Hemorrhagic Shock In Dogs Research Articles

Topical Melatonin Improves Gastric Microcirculatory Oxygenation During Hemorrhagic Shock in Dogs but Does Not Alter Barrier Integrity of Caco-2 Monolayers

Systemic administration of melatonin exerts tissue protective effects in the context of hemorrhagic shock. Intravenous application of melatonin prior to hemorrhage improves gastric microcirculatory perfusion and maintains intestinal barrier function in dogs. The aim of the present study was to analyze the effects of a topical mucosal melatonin application on gastric microcirculation during hemorrhagic shock in vivo and on mucosal barrier function in vitro. In a randomized cross-over study, six anesthetized female foxhounds received 3.3 mg melatonin or the vehicle as a bolus to the gastric and oral mucosa during physiological and hemorrhagic (−20% blood volume) conditions. Microcirculation was analyzed with reflectance spectrometry and laser doppler flowmetry. Systemic hemodynamic variables were measured with transpulmonary thermodilution. For analysis of intestinal mucosal barrier function in vitro Caco-2 monolayers were used. The transepithelial electrical resistance (TEER) and the passage of Lucifer Yellow (LY) from the apical to the basolateral compartment of Transwell chambers were measured. Potential barrier protective effects of melatonin against oxidative stress were investigated in the presence of the oxidant H2O2. During physiologic conditions topical application of melatonin had no effect on gastric and oral microcirculation in vivo. During hemorrhagic shock, gastric microcirculatory oxygenation (μHbO2) was decreased from 81 ± 8% to 50 ± 15%. Topical treatment with melatonin led to a significant increase in μHbO2 to 60 ± 13%. Topical melatonin treatment had no effect on gastric microcirculatory perfusion, oral microcirculation or systemic hemodynamics. Incubation of H2O2 stressed Caco-2 monolayers with melatonin did neither influence transepithelial electrical resistance nor LY translocation. Topical treatment of the gastric mucosa with melatonin attenuates the shock induced decrease in microcirculatory oxygenation. As no effects on local microcirculatory and systemic perfusion were recorded, the improved μHbO2 is most likely caused by a modulation of local oxygen consumption. In vitro melatonin treatment did not improve intestinal barrier integrity in the context of oxidative stress. These results extend the current knowledge on melatonin's protective effects during hemorrhage in vivo. Topical application of melatonin exerts differential effects on local microcirculation compared to systemic pretreatment and might be suitable as an adjunct for resuscitation of hemorrhagic shock.

Regional hypothermia improves gastric microcirculatory oxygenation during hemorrhage in dogs.

Mild systemic hypothermia increases gastric mucosal oxygenation (μHbO2) during hemorrhagic shock in dogs. In the context of critical blood loss hypothermia might be fatal due to adverse side effects. Selective regional hypothermia might overcome these limitations. The aim of our study was to analyze the effects of regional gastric and oral mucosal hypothermia on μHbO2 and perfusion (μflow). In a cross-over study six anesthetized dogs were subjected to local oral and gastric mucosal hypothermia (34°C), or maintenance of local normothermia during normovolemia and hemorrhage (-20% blood volume). Macro- and microcirculatory variables were recorded continuously. During normovolemia, local hypothermia increased gastric microcirculatory flow (μflow) without affecting oxygenation (μHbO2) or oral microcirculation. During mild hemorrhagic shock gastric μHbO2 decreased from 72±2% to 38±3% in the normothermic group. This was attenuated by local hypothermia, where μHbO2 was reduced from 74±3% to 52±4%. Local perfusion, oral microcirculation and macrocirculatory variables were not affected. Selective local hypothermia improves gastric μHbO2 during hemorrhagic shock without relevant side effects. In contrast to systemic hypothermia, regional mucosal hypothermia did not affect perfusion and oxygen supply during hemorrhage. Thus, the increased μHbO2 during local hypothermia rather indicates reduced mucosal oxygen demand.

Ultrasonographic Assessment of Caudal Vena Cava to Aorta Ratio as a Novel Endpoint in Hemorrhagic Shock Resuscitation in Dogs

Objective- The aim of this study was to assess ultrasonography-derived caudal vena cava to aorta ratio (CVC/Ao) as a novel endpoint in the resuscitation of experimental hemorrhagic shock in dogs. Design- Experimental study. Animals- Ten adult mongrel healthy dogs. Procedures- After induction of anesthesia (control assessments), hemorrhagic shock was induced by blood withdrawal to a mean arterial pressure of 40 to 50 mmHg within 30 minutes and then maintained in a hypovolemic situation for an additional 30 minutes (second and third stages of assessments). Afterward, the dogs were randomly assigned to two groups which received 20 ml/kg lactated Ringer's solution or 5 ml/kg Hydroxyethyl starch, in four consecutive 15 minutes intervals (fourth stage of assessments). One hour after the last resuscitation step, final ultrasonographic assessments were performed. Results- Hemorrhagic shock caused a significant decrease in the CVC and Ao diameters as well as the CVC/Ao (2.14 ± 0.28 cm, 0.85 ± 0.07 cm and 0.4 ± 0.06, respectively) (p<0.05). Following the fluid resuscitation, CVC/Ao increased and returned to pre-shock values in both groups. Conclusion and clinical relevance- Findings indicated that serial ultrasonographic assessment of the CVC/Ao can be a useful endpoint in the resuscitation of dogs with hemorrhagic shock.

Melatonin pretreatment improves gastric mucosal blood flow and maintains intestinal barrier function during hemorrhagic shock in dogs.

Melatonin improves hepatic perfusion after hemorrhagic shock and may reduce stress-induced gastric lesions. This study was designed to investigate whether pretreatment with melatonin may influence gastric mucosal microcirculatory perfusion (μflow), oxygenation (μHbO2 ), or intestinal barrier function during physiological and hemorrhagic conditions in dogs. In a randomized crossover study, five anesthetized foxhounds received melatonin 100μgkg-1 or vehicle (ethanol 5%) intravenously in the absence or presence of hemorrhagic shock (60minutes, -20% blood volume). Systemic hemodynamic variables, gastric mucosal perfusion, and oxygenation were recorded continuously; intestinal barrier function was assessed intermittently via xylose absorption. During hemorrhagic shock, melatonin significantly attenuated the decrease in μflow, compared with vehicle (-19±9 vs -43±10aU, P<.05), without influence on μHbO2 . A significant increase in xylose absorption was detected during hemorrhage in vehicle-treated dogs, compared with sham-operated animals (13±2 vs 8±1 relative amounts, P<.05); this was absent in melatonin-treated animals (6±1 relative amounts). Melatonin did not influence macrocirculation. Melatonin improves regional blood flow suggesting improved oxygen delivery in gastric mucosa during hemorrhagic shock. This could provide a mechanism for the observed protection of intestinal barrier function in dogs.

Effect of Topical Iloprost and Nitroglycerin on Gastric Microcirculation and Barrier Function during Hemorrhagic Shock in Dogs

Background: Topical drug application is used to avoid systemic side effects. The aim of this study was to analyze whether locally applied iloprost or nitroglycerin influence gastric mucosal perfusion, oxygenation, and barrier function during physiological and hemorrhagic conditions. Methods: In repeated experiments, 5 anesthetized dogs received iloprost, nitroglycerin, or normal saline during physiological and hemorrhagic (-20% blood volume) conditions. Macro- and microcirculatory variables were recorded continuously. Gastric barrier function was assessed via translocation of sucrose into the blood. Results: During hemorrhage, gastric mucosal oxygenation decreased from 77 ± 4 to 37 ± 7%. This effect was attenuated by nitroglycerin (78 ± 6 to 47 ± 13%) and iloprost (82 ± 4 to 54 ± 9%). Sucrose plasma levels increased during hemorrhage from 7 ± 4 to 55 ± 15 relative amounts. This was alleviated by nitroglycerin (5 ± 8 to 29 ± 38 relative amounts). These effects were independent of systemic hemodynamic variables. Conclusions: During hemorrhage, topical nitroglycerin and iloprost improve regional gastric oxygenation without affecting perfusion. Nitroglycerin attenuated the shock-induced impairment of the mucosal barrier integrity. Thus, local drug application improves gastric microcirculation without compromising systemic hemodynamic variables, and it may also protect mucosal barrier function.

The effects of etomidate for continuous infusion on adrenocortical function in hemorrhagic shock dogs

The effects of etomidate for continuous infusion on adrenocortical function in hemorrhagic shock dogs

Effects of goal-directed fluid therapy with different lactated Ringer's: hydroxyethyl starch ratios in hemorrhagic shock dogs.

The effects of goal-directed fluid therapy, with lactated Ringer's (LR) and 6% hydroxyethyl starch (HES) solution, on hemorrhagic shock dogs are unknown. We aimed to determine the optimal LR: HES ratio for the resuscitation of hemorrhagic shock dogs. Hemorrhagic shock was induced in 40 ventilated dogs by drawing an estimated 60% blood volume. The animals were randomly divided into five groups (N = 8) according to the LR: HES ratio of the resuscitation fluid (3:1, 2:1, 1:1, 1:2, and 1:3), and were then resuscitated for 24 h to reach the stroke volume variation (SVV) and hemoglobin (Hb) goals by fluid infusion and autologous blood perfusion. The extravascular lung water index (EVLWI), pH, partial pressure of oxygen (PaO2), base excess (BE), sodium, chloride, Hb and creatinine clearance (Clearcrea) were checked after 24 h (R24). The EVLWI of the 3:1 group at R24 were higher than that of the 1:3 group and the baseline value (P < 0.05), whereas the PaO2 was lower (P < 0.05). In contrast to the 3:1 group at R24 and baseline, plasma chloride and sodium in the 1:3 and 1:2 groups increased; however, pH, BE, and Clearcrea decreased (P < 0.05). No significant differences were found in the 1:1 and 2:1 groups at R24 compared with baseline (P > 0.05). Resuscitation with LR and HES at 2:1 and 1:1 ratios are superior in maintaining the acid-base, electrolyte, and lung water balances as well as renal function in hemorrhagic shock dogs than at ratios of 3:l, 1:2, and1:3.

Melatonin improves gastric mucosal microcirculatory perfusion and maintains intestinal barrier function during haemorrhagic shock in dogs

Vollmer, C.1; Wallenfang, M.1; Weber, A.2; Bauer, I.1; Mathes, A.1; Picker, O.1 Author Information

Dose-Dependent Hemodynamic, Biochemical, and Tissue Oxygen Effects of OC99 following Severe Oxygen Debt Produced by Hemorrhagic Shock in Dogs.

We determined the dose-dependent effects of OC99, a novel, stabilized hemoglobin-based oxygen-carrier, on hemodynamics, systemic and pulmonary artery pressures, surrogates of tissue oxygen debt (arterial lactate 7.2 ± 0.1 mM/L and arterial base excess −17.9 ± 0.5 mM/L), and tissue oxygen tension (tPO2) in a dog model of controlled severe oxygen-debt from hemorrhagic shock. The dose/rate for OC99 was established from a pilot study conducted in six bled dogs. Subsequently twenty-four dogs were randomly assigned to one of four groups (n = 6 per group) and administered: 0.0, 0.065, 0.325, or 0.65 g/kg of OC99 combined with 10 mL/kg lactated Ringers solution administered in conjunction with 20 mL/kg Hextend IV over 60 minutes. The administration of 0.325 g/kg and 0.65 g/kg OC99 produced plasma hemoglobin concentrations of 0.63 ± 0.01 and 1.11 ± 0.02 g/dL, respectively, improved systemic hemodynamics, enhanced tPO2, and restored lactate and base excess values compared to 0.0 and 0.065 g/kg OC99. The administration of 0.65 g/kg OC99 significantly elevated pulmonary artery pressure. Plasma hemoglobin concentrations of OC99 ranging from 0.3 to 1.1 g/dL, in conjunction with colloid based fluid resuscitation, normalized clinical surrogates of tissue oxygen debt, improved tPO2, and avoided clinically relevant increases in pulmonary artery pressure.

Assessment of shock index in healthy dogs and dogs in hemorrhagic shock

To compare the shock index (SI) in a population of healthy dogs to a population of dogs with confirmed hemorrhagic shock. Retrospective analysis of data collected prospectively from 2 previous studies. University teaching hospital. Seventy-eight healthy control dogs enrolled in a study to establish a reference interval for a tissue oxygen monitor; 38 dogs with confirmed hemorrhagic shock enrolled in a study to evaluate the tissue oxygen monitor in hemorrhagic shock. The heart rate and systolic blood pressure obtained during the respective studies were used to calculate the SI. None. Shock index was significantly higher in the hemorrhage group (median 1.37, range 0.78-4.35) than the control group (median 0.91, range 0.57-1.53); 92% of the dogs in hemorrhagic shock had an SI of >0.91. Compared with controls, dogs in hemorrhagic shock had significantly lower body temperatures (median 38.3°C, range 35.6-39.9°C versus median 38.7°C, range 37.5-39.9°C), higher heart rates (median 150/min, range 120-220/min versus median 110/min range 80-150/min), lower systolic blood pressures (mean 112 mm Hg, SD ±35.8 mm Hg versus mean 125 mm Hg, SD ±21.5 mm Hg), higher lactate concentrations (median 0.51 mmol/L, range 0.078-1.41 mmol/L versus median 0.11 mmol/L, range 0.033-0.33 mmol/L), and lower hemoglobin concentrations (median 81 g/L, range 56-183 g/L versus median 162.5 g/L, range 133-198 g/L). Shock index is a simple and easy calculation that can be used as an additional triage tool and should prompt further investigation for hemorrhage if the values are >0.9.

Erratum to: Dobutamine, not dopamine, improves gastric intramucosal pH during resuscitation from hemorrhagic shock in dogs

Erratum to: Dobutamine, not dopamine, improves gastric intramucosal pH during resuscitation from hemorrhagic shock in dogs

Hypothermia Improves Oral and Gastric Mucosal Microvascular Oxygenation during Hemorrhagic Shock in Dogs

Hypothermia is known to improve tissue function in different organs during physiological and pathological conditions. The aim of this study was to evaluate the effects of hypothermia on oral and gastric mucosal microvascular oxygenation (μHbO2) and perfusion (μflow) under physiological and hemorrhagic conditions. Five dogs were repeatedly anesthetized. All animals underwent each experimental protocol (randomized cross-over design): hypothermia (34°C), hypothermia during hemorrhage, normothermia, and normothermia during hemorrhage. Microcirculatory and hemodynamic variables were recorded. Systemic (DO2) and oral mucosal (μDO2) oxygen delivery were calculated. Hypothermia increased oral μHbO2 with no effect on gastric μHbO2. Hemorrhage reduced oral and gastric μHbO2 during normothermia (−36 ± 4% and −27 ± 7%); however, this effect was attenuated during additional hypothermia (−15 ± 5% and −11 ± 5%). The improved μHbO2 might be based on an attenuated reduction in μflow during hemorrhage and additional hypothermia (−51 ± 21 aU) compared to hemorrhage and normothermia (−106 ± 19 aU). μDO2 was accordingly attenuated under hypothermia during hemorrhage whereas DO2 did not change. Thus, in this study hypothermia alone improves oral μHbO2 and attenuates the effects of hemorrhage on oral and gastric μHbO2. This effect seems to be mediated by an increased μDO2 on the basis of increased μflow.

Cardiopulmonary effects of a new inspiratory impedance threshold device in acute hemorrhagic shock in dogs

To compare cardiovascular and respiratory effects of an inspiratory impedance threshold device (ITD) in dogs before and after induction of acute hemorrhagic shock. Prospective experimental randomized study. Eight healthy adult dogs. Dogs were anesthetized and maintained on spontaneous ventilation. Tidal volume (V(T)), systolic, mean and diastolic arterial blood pressure (SAP, MAP, DAP), central venous pressure (CVP), gastric P(CO2) (GBF) as an indicator of gastric perfusion, cardiac index (CI), systemic vascular resistance (SVR), oxygen delivery (DO(2)), and plasma lactate were monitored. To monitor respiratory compliance (RC) and respiratory resistance (ResR), animals were briefly placed on mechanical ventilation. Dogs were studied under 4 different conditions: (1) baseline (euvolemic state) (MAP > 60 mm Hg) with and without the ITD and (2) acute hemorrhagic shock (hypovolemic state) (target MAP of 40 mm Hg) with and without ITD. These 4 conditions were performed during one anesthetic period, allowing time for stabilization of parameters for each condition. Data were analyzed by ANOVA for repeated measure mixed models. No cardiovascular changes were detected between groups with and without use of ITD during euvolemic states. During acute hemorrhagic hypovolemic state, CI and DO(2) were higher with the ITD (2.9 ± 0.6 L/min/m(2)) and (326.5 ± 86.8 mL/min) compared with no ITD (1.8 ± 0.6 L/min/m(2)) and (191.3 ± 58.1 mL/min), respectively. The use of ITD during hypovolemia also increased SAP and MAP. There was an increase in ResR and decreased RC with the ITD in both euvolemic and hypovolemic states. The use of an ITD in dogs during acute hemorrhagic hypovolemic shock improved cardiovascular parameters but had negative effects on RC and ResR.

Assessment of microcirculatory changes by use of sidestream dark field microscopy during hemorrhagic shock in dogs

To directly assess microcirculatory changes associated with induced hemorrhagic shock by use of sidestream dark field microscopy (SDM) and correlate those values with concurrently measured macrovascular and blood gas variables in healthy anesthetized dogs. 12 adult dogs. Dogs were anesthetized and splenectomized. Instrumentation and catheterization were performed for determination of macrohemodynamic and blood gas variables. Hemorrhagic shock was induced via controlled hemorrhage to a mean arterial blood pressure (MAP) of 40 mm Hg. Dogs were maintained in the shock state (MAP, 35 to 45 mm Hg) for 60 minutes. An SDM device was used to image microcirculation of buccal mucosa, and vascular analysis software was used to determine microcirculatory variables. These values were compared with other cardiovascular and blood gas variables to determine correlations. Following hemorrhage, there was a significant decrease in microvascular variables (mean ± SD), including proportion of perfused vessels (82.77 ± 8.32% vs 57.21 ± 28.83%), perfused vessel density (14.86 ± 2.64 mm/m(2) vs 6.66 ± 4.75 mm/m(2)), and microvascular flow index (2.54 ± 0.52 vs 1.59 ± 0.85). Perfused vessel density individually correlated well with macrovascular variables, with heart rate (zero order, partial correlation, and part correlation coefficients = -0.762, -0.884, and -0.793, respectively) and oxygen extraction ratio (-0.734, -0.832, and -0.746, respectively) being the most important predictors. SDM allowed real-time imaging of the microvasculature and has potential as an effective tool in experimental and clinical applications for monitoring microcirculatory changes associated with hemorrhagic shock and resuscitation in dogs.

The effects of stimulation at acupoint ST36 points against hemorrhagic shock in dogs

The aim of this study is to investigate the effects of electroacupuncturing (EA) zusanli points on levels of basic hemodynamics, lactate, and cytokines in dogs with hemorrhagic shock. Thirty healthy dogs were randomly divided into 5 groups: sham hemorrhagic shocked group, hemorrhagic shocked group, EA group, nonacupuncturing group, and EA after vagotomy group. Zusanli points were electroacupunctured with constant voltage (10-15 V, 30 Hz) for 30 minutes immediately after the shock models were established. Before the stimulation, a blood pressure transducer was implanted into the right femoral artery for continuous recording of mean arterial pressure (MAP), and a 5F Swan-Ganz pediatric catheter was implanted into the pulmonary artery. The levels of serum tumor necrosis factor α (TNF- α) in the femoral artery were detected at 0, 120, and 180 minutes after hemorrhage. The levels of serum lactate in the femoral artery were detected before hemorrhage (−45 minutes), at 0 minute, and at 180 minutes. In the hemorrhagic shocked group, the levels of MAP, cardiac output, cardiac index, central venous pressure, and pulmonary arterial wedge pressure decreased significantly; at the same time, the levels of serum TNF- α and serum lactate increased significantly. There were no differences between these groups and the hemorrhagic group, but they were different from the sham hemorrhagic shocked group. In the EA group, the levels of MAP, cardiac output, cardiac index, central venous pressure, and pulmonary arterial wedge pressure gradually increased, but the content of serum TNF- α and lactate obviously decreased. The results suggested that EA zusanli points produce a protective effect on hemorrhagic shock in dogs.

The change in bone marrow after intraosseous hypertonic saline-hydroxyethyl starch infusion for resuscitation of hemorrhagic shock in dog

To observe the change in bone marrow after intraosseous hypertonic saline- hydroxyethyl starch (HSH) in dogs with hemorrhagic shock. Eighteen male dogs were randomly divided into sham group, normal saline (NS) group (0.9% sodium chloride) and HSH group (7.5% sodium chloride-6% hydroxyethyl starch). Wiggers graded controlled hemorrhagic shock model was reproduced in NS and HSH groups, and above solutions were injected into bone marrow of the tibia in low dosage (4 ml/kg) rapidly (within 5 minutes). The sham group did not lose blood or receive infusion. CD34(+) expression of peripheral blood and bone marrow, and the change in picture of different hematopoietic series in bone marrow were examined before and after bone marrow resuscitation. Pathological change in bone marrow was examined after different resuscitation fluid infusion. After 48 hours of resuscitation, the percentage of CD34(+) in bone marrow and peripheral blood in HSH group were significantly higher than that of NS group [peripheral blood: (6.915+/-1.178)% vs. (4.848+/-0.527)%, bone marrow: (7.900+/-0.648)% vs. (6.875+/- 0.403)% , both P<0.05]. One week after resuscitation, the erythrocyte count and granulocytic count in NS group were significantly increased compared with sham group (erythrocyte count: 0.289+/-0.016 vs. 0.253+/-0.014, granulocytic count: 0.615+/-0.019 vs. 0.560+/-0.013, both P<0.05], lymphocytic count was significantly decreased (0.049+/-0.007 vs. 0.132+/-0.015, P<0.05). In the HSH group, erythrocyte count (0.273+/-0.012), lymphocytic count (0.162+/-0.014) were all significantly increased (both P<0.05), while granulocytic count (0.517+/-0.038) was significantly decreased (P<0.05). After 4 week of resuscitation, the change in hemopoiesis series in NS group and HSH group recovered to normal level. The bone marrow morphology changed slightly, and no bone necrosis occurred. HSH in small amount through intraosseous space is safe and effective as a fluid resuscitation measure for shock, and little change in bone marrow has been found after the infusion.

Does the Choice of the Halogenated Anesthetic Influence Renal Function during Hemorrhagic Shock and Resuscitation?

Introduction. Halogenated anesthetics can cause changes in the variables that modify the cardiac output necessary to maintain renal hemodynamic during hemorrhagic shock and resuscitation. However, halogenated anesthetics seem to protect against renal ischemia-reperfusion injury. In a model of pressure-guided hemorrhagic shock in dogs, we studied the comparative effects of three halogenated anesthetics—halothane, sevoflurane, and isoflurane—at equipotent concentrations on renal responses after resuscitation. Methods. Thirty dogs were anesthetized with 1.0 minimum alveolar anesthetic concentration (MAC) of halothane, sevoflurane, or isoflurane. The dogs were splenectomized and hemorrhaged to hold mean arterial pressure at 40–50 mm Hg over 45 min and then resuscitated with the shed blood volume. Hemodynamic variables were measured at baseline, after 45 min of hemorrhage, and 15 and 60 min after resuscitation. Renal variables were measured at baseline and 15 and 60 min after resuscitation. Results. Hemorrhage induced reductions of mean arterial pressure, filling pressures, and cardiac index (p < 0.05), without significant differences among groups (p > 0.05). After 60 min of shed blood replacement, all groups restored hemodynamic and renal variables to the prehemorrhage levels (p > 0.05), without significant differences among groups (p > 0.05), with the exception of sodium fractional excretion, the values for which were significantly higher in isoflurane group, in relation to the other groups after 15 min of re-transfusion (p < 0.05), and renal vascular resistance, the values for which remain lower than baseline in halothane group (p < 0.05). Conclusions. We conclude that no difference could be detected between choosing equipotent doses of halothane, sevoflurane, or isoflurane in relation to renal variables in dogs submitted to pressure-adjusted hemorrhagic shock and resuscitation.

Gastric Mucosal Perfusion in Dogs: Effects of Halogenated Anesthetics and of Hemorrhage

The gastrointestinal tract is one of the first organs affected by hypoperfusion during hemorrhagic shock. The hemodynamics and oxygen transport variables during hemorrhagic shock and resuscitation can be affected by the anesthetics used. In a model of pressure-guided hemorrhagic shock in dogs, we studied the effects of three halogenated anesthetics—halothane, sevoflurane, and isoflurane—at equipotent concentrations on gastric oxygenation. Thirty dogs were anesthetized with 1.0 minimum alveolar anesthetic concentration (MAC) of either halothane, sevoflurane, or isoflurane. A gastric tonometer was placed in the stomach to determine mucosal gastric CO2 (PgCO2) and for the calculation of gastric-arterial PCO2 gradient (PCO2 gap). The dogs were splenectomized and hemorrhaged to hold mean arterial pressure at 40–50 mm Hg over 45 min and then resuscitated with the shed blood volume. Hemodynamics, systemic oxygenation, and PCO2 gap were measured at baseline, after 45 min of hemorrhage, and at 15 and 60 min after blood resuscitation. Hemorrhage induced reductions of mean arterial pressure and cardiac index, while systemic oxygen extraction increased (p <. 05), without significant differences among groups (p >. 05). Halothane group showed significant lower PCO2 gap values than the other groups (p <. 05). After 60 min of shed blood replacement, all groups restored hemodynamics, systemic oxygenation, and PCO2 gap to the prehemorrhage levels (p >. 05), without significant differences among groups (p >. 05). We conclude that halothane is superior to preserve the gastric mucosal perfusion in comparison to isoflurane and sevoflurane, in dogs submitted to pressure-guided hemorrhagic shock at equipotent doses of halogenated anesthetics.

Continuous cardiac output monitoring via arterial pressure waveform analysis following severe hemorrhagic shock in dogs*

To determine agreement and correlation between cardiac output determined by arterial pressure waveform analysis (PulseCO) and the lithium dilution indicator technique (LiDCO) during severe hemorrhagic shock and after fluid resuscitation in dogs. Prospective experimental study. University research laboratory. Twelve adult mongrel dogs. Dogs were anesthetized, and selected arteries and veins were catheterized. Baseline cardiac output was determined by LiDCO and used to calibrate the PulseCO. Hemorrhagic shock was induced by withdrawing blood to achieve and maintain a mean arterial pressure of 30-40 mm Hg for 60 mins, and cardiac output was measured again using both methods. All dogs were resuscitated by administering lactated Ringer's solution intravenously to achieve and maintain a mean arterial pressure between 60 and 70 mm Hg. PulseCO and LiDCO values were measured at 10 and 120 mins after resuscitation. Mean baseline cardiac output was 2.93 +/- 0.45 L/min. PulseCO values overestimated cardiac output compared with LiDCO during hemorrhagic shock (2.25 vs. 0.78 L/min). There were no differences in cardiac output determined by PulseCO and LiDCO at 10 and 120 mins after fluid resuscitation. Bland-Altman analysis suggested that PulseCO values were inaccurate after hemorrhage, producing significant bias with wide limits of agreement and percentage error (1.47 +/- 1.46 L/min; 97%). Bias was small but the limits of agreement and percentage error were large for cardiac output at 10 and 120 mins after resuscitation (-0.1 +/- 1.88 [98%] and -0.17 +/- 1.32 [71%] L/min, respectively). There appeared to be a negative but not significant correlation after hemorrhage (r = -.45; p = .15). PulseCO determination of cardiac output does not accurately predict rapid decreases in cardiac output or the effects of fluid resuscitation in dogs. Recalibration of PulseCO may be necessary after any apparent or suspected decrease in cardiac preload, afterload, or contractility.

Determination of Optimal Dose of Arginine Vasopressin in Hemorrhagic Shock in Dogs

The hemodynamic effects of vasopressin of high/low doses on dogs were investigated using experimentally induced hemorrhagic shock model. Experimental groups were categorized according to administered doses of vasopressin (0.1, 0.4 and 1.6 IU/kg) and hemodynamic parameters were measured before and after the graded-dose administration of vasopressin. Administration of high- and middle-dose vasopressin (0.4 and 1.6 IU/kg) showed superior increase in blood pressure and systemic vascular resistance, compared with those of low-dose one (0.1 IU/kg). Results of systolic arterial pressure and mean arterial pressure in 1.6 IU/kg-administered group revealed lower efficacy than that in 0.4 IU/kg group in spite of administration of higher dose. This study demonstrates that 0.4 IU/kg of vasopressin can be used as the most effective dose for improving hemodynamic condition in the decompensatory phase of hemorrhagic shock in dogs.