 1.47 kPa (15 cm H2O). Twenty critical care nurses volunteered for the study and ventilated the manikin for 1 min with a respiratory rate of 20 min(-1) with each ventilation device in random order. The mouth-to-bag-resuscitator versus paediatric self-inflating bag resulted in significantly (P < 0.05) higher lung tidal volumes (302 +/- 41 ml versus 233 +/- 22 ml), and peak airway pressure (10 +/- 1 cm H2O versus 9 +/- 1 cm H2O), but comparable inspiratory time fraction (28 +/- 5% versus 27 +/- 5%, Ti/Ttot), peak inspiratory flow rate (0.6 +/- .01 l/s versus 0.6 +/- 0.2 l/s), and stomach inflation (149 +/- 495 ml/min versus 128 +/- 278 ml/min). In comparison with the adult self-inflating bag, there was significantly (P < 0.05) less gastric inflation (3943 +/- 4896 ml/min versus 149 +/- 495 ml/min versus 128 +/- 278 ml/min, respectively) with both devices, but the standard adult self-inflating bag had significantly higher lung tidal volumes (566 +/- 77 ml), peak airway pressure (13 +/- 1 cm H2O), and peak inspiratory flow rate (0.8 +/- 0.11 l/s). In conclusion, comparing the mouth-to-bag-resuscitator with small tidal volumes versus the paediatric self-inflating-bag during simulated ventilation of an unintubated patient in respiratory arrest resulted in comparable marginal stomach inflation, but significantly reduced the likelihood of gastric inflation compared to the adult self-inflating-bag. Lung tidal volumes were improved from approximately 250 ml with the paediatric self-inflating-bag to approximately 300 ml with the mouth-to-bag-resuscitator.

Mechanical versus manual ventilation via a face mask during the induction of anesthesia: a prospective, randomized, crossover study.

UNLABELLED: One approach to make ventilation safer in an unprotected airway has been to limit tidal volumes; another one might be to limit peak airway pressure, although it is unknown whether adequate tidal volumes can be delivered. Accordingly, the purpose of this study was to evaluate the quality of automatic pressure-controlled ventilation versus manual circle system face-mask ventilation regarding ventilatory variables in an unprotected airway. We studied 41 adults (ASA status I-II) in a prospective, randomized, crossover design with both devices during the induction of anesthesia. Respiratory variables were measured with a pulmonary monitor (CP-100). Pressure-controlled mask ventilation versus circle system ventilation resulted in lower (mean +/- SD) peak airway pressures (10.6 +/- 1.5 cm H(2)O versus 14.4 +/- 2.4 cm H(2)O; P < 0.001), delta airway pressures (8.5 +/- 1.5 cm H(2)O versus 11.9 +/- 2.3 cm H(2)O; P < 0.001), expiratory tidal volume (650 +/- 100 mL versus 680 +/- 100 mL; P = 0.001), minute ventilation (10.4 +/- 1.8 L/min versus 11.6 +/- 1.8 L/min; P < 0.001), and peak inspiratory flow rates (0.81 +/- 0.06 L/s versus 1.06 +/- 0.26 L/s; P < 0.001) but higher inspiratory time fraction (48% +/- 0.8% versus 33% +/- 7.7%; P < 0.001) and end-tidal carbon dioxide (34 +/- 3 mm Hg versus 33 +/- 4 mm Hg; not significant). We conclude that in this model of apneic patients with an unprotected airway, pressure-controlled ventilation resulted in reduced inspiratory peak flow rates and peak airway pressures when compared with circle system ventilation, thus providing an additional patient safety effect during mask ventilation. IMPLICATIONS: In this model of apneic patients with an unprotected airway, pressure-controlled ventilation resulted in reduced inspiratory peak flow rates and lower peak airway pressures when compared with circle system ventilation, thus providing an additional patient safety effect during face-mask ventilation.

A pilot study to evaluate the SMART BAG: a new pressure-responsive, gas-flow limiting bag-valve-mask device.

UNLABELLED: Reducing inspiratory flow rate and peak airway pressure may be important to minimize the risk of stomach inflation when ventilating an unprotected airway with positive pressure ventilation. In this study, we assessed the effects of a standard self-inflating bag compared with a new pressure-responsive, inspiratory gas flow-limiting device (SMART BAG) on respiratory mechanics in 60 adult patients undergoing routine induction of anesthesia. Respiratory variables were measured using a pulmonary monitor. The SMART BAG resulted in significantly decreased inspiratory flow rate and peak airway pressure while providing adequate tidal volume delivery. IMPLICATIONS: The SMART BAG, a new pressure-responsive, peak inspiratory gas flow-limiting bag-valve mask device, limits inspiratory gas flow from up to 120 L/min in a standard self-inflating bag to approximately 40 L/min. It is designed for use by all levels of health care professionals and has been proven in a clinical pilot study to effectively ventilate patients in respiratory arrest.

The effects of nifedipine on ventricular fibrillation mean frequency in a porcine model of prolonged cardiopulmonary resuscitation.

UNLABELLED: We assessed the effects of a calcium channel blocker versus saline placebo on ventricular fibrillation mean frequency and hemodynamic variables during prolonged cardiopulmonary resuscitation (CPR). Before cardiac arrest, 10 animals were randomly assigned to receive either nifedipine (0.64 mg/kg; n = 5) or saline placebo (n = 5) over 10 min. Immediately after drug administration, ventricular fibrillation was induced. After 4 min of cardiac arrest and 18 min of basic life support CPR, defibrillation was attempted. Ninety seconds after the induction of cardiac arrest, ventricular fibrillation mean frequency was significantly (P < 0.01) increased in nifedipine versus placebo pigs (mean +/- SD: 12.4 +/- 2.1 Hz versus 8 +/- 0.7 Hz). From 2 to 18.5 min after the induction of cardiac arrest, no differences in ventricular fibrillation mean frequency were detected between groups. Before defibrillation, ventricular fibrillation mean frequency was significantly (P < 0.05) increased in nifedipine versus placebo animals (9.7 +/- 1.2 Hz versus 7.1 +/- 1.3 Hz). Coronary perfusion pressure was significantly lower in the nifedipine than in the placebo group from the induction of ventricular fibrillation to 11.5 min of cardiac arrest; no animal had a return of spontaneous circulation after defibrillation. In conclusion, nifedipine, but not saline placebo, prevented a rapid decrease of ventricular fibrillation mean frequency after the induction of cardiac arrest and maintained ventricular fibrillation mean frequency at approximately 10 Hz during prolonged CPR; this was nevertheless associated with no defibrillation success. IMPLICATIONS: This study evaluates the effects of a calcium channel blocker on ventricular fibrillation mean frequency, hemodynamic variables, and resuscitability during prolonged cardiopulmonary resuscitation (CPR) in pigs. Nifedipine, but not saline placebo, prevented a rapid decrease of ventricular fibrillation mean frequency after the induction of cardiac arrest and maintained ventricular fibrillation mean frequency at approximately 10 Hz during prolonged CPR but did not improve resuscitability.

Survival with full neurologic recovery after prolonged cardiopulmonary resuscitation with a combination of vasopressin and epinephrine in pigs.

UNLABELLED: We sought to determine the effects of a combination of vasopressin and epinephrine on neurologic recovery in comparison with epinephrine alone and saline placebo alone in an established porcine model of prolonged cardiopulmonary resuscitation (CPR). After 4 min of cardiac arrest, followed by 3 min of basic life support CPR, 17 animals were randomly assigned to receive, every 5 min, either a combination of vasopressin and epinephrine (vasopressin [IU/kg]/epinephrine [ micro g/kg]: 0.4/45, 0.4/45, and 0.8/45; n = 6), epinephrine alone (45, 45, and 200 micro g/kg; n = 6), or saline placebo alone (n = 5). After 22 min of cardiac arrest, including 18 min of CPR, defibrillation was attempted to achieve the return of spontaneous circulation. Aortic diastolic pressure was significantly (P < 0.01) increased 90 s after each of 3 vasopressin/epinephrine injections versus epinephrine alone versus saline placebo alone (mean +/- SEM: 69 +/- 3 mm Hg versus 45 +/- 3 mm Hg versus 29 +/- 2 mm Hg, 63 +/- 4 mm Hg versus 27 +/- 3 mm Hg versus 23 +/- 1 mm Hg, and 52 +/- 4 mm Hg versus 21 +/- 3 mm Hg versus 16 +/- 3 mm Hg, respectively). Spontaneous circulation was restored in six of six vasopressin/epinephrine pigs, whereas six of six epinephrine and five of five saline placebo pigs died (P < 0.01). Neurologic evaluation 24 h after successful resuscitation revealed only an unsteady gait and was normal 5 days after the experiment in all vasopressin/epinephrine-treated animals. In conclusion, in this porcine model of prolonged CPR, repeated vasopressin/epinephrine administration, but not epinephrine or saline placebo alone, ensured long-term survival with full neurologic recovery. IMPLICATIONS: We present a study to evaluate the effects of a combination of vasopressin and epinephrine during prolonged cardiopulmonary resuscitation on neurological outcome in pigs. We found that all pigs treated with a combination of vasopressin and epinephrine could be resuscitated and had full neurologic recovery observed over an entire period of 5 days.

Decreasing peak flow rate with a new bag-valve-mask device: effects on respiratory mechanics, and gas distribution in a bench model of an unprotected airway.

Reducing inspiratory flow rate and peak airway pressure may be important in order to minimise the risk of stomach inflation when ventilating an unprotected airway with positive pressure ventilation. The purpose of this study was to assess the effects of a newly developed bag-valve-mask device (SMART BAG), O-Two Systems International, Ont., Canada) that limits peak inspiratory flow. A bench model simulating a patient with an unintubated airway was used consisting of a face mask, manikin head, training lung (lung compliance, 100 ml/cm H(2)O, airway resistance 4 cm H(2)O/l/s, lower oesophageal sphincter pressure 20 cm H(2)O and simulated stomach). Twenty nurses were randomised to each ventilate the manikin using a standard single person technique for 1 min (respiratory rate, 12/min) with either a standard adult self-inflating bag, or the SMART BAG. The volunteers were blinded to the experimental design of the model until completion of the experimental protocol. The SMART BAG vs. standard self-inflating bag resulted in significantly (P<0.05) lower mean+/-S.D. peak inspiratory flow rates (32+/-2 vs. 61+/-13 l/min), peak inspiratory pressure (12+/-2 vs. 17+/-2 cm H(2)O), lung tidal volumes (525+/-111 vs. 680+/-154 ml) and stomach tidal volumes (0+/-0 vs. 17+/-36 ml), longer inspiratory times (1.9+/-0.3 vs. 1.5+/-0.3 s), but significantly higher mask leakage (26+/-13 vs. 14+/-8%); mask tidal volumes (700+/-104 vs. 785+/-172 ml) were comparable. The mask leakage observed is not an uncommon factor in bag-valve-mask ventilation with leakage fractions of 25-40% having been previously reported. The differences observed between the standard BVM and the SMART BAG are due more to the anatomical design of the mask and the non-anatomical shape of the manikin face than the function of the device. Future studies should remove the mask to manikin interface and should introduce a standardized mask leakage fraction. The use of a two-person technique may have removed the problem of mask leakage. In conclusion, using the SMART BAG during simulated ventilation of an unintubated patient in respiratory arrest significantly decreased inspiratory flow rate, peak inspiratory pressure, stomach tidal volume, and resulted in a significantly longer inspiratory time when compared to a standard self-inflating bag.

Optimizing bag-valve-mask ventilation with a new mouth-to-bag resuscitator.

When ventilating an unintubated patient with a self-inflating bag, high peak inspiratory flow rates may result in high peak airway pressure with subsequent stomach inflation; this may occur frequently when rescuers without daily experience in bag-valve-mask ventilation need to perform advanced airway management. The purpose of this study was to assess the effects of a newly developed self-inflating bag (mouth-to-bag resuscitator; Ambu, Glostrup, Denmark) that limits peak inspiratory flow. A bench model simulating a patient with an unintubated airway was used, consisting of a face mask, manikin head, training lung (lung compliance, 100 ml/0.098 kPa (100 ml/cm H(2)O)); airway resistance, 0.39 kPa/l per second (4 cm H(2)O/l/s), oesophagus (LESP, 1.96 kPa (20 cm H(2)O)) and simulated stomach. Twenty nurses were randomised to ventilate the manikin for 1 min (respiratory rate: 12 per minute) with either a standard self-inflating bag or the mouth-to-bag resuscitator, which requires the rescuer to blow up a single-use balloon inside the self-inflating bag, which in turns displaces air towards the patient. When supplemental oxygen is added, ventilation with up to 100% oxygen may be obtained, since expired air is only used as the driving gas. The mouth-to-bag resuscitator therefore allows two instead of one hand sealing the mask on the patient's face. The volunteers were blinded to the experimental design of the model until completion of the experimental protocol. The mouth-to-bag resuscitator versus standard self-inflating bag resulted in significantly (P<0.05) higher mean+/-S.D. mask tidal volumes (1048+/-161 vs. 785+/-174 ml) and lung tidal volumes (911+/-148 vs. 678+/-157 ml), longer inspiratory times (1.7+/-0.4 vs. 1.4+/-0.4 s), but significantly lower peak inspiratory flow rates (50+/-9 vs. 62+/-13 l/min) and mask leakage (10+/-4 vs. 15+/-9%); peak inspiratory pressure (17+/-2 vs. 17+/-2 cm H(2)O) and stomach tidal volumes (16+/-30 vs. 18+/-35 ml) were comparable. In conclusion, employing the mouth-to-bag resuscitator during simulated ventilation of an unintubated patient in respiratory arrest significantly decreased inspiratory flow rate and improved lung tidal volumes, while decreasing mask leakage.

Vasopressin, but not fluid resuscitation, enhances survival in a liver trauma model with uncontrolled and otherwise lethal hemorrhagic shock in pigs.

BACKGROUND: The authors compared the effects of vasopressin fluid resuscitation on survival in a liver trauma model with uncontrolled and otherwise lethal hemorrhagic shock in pigs. METHODS: A midline laparotomy was performed on 23 domestic pigs, followed by an incision, and subsequent finger fraction across the right medial liver lobe. During hemorrhagic shock, animals were randomly assigned to receive either 0.4 U/kg vasopressin (n = 9), or fluid resuscitation (n = 7), or saline placebo (n = 7), respectively. A continuous infusion of 0.08 U x kg(-1) x min(-1) vasopressin in the vasopressin group, or normal saline was subsequently administered in the fluid resuscitation and saline placebo group, respectively. After 30 min of experimental therapy, bleeding was controlled by surgical intervention, and blood transfusion and rapid fluid infusion were subsequently performed. RESULTS: Maximum mean arterial blood pressure during experimental therapy in the vasopressin-treated animals was significantly higher than in the fluid resuscitation and saline placebo groups (mean +/- SD, 72 +/- 26 vs 38 +/- 16 vs 11 +/- 7 mmHg, respectively; P< 0.05). Subsequently, mean arterial blood pressure remained at approximately 40 mmHg in all vasopressin-treated animals, whereas mean arterial blood pressure in all fluid resuscitation and saline placebo pigs was close to aortic hydrostatic pressure (approximately 15 mmHg) within approximately 20 min of experimental therapy initiation. Total blood loss was significantly higher in the fluid resuscitation pigs compared with vasopressin or saline placebo after 10 min of experimental therapy (65 +/- 6 vs 42 +/- 4 vs 43 +/- 6 ml/kg, respectively; P< 0.05). Seven of seven fluid resuscitation, and seven of seven saline placebo pigs died within approximately 20 min of experimental therapy, while 8 of 9 vasopressin animals survived more than 7 days (P < 0.05). CONCLUSIONS: Vasopressin, but not fluid resuscitation or saline placebo, ensured survival with full recovery in this liver trauma model with uncontrolled and otherwise lethal hemorrhagic shock in pigs.