Lf Poli de Figueiredo

Hypertonic acetate-ααhemoglobin 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.

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 Ringers 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.

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.

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.

Effects of hypertonic saline and lactated Ringer's solutions on bacterial translocation in a rat model of intestinal obstruction and ischemia

Clinical evidence suggests that bacterial translocation (BT) may not be the primary cause in the development of sepsis and multiple organ dysfunction. However, BT has an important role in the activation of the immune system. Therapies have been extensively investigated to improve tissue perfusion and reduce intestinal ischemia. The aim of this study is to evaluate the effects of hypertonic saline (HSS) 7.5% and lactated Ringers (LR) solutions on intestinal BT in rats that underwent intestinal obstruction and ischaemia (IO).

Early fluid replacement with hypertonic isoncotic solution guided by mixed venous oxygen saturation in experimental hypodynamic sepsis

Volume replacement is one of the cornerstones in the management of sepsis. The type and amount of fluid are still controversial.

PULSE PRESSURE RESPIRATORY VARIATION AS EARLY MARKER OF CARDIAC OUTPUT FALL IN EXPERIMENTAL HEMORRHAGIC SHOCK

Pulse pressure (DeltaPp) and systolic pressure (DeltaPs) variations have been recommended as predictors of fluid responsiveness in critically ill patients. We hypothesized that changes in DeltaPp and DeltaPs parallel alterations in stroke volume (SV) and cardiac output (CO) during hemorrhage, shock, and resuscitation. In anesthetized and mechanically ventilated mongrel dogs, a graded hemorrhage (20 mL/min) was induced to a target mean arterial pressure (MAP) of 40 mm Hg, which was maintained for additional 30 min. Total shed-blood volume was then retransfused at a 40 mL/min rate. CO, SV, right atrial pressure (RAP), pulmonary artery occlusion pressure (PAOP), and continuous mixed venous oxygen saturation (SvO(2)) were assessed. Both DeltaPp and DeltaPs were calculated from direct arterial pressure waveform. Removal of about 9% of estimated blood volume promoted a reduction in SV (14.8 +/- 2.2 to 10.6 +/- 1.3 mL, P < 0.05). At approximately 18% blood volume removal, significant changes in CO (2.4 +/- 0.2 to 1.5 +/- 0.2 mL/min, P < 0.05), DeltaPp (12.6 +/- 1.4 to 15.8 +/- 2.0%, P < 0.05), and SvO(2) (82 +/- 1.4 to 73 +/- 1.7%, P < 0.05) were observed. Alterations in MAP, RAP, PAOP, and DeltaPs could be detected only after each animal had lost over 36% of estimated initial blood volume. There was correlation between blood volume loss and SV, CO, and SvO(2), as well as between blood loss and MAP, DeltaPp, and DeltaPs. Blood volume loss showed no correlation with cardiac filling pressures. DeltaPp is a useful, early marker of SV and CO for the assessment of cardiac preload changes in hemorrhagic shock, while cardiac filling pressures are not.

Bone marrow cellularity after hemorrhagic shock and fluid resuscitation with hypertonic saline or lactated Ringer's solution

Qualitative alterations in the bone marrow morphology have been described after shock and fluid resuscitation. However, quantitative cellularity must also be addressed.

Is intestinal tonometry a reliable method to detect histological changes after small bowel transplantation

Postoperative complications after intestinal transplantation can be attributed to hypothermic storage and reperfusion injury. In this study, we sought to obtain evidence that intestinal pCO2 measurement can be a useful method for monitoring graft perfusion and early histological changes after small-bowel transplantation. Additionally, we evaluated the initial effects of isolated intestinal hypothermic perfusion (IHP) (at 4°C) on mucosal and serosal blood flow distribution, and we correlated these findings with other systemic and regional markers of mesenteric ischemia.

Intestinal blood flow and pCO2 gradients in arterial and venous mesenteric blood flow obstruction

In this study, we evaluated the systemic and regional pCO2 gradients changes induced by arterial and venous mesenteric blood flow obstruction. In addition, we sought to obtain evidence that systemic markers of splanchnic hypoperfusion can detect the initial changes after intestinal ischemia induced by arterial or venous blood flow interruption.