Hyperbaric oxygen therapy induces kidney protection in an ischemia/reperfusion model in rats.

Ischemia/reperfusion (I/R) injury remains a major cause of graft dysfunction, which impacts short- and long-term follow-up. Hyperbaric oxygen therapy (HBO), through plasma oxygen transport, has been currently used as an alternative treatment for ischemic tissues. The aim of this study was to analyze the effects of HBO on kidney I/R injury model in rats, in reducing the harmful effect of I/R. The renal I/R model was obtained by occluding bilateral renal pedicles with nontraumatic vascular clamps for 45 minutes, followed by 48 hours of reperfusion. HBO therapy was delivered an hypebaric chamber (2.5 atmospheres absolute). Animals underwent two sessions of 60 minutes each at 6 hours and 20 hours after initiation of reperfusion. Male Wistar rats (n = 38) were randomized into four groups: sham, sham operated rats; Sham+HBO, sham operated rats exposed to HBO; I/R, animals submitted to I/R; and I/R+HBO, I/R rats exposed to HBO. Blood, urine, and kidney tissue were collected for biochemical, histologic, and immunohistochemical analyses. The histopathological evaluation of the ischemic injury used a grading scale of 0 to 4. HBO attenuated renal dysfunction after ischemia characterized by a significant decrease in blood urea nitrogen (BUN), serum creatinine, and proteinuria in the I/R+HBO group compared with I/R alone. In parallel, tubular function was improved resulting in significantly lower fractional excretions of sodium and potassium. Kidney sections from the I/R plus HBO group showed significantly lower acute kidney injury scores compared with the I/R group. HBO treatment significantly diminished proliferative activity in I/R (P < .05). There was no significant difference in macrophage infiltration or hemoxygenase-1 expression. In conclusion, HBO attenuated renal dysfunction in a kidney I/R injury model with a decrease in BUN, serum creatinine, proteinuria, and fractional excretion of sodium and potassium, associated with reduced histological damage.

Systemic and regional hemodynamic effects of enalaprilat infusion in experimental normotensive sepsis.

Angiotensin-converting enzyme inhibitors have been shown to improve splanchnic perfusion in distinct shock states. We hypothesized that enalaprilat potentiates the benefits of early fluid resuscitation in severe experimental sepsis, particularly in the splanchnic region. Anesthetized and mechanically ventilated mongrel dogs received an intravenous infusion of live Escherichia coli over a period of 30 min. Thereafter, two interventions were performed: fluid infusion (normal saline, 32 mL/kg over 30 min) and enalaprilat infusion (0.02 mg kg(-1) min(-1) for 60 min) in randomized groups. The following groups were studied: controls (fluid infusion, N = 4), E1 (enalaprilat infusion followed by fluid infusion, N = 5) and E2 (fluid infusion followed by enalaprilat infusion, N = 5). All animals were observed for a 120 min after bacterial infusion. Mean arterial pressure, cardiac output (CO), portal vein blood flow (PVBF), systemic and regional oxygen-derived variables, and lactate levels were measured. Rapid and progressive reductions in CO and PVBF were induced by the infusion of live bacteria, while minor changes were observed in mean arterial pressure. Systemic and regional territories showed a significant increase in oxygen extraction and lactate levels. Widening venous-arterial and portal-arterial pCO2 gradients were also detected. Fluid replacement promoted transient benefits in CO and PVBF. Enalaprilat after fluid resuscitation did not affect systemic or regional hemodynamic variables. We conclude that in this model of normotensive sepsis inhibition of angiotensin-converting enzyme did not interfere with the course of systemic or regional hemodynamic and oxygen-derived variables.

Mechanisms of action of hypertonic saline resuscitation in severe sepsis and septic shock.

Small volumes of 7.5% NaCl (2400mOsm/L) have been extensive evaluated in animal models of hemorrhagic shock and in clinical trials of post-traumatic hypotension and as volume support for complex cardiovascular procedures. Hypertonic solutions promote immediate blood volume expansion, restore cardiac output and regional blood flows, improve microcirculation and modulate immune responses, thereby decreasing inflammatory responses triggered by shock and trauma. A large number of very interesting in vivo and in vitro experiments highlighted that hypertonic saline resuscitation may decrease susceptibility to post-traumatic sepsis, modulate trauma and sepsis-induced immune dysfunction, inflammatory response and apoptosis. All those long-term benefits associated with hypertonic resuscitation may be of potential relevance for the management of severe sepsis and septic shock In this review, we describe the mechanisms of action of hypertonic saline based on experimental studies as well as its efficacy and safety based on its clinical use. We believe those studies support the need for additional experimental and clinical studies before the widespread use of hypertonic solutions for the treatment of severe sepsis and septic shock.

Anatomical study of the gastrocnemius venous network and proposal for a classification of the veins.

OBJECTIVES: To present a detailed description of the gastrocnemius venous network. DESIGN: Anatomical study in cadavers. MATERIAL AND METHODS: Forty lower limbs from 20 adult male cadavers were studied. All gastrocnemius veins were dissected from the gastrocnemius muscle heads proximally toward their drainage site. RESULTS: Eighty heads of 40 gastrocnemius muscles showed 438 gastrocnemius veins. The number of veins per muscle head varied between 2 and 12. There were 221 gastrocnemius trunks distributed as 95 main gastrocnemius trunks, 81 axial and 45 collateral ones. From the 95 main gastrocnemius trunks, 83 (87%) drained into the popliteal vein. Direct observation of the gastrocnemius venous network allowed us to classify the anatomical distribution as four distinct types. CONCLUSIONS: The majority of main gastrocnemius venous trunks drain into the popliteal vein. There is wide variability in the number of gastrocnemius veins. We propose a classification of four distinct types of anatomical pattern.

Active spleno-femoral shunt avoids splanchnic congestion during portal triad occlusion: an experimental study.

UNLABELLED: Portal triad occlusion (PTO) is often performed during hepatic resections for trauma or malignancies to minimize intraoperative blood loss. The pringle maneuver is also regularly required during liver transplantation. This maneuver leads to temporary hepatic ischemia and may be associated with splanchnic blood flow congestion, promoting undesirable hemodynamic disturbances in some patients. Veno-venous bypass is a useful, easily performed technique that may avoid those deleterious hemodynamic effects of PTO. We tested the hypothesis that an active spleno-femoral shunt maintains hemodynamic stability and promotes complete decompression of the mesenteric bed, avoiding intestinal mucosal blood congestion, during PTO. METHODS: Seven dogs (17.2 +/- 0.9 kg) were subjected to 45 minutes of hepatic ischemia during which there was an active spleno-femoral shunt. Systemic hemodynamics were evaluated through Swan-Ganz and arterial catheters. Splanchnic perfusion was assessed by portal vein blood flow and hepatic artery blood flow (PVBF and HABF, ultrasonic flowprobe), intestinal mucosal-arterial pCO(2) gradient (D(t-a)pCO(2), tonometry), and regional O(2)-derived variables. RESULTS: No significant changes in systemic and regional parameters were observed during the ischemia period. During reperfusion, a significant decrease in mean arterial pressure, PVBF, and arterial pH was observed. A significant increase in ALT and D(t-a)pCO(2) (4.8 +/- 2.5 to 18.9 +/- 3 mm Hg) was also observed following hepatic blood flow restoration. CONCLUSION: Spleno-femoral shunt maintains systemic hemodynamic stability, with an effective decompression of the splanchnic bed during portal triad occlusion. The deleterious hemodynamic and metabolic effects observed during reperfusion period, such as transitory hypotension, high D(t-a)pCO(2), and acidemia, were associated with an isolated hepatic ischemia-reperfusion injury, not with the blood congestion in the splanchnic bed.

Short-lasting systemic and regional benefits of early crystalloid infusion after intravenous inoculation of dogs with live Escherichia coli.

We investigated the systemic and regional hemodynamic effects of early crystalloid infusion in an experimental model of septic shock induced by intravenous inoculation with live Escherichia coli. Anesthetized dogs received an intravenous infusion of 1.2 x 10(10) cfu/kg live E. coli in 30 min. After 30 min of observation, they were randomized to controls (no fluids; N = 7), or fluid resuscitation with lactated Ringer's solution, 16 ml/kg (N = 7) or 32 ml/kg (N = 7) over 30 min and followed for 120 min. Cardiac index, portal blood flow, mean arterial pressure, systemic and regional oxygen-derived variables, blood lactate, and gastric PCO2 were assessed. Rapid and progressive cardiovascular deterioration with reduction in cardiac output, mean arterial pressure and portal blood flow (approximately 50, approximately 25 and approximately 70%, respectively) was induced by the live bacteria challenge. Systemic and regional territories showed significant increases in oxygen extraction and in lactate levels. Significant increases in venous-arterial (approximately 9.6 mmHg), portal-arterial (approximately 12.1 mmHg) and gastric mucosal-arterial (approximately 18.4 mmHg) PCO2 gradients were also observed. Early fluid replacement, especially with 32 ml/kg volumes of crystalloids, promoted only partial and transient benefits such as increases of approximately 76% in cardiac index, of approximately 50% in portal vein blood flow and decreases in venous-arterial, portal-arterial, gastric mucosal-arterial PCO2 gradients (7.2 +/- 1.0, 7.2 +/- 1.3 and 9.7 +/- 2.5 mmHg, respectively). The fluid infusion promoted only modest and transient benefits, unable to restore the systemic and regional perfusional and metabolic changes in this hypodynamic septic shock model.

Short-lasting systemic and regional benefits of early crystalloid infusion after intravenous inoculation of dogs with live Escherichia coli

We investigated the systemic and regional hemodynamic effects of early crystalloid infusion in an experimental model of septic shock induced by intravenous inoculation with live Escherichia coli. Anesthetized dogs received an intravenous infusion of 1.2 x 10(10) cfu/kg live E. coli in 30 min. After 30 min of observation, they were randomized to controls (no fluids; N = 7), or fluid resuscitation with lactated Ringer's solution, 16 ml/kg (N = 7) or 32 ml/kg (N = 7) over 30 min and followed for 120 min. Cardiac index, portal blood flow, mean arterial pressure, systemic and regional oxygen-derived variables, blood lactate, and gastric PCO2 were assessed. Rapid and progressive cardiovascular deterioration with reduction in cardiac output, mean arterial pressure and portal blood flow (about 50, about 25 and about 70 percent, respectively) was induced by the live bacteria challenge. Systemic and regional territories showed significant increases in oxygen extraction and in lactate levels. Significant increases in venous-arterial (about 9.6 mmHg), portal-arterial (about 12.1 mmHg) and gastric mucosal-arterial (about 18.4 mmHg) PCO2 gradients were also observed. Early fluid replacement, especially with 32 ml/kg volumes of crystalloids, promoted only partial and transient benefits such as increases of about 76 percent in cardiac index, of about 50 percent in portal vein blood flow and decreases in venous-arterial, portal-arterial, gastric mucosal-arterial PCO2 gradients (7.2 ± 1.0, 7.2 ± 1.3 and 9.7 ± 2.5 mmHg, respectively). The fluid infusion promoted only modest and transient benefits, unable to restore the systemic and regional perfusional and metabolic changes in this hypodynamic septic shock model.

Hepatic arterial buffer response fails to restore hepatic oxygenation after temporary liver dearterialization in canines.

BACKGROUND: Hepatic artery thrombosis is a rare but extremely troublesome condition after liver transplantation. Recently, urgent arterial revascularization has been used as rescue therapy, leading to improved graft and patient survivals. Hepatic artery ligation produces a progressive reduction in portal vein blood flow. Theoretically, a hyperemic response may be expected following hepatic artery reperfusion (hepatic artery buffer response, HABR). In this study, we tested the hypothesis that HABR can maintain adequate liver oxygenation after temporary liver dearterialization. METHODS: Seven dogs (19.7 +/- 1.2 kg) subjected to 60 minutes of hepatic artery occlusion were observed for 120 minutes thereafter. Systemic hemodynamics was evaluated through Swan-Ganz and arterial catheters, and splanchnic perfusion by portal vein and hepatic artery blood flows (PVBF and HABF) via an ultrasonic flowprobe. Liver enzymes (ALT and LDH) and systemic and hepatic oxygen delivery (DO2hepat) were calculated using standard formulae. RESULTS: Hepatic artery occlusion induced a progressive reduction in PVBF and DO2hepat. A complete restoration of HABF after hepatic artery declamping was observed; however, the DO2hepat (33.3 +/- 5.9 to 16.5 +/- 5.9 mL/min) did not return to the baseline levels. CONCLUSION: Temporary hepatic artery occlusion induced a progressive decrease in portal vein blood flow during ischemia, an effect that continued during the reperfusion period. The hepatic artery blood flow was promptly restored after declamping. However, HABR was not able to restore hepatic oxygen delivery to baseline levels during the reperfusion period.

Effects of intra-aortic balloon occlusion on intestinal perfusion, oxygen metabolism and gastric mucosal PCO2 during experimental hemorrhagic shock.

BACKGROUND: Aortic occlusion has been suggested for the initial treatment of severe uncontrolled hemorrhagic shock. Our objective is to determine the impact of aortic occlusion, during hemorrhagic shock, on splanchnic mucosal perfusion and to correlate these findings with other systemic and regional markers of splanchnic ischemia. METHODS: Fourteen dogs (17 +/- 1.7 kg) anesthetized with pentobarbital were bled to a mean arterial pressure (MAP) of 40 mm Hg. After 30 min, the animals were randomly assigned to controls (no aortic occlusion, n = 7) and transfemoral aortic occlusion (TAO) at T9 level (n = 7). Superior mesenteric artery blood flow (SMABF, ultrasonic flow probe), gastric mucosal PCO2 (gastric tonometry) and splanchnic oxygen extraction ratio (O2ERsplanc) were evaluated for 120 min. RESULTS: Hemorrhage caused a marked reduction in SMABF and increases in PCO2-gap and O2ERsplanc in both groups. TAO significantly improved MAP and further increased the PCO2-gap and O2ERsplanc, with a decreased SMABF. After reperfusion, SMABF, MAP and O2ERsplanc returned to pre-occlusion values, although the PCO2-gap remained higher in the TAO group. CONCLUSION: Aortic occlusion promotes blood pressure restoration with an additional insult to mucosal perfusion, which could be adequately predicted by global and/or splanchnic oxygen-derived variables during ischemia, but not during the early reperfusion period.

Effects of N-acetylcysteine in hepatic ischemia-reperfusion injury during hemorrhagic shock.

This article seeks to standardize an experimental model of liver ischemia-reperfusion in rats following hemorrhagic shock modulated by N-acetylcysteine (NAC). Twenty-seven adult Wistar rats were randomized into three groups: the HS-IR-Garm underwent hemorrhagic shock with selective hepatic ischemia followed by reperfusion; the HSIR + NAC-G, the same procedure plus NAC; and the control group, only venous catheterization. Blood was withdrawn for 10 minutes until MABP reached 35 mm Hg, which was maintained for 1 hour. The blood was then reinjected as required to maintain MABP at that level. Ringer's lactate solution was infused in a volume equivalent to three times the shed blood, over a period of 15 minutes. Half of the shed blood was reinfused over 5 minutes. HSIR + NAC-G received 150 mg/kg of NAC, during treatment of the shock, and again 10 minutes before reperfusion and continued for 30 minutes. Finally, both groups were subjected to 40 minutes of warm selective hepatic ischemia and reperfusion for 1 hour. Data were analyzed by nonparametric tests (P < or =.05). Liver enzyme levels were higher in HS-IR-G (DHL = 6094 +/- 1688, AST = 746 +/- 175, and ALT = 457 +/- 90) than in HSIR + NAC-G group (DHL = 2920 +/- 284, AST = 419 +/- 113, and ALT = 253 +/- 26). The values in the control group were lower than both experimental groups (DHL = 965 +/- 173, AST = 163 +/- 42, and ALT = 82 +/- 28). Our data showed that liver ischemia-reperfusion injury following hemorrhagic shock produces important hepatic damage and that NAC reduces injury in this rat model.

Increases in fines and driver licence withdrawal have effectively reduced immediate deaths from trauma on Brazilian roads: first-year report on the new traffic code.

Road accidents are a major cause of death in Brazil, with rates increasing steadily for years. Our objective here is to report the impact of the new Brazilian Traffic Code, introduced in 1998. Its main new features include a large increase in fines and a rigid penalty scoring system that leads to driver license withdrawal. Speed limits have actually been raised on many roads, but adherence to the rules has been monitored more closely. We compare the incidence of injured patients and immediate deaths in road accidents and emergency room admissions to a level I trauma centre in downtown São Paulo between January and December 1998 with corresponding data from between January and December 1997. There was an overall 21.3% reduction in the number of accidents and a 24.7% reduction in immediate deaths, saving 5962 lives on Brazilian highways. Tickets issued fell by 49.5% (601977 during 1997 to 304785 during 1998). Motor vehicle accident-related emergency room admissions decreased by 33.2%. We conclude that very costly tickets and threatened driver licences have proved very effective in decreasing immediate deaths from trauma. Further advances in educational programmes associated with road and vehicle safety measures are likely to provide the much needed further reduction in the still high trauma mortality on Brazilian roads and streets.

Radioisotope blood volume measurement in uncontrolled retroperitoneal haemorrhage induced by a transfemoral iliac artery puncture.

Standard-of-care, large volume crystalloid infusion, in the setting of uncontrolled bleeding, has been challenged and it is not known if fluid resuscitation increases retroperitoneal hemorrhage. We developed an experimental model of retroperitoneal haemorrhage to correlate haemodynamic and metabolic alterations with the blood volume loss. Anaesthetised, spontaneously breathing dogs (17.1+/-0.56 kg) were randomised to unilateral (UL, n=11) or bilateral (BL, n=11) iliac artery puncture, using a metallic device introduced through the femoral arteries and followed for 120 min. Initial and final blood volumes were determined using radioactive tracers, 99mTC and 51Cr, respectively. UL was associated with a stable arterial pressure and a moderate decrease in cardiac output and oxygen delivery. BL induced an abrupt and sustained decrease in mean arterial pressure, from 131.9+/-5.9 to 88.6+/-10.8 mmHg, and a much greater reduction in cardiac output, oxygen delivery and consumption than UL throughout the experiment. Total retroperitoneal blood loss after BL was 36.8+/-3.2 ml/kg, while after UL was 25.1+/-3.4 ml/kg (P=0.0262). We conclude that a transfemoral bilateral iliac artery puncture produces a clinically relevant model of uncontrolled retroperitoneal haemorrhage, with hypotension and low flow state, while a unilateral iliac artery lesion causes a compensated shock state.

Hypertonic saline dextran produces early (8-12 hrs) fluid sparing in burn resuscitation: a 24-hr prospective, double-blind study in sheep.

OBJECTIVE: Resuscitation of large burn injuries must quickly restore and maintain cardiovascular function and fluid balance while minimizing secondary edema-related damage. We tested the hypothesis that two 4-mL x kg(-1) doses of hypertonic saline dextran (HSD; 7.5% NaCl/6% dextran-70) can produce prolonged reduction in fluid requirements after burn injury. DESIGN: Prospective, pseudo randomized, double-blind study. SETTING: Animal research laboratory. SUBJECTS: Female adult Merino sheep (n = 12). INTERVENTIONS: Sheep were given a 40% total body surface area full-thickness flame burn under halothane anesthesia. One hour after the burn, the conscious animals received an initial dose of 4 mL x kg(-1) HSD (n = 6) or normal saline (NS; NaCl 0.9%) (n = 6) intravenously during 30 mins. This was followed by lactated Ringer's solution, infused to a target urine output of 1 mL x kg(-1) x hr(-1) throughout the 24-hr study. A second 4-mL x kg(-1) dose of HSD or NS was started at 12 hrs, and infused during 5 hrs. MEASUREMENTS AND MAIN RESULTS: Hourly urine output measurements were used to guide the infusion rate of the lactated Ringer's. The initial infusion of HSD 1 hr after the burn injury promptly restored cardiac index, promoted diuresis, and reduced fluid requirements compared with the NS controls (73% reduction for HSD relative to NS at 8 hrs). Subsequent rebound fluid accumulation resulted in similar net fluid balances in both groups within 12 hrs after the burn. The second dose of HSD, given at 12 hrs, was without effect on hemodynamics and fluid balance. CONCLUSIONS: We conclude a considerable initial, but not sustained fluid-sparing effect of early HSD, and no effect of a late, slowly infused HSD dose in this two-dose regimen.

Thermal filament continuous thermodilution cardiac output delayed response limits its value during acute hemodynamic instability.

BACKGROUND: It has been suggested that measurement of continuous cardiac output (CCO) is an advancement in the management of critically ill patients. Our objective was to determine the accuracy of CCO during the rapid hemodynamic changes induced by hemorrhage and resuscitation. METHODS: In 12 anesthetized dogs (20.2+/-0.9 kg), pulmonary artery blood flow, our "gold standard" cardiac output, was measured with an sonographic flowprobe, whereas CCO, intermittent bolus cardiac output (ICO), and mixed venous oxygen saturation were measured with a thermodilution fiberoptic pulmonary artery catheter with a thermal filament. A graded hemorrhage (20 mL/min) was produced to a mean arterial pressure of 40 mm Hg, which was maintained at this level for 30 minutes. Total shed blood volume (701+/-53 mL) was retransfused at a rate of 40 mL/min, over 30 minutes, after which a massive hemorrhage (100 mL/min) was produced over 10 minutes. RESULTS: Hemorrhage induced significant decreases in mean arterial pressure, mixed venous oxygen saturation, and oxygen delivery, which were all restored during early resuscitation. However, CCO showed a delayed response after hemorrhage and resuscitation, compared with pulmonary blood flow, throughout the study (r = 0.549), matching only at baseline and at the end of both graded hemorrhage and resuscitation periods. There was a good correlation between ICO and pulmonary artery blood flow (r = 0.964) and no significant differences between them throughout the study. CONCLUSION: CCO has a delayed response during acute hemodynamic changes induced by hemorrhage and resuscitation. When sudden changes in mean arterial pressure or in mixed venous oxygen saturation are detected, cardiac output must be estimated by the standard bolus thermodilution technique, not by CCO.

Impact of previous thoracic aneurysm repair on thoracoabdominal aortic aneurysm management.

BACKGROUND: The purpose of this study was to determine the impact of previous thoracic aortic aneurysm repair (PTAR) on subsequent thoracoabdominal aortic aneurysm operations. METHODS: A retrospective review of 723 thoracoabdominal aortic aneurysm repairs over a 10-year period facilitated comparison of 179 patients (24.8%) with PTAR and 544 patients (75.2%) without PTAR. RESULTS: Patients with PTAR had more chronic dissections and extensive thoracoabdominal aortic aneurysms, and consequently required longer clamp and ischemic times and more intraoperative transfusions. Patients without PTAR were older, had more preoperative comorbid disease, and had more symptomatic or ruptured aneurysms. Although differences did not reach statistical significance, patients without PTAR tended toward increased in-hospital mortality (8.5% versus 4.5%; p = 0.078) and postoperative paraplegia/paraparesis rates (6.5% versus 2.8%; p = 0.069). More patients without PTAR had cardiac complications (11.3% versus 5.6%; p = 0.028) and required chronic hemodialysis (5.9% versus 1.1%; p = 0.009). CONCLUSIONS: The presence of a PTAR did not adversely affect the outcome of thoracoabdominal aortic aneurysm repair. After thoracic aortic aneurysm repair, life-long radiologic surveillance and early surgical treatment are justified.

Hemodynamic effects of isovolemic hemodilution during descending thoracic aortic cross clamping and lower torso reperfusion.

BACKGROUND: Isovolemic hemodilution has been suggested for blood conservation and to improve hemodynamic tolerance to abdominal aortic cross clamping. However, the hemodynamic effects of hemodilution during descending thoracic aortic cross clamping (DAC) have not been established. We evaluated them in anesthetized swine. METHODS: Hemodilution (n = 7) was produced by the isovolemic exchange of blood for 6% hetastarch to a target hematocrit of 20%. Hematocrit in control pigs (n = 7) remained at 30%. DAC was performed at the T9 level for 45 minutes. During a 60-minute reperfusion period, control pigs were infused with lactated Ringer's solution; shed blood was returned to hemodilution pigs, followed by lactated Ringer's. If hypotension occurred despite left atrial pressure of 10 mm Hg or greater, boluses of phenylephrine were given to keep mean arterial pressure above 60 mm Hg. RESULTS: Hemodilution caused a marked reduction in hematocrit and in global oxygen delivery (DO2). DAC produced a significant increase in proximal arterial pressure, cardiac index, and DO2 and oxygen consumption (VO2) was markedly reduced in both groups. A significant increase in systemic vascular resistance during DAC occurred only in control pigs. After reperfusion, vascular resistance was significantly lower than baseline in hemodilution pigs, requiring a sixfold greater dose of phenylephrine to avoid hypotension. A lower global DO2 and supply-limited VO2 were also observed in hemodilution pigs. CONCLUSIONS: Isovolemic hemodilution maintains hemodynamic stability during DAC. During lower torso reperfusion, however, hemodilution caused hemodynamic instability, decreased global DO2, and limited VO2, which may offset its potential benefits.

Hypertonic acetate-alpha alpha hemoglobin for small volume resuscitation of hemorrhagic shock.

Hypertonic acetate solution in small volumes greatly improves cardiac output and corrects acid-base disturbances in hemorrhaged animals. We hypothesized that the combination of alpha alpha-crosslinked human hemoglobin (alpha alpha Hb), an oxygen carrier and vasoconstrictor, with hypertonic sodium acetate (HAHb), a vasodilator, may be effective for small volume resuscitation of hemorrhagic shock. Six pigs hemorrhaged to a mean arterial pressure of 40 mmHg for 60 min (bled volume: 23.6 +/- 2.5 ml.kg-1) received a single bolus of 4 ml.kg-1 of HAHb infused over two min. HAHb restored arterial pressure, increased systemic vascular resistance and caused a modest increase in cardiac output and SvO2, while pulmonary arterial pressure and vascular resistance were markedly increased. In two animals, transient severe hypotension and low cardiac output may have been due to acute pulmonary hypertension during injection. Compared to our previous study, in which animals received 4 ml-kg-1 of alpha alpha Hb alone, HAHb produced higher cardiac output and a smaller increase in systemic and pulmonary vascular resistance. However, slower, titrated infusions may be needed when hemoglobin solutions are combined with drugs or solutions that cause vasodilation in order to decrease the likelihood of acute hemodynamic instability.

Hemodynamic improvement in hemorrhagic shock by aortic balloon occlusion and hypertonic saline solutions.

The initial treatment of uncontrolled hemorrhage shock from an abdominal source is controversial. The hemodynamic effects of transfemoral diaphragmatic aortic occlusion with a balloon followed by a single bolus of hypertonic saline solutions have been evaluated in 28 dogs. The animals were submitted to pressure-driven hemorrhage for 90 min, according to mean arterial pressure in the abdominal aorta and randomized into four groups, according to the treatment employed at 34 min after hemorrhage. Group 1 dogs (controls) received isotonic NaCl (0.9%, 208 mOsm/l, 4 ml/kg) without aortic occlusion; group 2 underwent aortic occlusion and received isotonic NaCl (0.9%, 308 mOsm/l, 4 ml/kg): group 3 were occluded and received hypertonic NaCl (7.5%, 2400 mOsm/l, 4 ml/kg); group 4 were occluded and received hypertonic sodium acetate (10.5%, 2400 mOsm/l, 4 ml/kg). There were no significant differences between groups at basal measures and also after 30 min of continuous bleeding, when animals presented with severe shock, and significant decreases in mean arterial pressure, cardiac index, systolic index and cardiac filling pressures; the systemic vascular resistance index was increased. Control animals remained in severe shock throughout the experiment and three died. The recovery of mean arterial pressure in aortic-occluded dogs given isotonic NaCl was associated with a marked increase in systemic vascular resistance index, without improvements in cardiac index, systolic index and cardiac filling pressures. In occluded dogs given hypertonic NaCl and NaAc the mean arterial pressure recovery lasted longer, with lower increases in systemic vascular resistance index, while the cardiac index, systolic index and cardiac filling pressures showed a marked albeit transient increase. Injection of hypertonic saline following aortic occlusion produced significantly better hemodynamic profiles and should be seriously considered for the first treatment in severe uncontrolled hemorrhagic shock from an abdominal vascular source.