The Retrograde Ventriculosinusal Shunt in an Animal Experimental Model of Hydrocephalus.

Currently, hydrocephalus treatment is performed mainly with ventriculoperitoneal shunting. This experimental study aims at assessing whether the experimental model of hydrocephalus in dogs is applicable to the laboratory study of the retrograde ventriculosinusal shunt (RVSS). Four mongrel dogs were assessed. After randomization, the animals were divided into two groups: an experimental group that underwent the induction of hydrocephalus/RVSS and a control group, for the measurement of the mean arterial pressure, intracranial pressure and pressure in the superior sagittal sinus (SSS). The controls presented a mean arterial pressure of 68 mm Hg (71 and 65), an intracranial pressure of 163 mm H2O (149.6 and 176.8) and a pressure at the SSS of 40 mm H2O (40 and 40). The kaolin injection into the cisterna magna at a concentration of 0.3 mg/ml was capable of inducing the clinical and radiological mechanism of hydrocephalus (intracranial pressure = 250 mm H2O, pressure at the SSS = 50 mm H2O). The caliber of the SSS was 2.5 ± 1.0 mm. The fact that the SSS caliber of the dog was the same size as the external diameter of the catheter used resulted in the complete obstruction of the SSS when the catheter was inserted. We believe we could design and perform an experimental model to test the RVSS. It is applicable and feasible. The model of hydrocephalus, the surgical apparatus and the scenario were adequate, but the shunt system needs to be proportionally made to the canine anatomy.

Local and remote ischemic preconditioning protect against intestinal ischemic/reperfusion injury after supraceliac aortic clamping

OBJECTIVES: This study tests the hypothesis that local or remote ischemic preconditioning may protect the intestinal mucosa against ischemia and reperfusion injuries resulting from temporary supraceliac aortic clamping. METHODS: Twenty-eight Wistar rats were divided into four groups: the sham surgery group, the supraceliac aortic occlusion group, the local ischemic preconditioning prior to supraceliac aortic occlusion group, and the remote ischemic preconditioning prior to supraceliac aortic occlusion group. Tissue samples from the small bowel were used for quantitative morphometric analysis of mucosal injury, and blood samples were collected for laboratory analyses. RESULTS: Supraceliac aortic occlusion decreased intestinal mucosal length by reducing villous height and elevated serum lactic dehydrogenase and lactate levels. Both local and remote ischemic preconditioning mitigated these histopathological and laboratory changes. CONCLUSIONS: Both local and remote ischemic preconditioning protect intestinal mucosa against ischemia and reperfusion injury following supraceliac aortic clamping. .

Local and remote ischemic preconditioning protect against intestinal ischemic/reperfusion injury after supraceliac aortic clamping.

OBJECTIVES: This study tests the hypothesis that local or remote ischemic preconditioning may protect the intestinal mucosa against ischemia and reperfusion injuries resulting from temporary supraceliac aortic clamping. METHODS: Twenty-eight Wistar rats were divided into four groups: the sham surgery group, the supraceliac aortic occlusion group, the local ischemic preconditioning prior to supraceliac aortic occlusion group, and the remote ischemic preconditioning prior to supraceliac aortic occlusion group. Tissue samples from the small bowel were used for quantitative morphometric analysis of mucosal injury, and blood samples were collected for laboratory analyses. RESULTS: Supraceliac aortic occlusion decreased intestinal mucosal length by reducing villous height and elevated serum lactic dehydrogenase and lactate levels. Both local and remote ischemic preconditioning mitigated these histopathological and laboratory changes. CONCLUSIONS: Both local and remote ischemic preconditioning protect intestinal mucosa against ischemia and reperfusion injury following supraceliac aortic clamping.

Entrapped victims in motor vehicle collisions: characteristics and prehospital care in the city of São Paulo, Brazil.

OBJECTIVE: To examine the severity of trauma in entrapped victims and to identify risk factors for mortality and morbidity. INTRODUCTION: Triage and rapid assessment of trauma severity is essential to provide the needed resources during prehospital and hospital phases and for outcome prediction. It is expected that entrapped victims will have greater severity of trauma and mortality than non-entrapped subjects. METHODS: A transverse, case-control, retrospective study of 1203 victims of motor vehicle collisions treated during 1 year by the prehospital service in São Paulo, Brazil was carried out. All patients were drivers, comprising 401 entrapped victims (33.3%) and 802 non-entrapped consecutive controls (66.7%). Sex, age, mortality rates, Glasgow Coma Scale (GCS), Revised Trauma Score (RTS), corporal segments, timing of the prehospital care and resource use were compared between the groups. The results were analysed by χ², Zres, analysis of variance and Bonferroni tests. RESULTS: Entrapped victims were predominantly men (84.8%), aged 32 ± 13.1 years, with immediate mortality of 10.2% and overall mortality of 11.7%. They had a probability of death at the scene 8.2 times greater than that of non-entrapped victims. The main cause of death was hemorrhage for entrapped victims (45.2%) and trauma for non-entrapped victims. Of the entrapped victims who survived, 18.7% had a severe GCS (OR = 10.62), 12% a severe RTS (OR = 9.78) and 23.7% were in shock (OR = 3.38). Entrapped victims were more commonly transported to advanced life support units and to tertiary hospitals. CONCLUSION: Entrapped victims had greater trauma severity, more blood loss and a greater mortality than respective, non-entrapped controls.

Entrapped victims in motor vehicle collisions: characteristics and prehospital care in the city of São Paulo, Brazil

OBJECTIVE: To examine the severity of trauma in entrapped victims and to identify risk factors for mortality and morbidity. INTRODUCTION: Triage and rapid assessment of trauma severity is essential to provide the needed resources during prehospital and hospital phases and for outcome prediction. It is expected that entrapped victims will have greater severity of trauma and mortality than non-entrapped subjects. METHODS: A transverse, case-control, retrospective study of 1203 victims of motor vehicle collisions treated during 1 year by the prehospital service in São Paulo, Brazil was carried out. All patients were drivers, comprising 401 entrapped victims (33.3 percent) and 802 non-entrapped consecutive controls (66.7 percent). Sex, age, mortality rates, Glasgow Coma Scale (GCS), Revised Trauma Score (RTS), corporal segments, timing of the prehospital care and resource use were compared between the groups. The results were analysed by χ2, Zres, analysis of variance and Bonferroni tests. RESULTS: Entrapped victims were predominantly men (84.8 percent), aged 32±13.1 years, with immediate mortality of 10.2 percent and overall mortality of 11.7 percent. They had a probability of death at the scene 8.2 times greater than that of non-entrapped victims. The main cause of death was hemorrhage for entrapped victims (45.2 percent) and trauma for non-entrapped victims. Of the entrapped victims who survived, 18.7 percent had a severe GCS (OR = 10.62), 12 percent a severe RTS (OR = 9.78) and 23.7 percent were in shock (OR = 3.38). Entrapped victims were more commonly transported to advanced life support units and to tertiary hospitals. CONCLUSION: Entrapped victims had greater trauma severity, more blood loss and a greater mortality than respective, non-entrapped controls.

Microcirculatory effects of local and remote ischemic preconditioning in supraceliac aortic clamping.

INTRODUCTION: Supraceliac aortic clamping in major vascular procedures promotes splanchnic ischemia and reperfusion (I/R) injury that may induce endothelial dysfunction, widespread inflammation, multiorgan dysfunction, and death. We tested the hypothesis that local or remote ischemic preconditioning (IPC) may be protective against injury after supraceliac aortic clamping through the modulation of mesenteric leukocyte-endothelial interactions, as evaluated with intravital microscopy and expression of adhesion molecules. METHODS: Fifty-six male Wistar rats (weight, 190 to 250 g), were divided into four groups of 14 rats each: control-sham surgery without aortic occlusion; I/R through supraceliac aortic occlusion for 20 minutes, followed by 120 minutes of reperfusion; local IPC through supraceliac aortic occlusion for two cycles of 5 minutes of ischemia and 5 minutes of reperfusion, followed by the same protocol of the IR group; remote IPC through infrarenal aortic occlusion for two cycles of 10 minutes of ischemia and 10 minutes of reperfusion, followed by the same protocol of the IR group. Seven animals per group were used to evaluate in vivo leukocyte-endothelial interactions in postcapillary venules with intravital microscopy and another seven animals per group were used to collect mesentery samples for immunohistochemistry demonstration of adhesion molecules expression. RESULTS: Supraceliac aortic occlusion increased the number of rolling leukocytes with slower velocities and increased the number of adherent leukocytes to the venular surface and leukocyte migration to the interstitium. The expression of P-selectin, E-selectin, and intercellular adhesion molecule-1 was also increased significantly after I/R. Local or remote IPC reduced the leukocyte recruitment in vivo and normalized the expression of adhesion molecules. CONCLUSIONS: Local or remote IPC reduces endothelial dysfunction on mesenteric microcirculation caused by I/R injury after supraceliac aortic clamping.

Vasodilation increases pulse pressure variation, mimicking hypovolemic status in rabbits.

OBJECTIVE: To test the hypothesis that pulse pressure respiratory variation (PPV) amplification, observed in hypovolemia, can also be observed during sodium nitroprusside (SNP)-induced vasodilation. INTRODUCTION: PPV is largely used for early identification of cardiac responsiveness, especially when hypovolemia is suspected. PPV results from respiratory variation in transpulmonary blood flow and reflects the left ventricular preload variations during respiratory cycles. Any factor that decreases left ventricular preload can be associated with PPV amplification, as seen in hypovolemia. METHODS: Ten anesthetized and mechanically ventilated rabbits underwent progressive hypotension by either controlled hemorrhage (Group 1) or intravenous SNP infusion (Group 2). Animals in Group 1 (n = 5) had graded hemorrhage induced at 10% steps until 50% of the total volume was bled. Mean arterial pressure (MAP) steps were registered and assumed as pressure targets to be reached in Group 2. Group 2 (n = 5) was subjected to a progressive SNP infusion to reach similar pressure targets as those defined in Group 1. Heart rate (HR), systolic pressure variation (SPV) and PPV were measured at each MAP step, and the values were compared between the groups. RESULTS: SPV and PPV were similar between the experimental models in all steps (p > 0.16). SPV increased earlier in Group 2. CONCLUSION: Both pharmacologic vasodilation and graded hemorrhage induced PPV amplification similar to that observed in hypovolemia, reinforcing the idea that amplified arterial pressure variation does not necessarily represent hypovolemic status but rather potential cardiovascular responsiveness to fluid infusion.

Vasodilation increases pulse pressure variation, mimicking hypovolemic status in rabbits

OBJECTIVE: To test the hypothesis that pulse pressure respiratory variation (PPV) amplification, observed in hypovolemia, can also be observed during sodium nitroprusside (SNP)-induced vasodilation. INTRODUCTION: PPV is largely used for early identification of cardiac responsiveness, especially when hypovolemia is suspected. PPV results from respiratory variation in transpulmonary blood flow and reflects the left ventricular preload variations during respiratory cycles. Any factor that decreases left ventricular preload can be associated with PPV amplification, as seen in hypovolemia. METHODS: Ten anesthetized and mechanically ventilated rabbits underwent progressive hypotension by either controlled hemorrhage (Group 1) or intravenous SNP infusion (Group 2). Animals in Group 1 (n = 5) had graded hemorrhage induced at 10 percent steps until 50 percent of the total volume was bled. Mean arterial pressure (MAP) steps were registered and assumed as pressure targets to be reached in Group 2. Group 2 (n = 5) was subjected to a progressive SNP infusion to reach similar pressure targets as those defined in Group 1. Heart rate (HR), systolic pressure variation (SPV) and PPV were measured at each MAP step, and the values were compared between the groups. RESULTS: SPV and PPV were similar between the experimental models in all steps (p > 0.16). SPV increased earlier in Group 2. CONCLUSION: Both pharmacologic vasodilation and graded hemorrhage induced PPV amplification similar to that observed in hypovolemia, reinforcing the idea that amplified arterial pressure variation does not necessarily represent hypovolemic status but rather potential cardiovascular responsiveness to fluid infusion.

Pulse pressure respiratory variation as an 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.

Low hematocrit impairs gastric mucosal CO2 removal during experimental severe normovolemic hemodilution.

OBJECTIVE: The net effects of acute normovolemic hemodilution with different hemoglobin levels on splanchnic perfusion have not been elucidated. The hypothesis that during moderate and severe normovolemic hemodilution, systemic and splanchnic hemodynamic parameters, oxygen-derived variables, and biochemical markers of anaerobic metabolism do not reflect the adequacy of gastric mucosa, was tested in this study. METHODS: Twenty one anesthetized mongrel dogs (16 +/- 1 kg) were randomized to controls (CT, n = 7, no hemodilution), moderate hemodilution (hematocrit 2 5% +/- 3%, n = 7) or severe hemodilution (severe hemodilution, hematocrit 15% +/- 3%, n = 7), through an isovolemic exchange of whole blood and 6% hydroxyethyl starch, at a 20 mL/min rate, to the target hematocrit. The animals were followed for 120 min after hemodilution. Cardiac output (CO, L/min), portal vein blood flow (PVF, mL/min), portal vein-arterial and gastric mucosa-arterial CO2 gradients (PV-artCO2 and PCO2 gap, mm Hg, respectively) were measured throughout the experiment. RESULTS: Exchange blood volumes were 33.9 +/- 3.3 and 61.5 +/- 5.8 mL/kg for moderate hemodilution and severe hemodilution, respectively. Arterial pressure and systemic and regional lactate levels remained stable in all groups. There were initial increases in cardiac output and portal vein blood flow in both moderate hemodilution and severe hemodilution; systemic and regional oxygen consumption remained stable largely due to increases in oxygen extraction rate. There was a significant increase in the PCO2-gap value only in severe hemodilution animals. CONCLUSION: Global and regional hemodynamic stability were maintained after moderate and severe hemodilution. However, a very low hematocrit induced gastric mucosal acidosis, suggesting that gastric mucosal CO2 monitoring may be useful during major surgery or following trauma.

Leukocyte-endothelium interactions after hemorrhagic shock/reperfusion and cecal ligation/puncture: an intravital microscopic study in rat mesentery.

Hemorrhagic shock/reperfusion (HS/R) followed by sepsis triggers systemic microcirculatory disturbances that may induce multiple organ failure. The present study evaluated the effects of HS/R and cecal ligation and puncture, followed by necrotic cecal resection/peritoneal lavage (REL) on leukocyte-endothelium interactions at the mesentery. Eighty-one anesthetized Wistar rats (200-250 g) were randomly assigned to a first injury: (1) control-HS-no hemorrhagic shock/no reperfusion group, (2) HS/blood-HS/R with 25% shed blood, and (3) HS/blood + LR-HS/R with 25% of the shed blood + lactated Ringer's solution, 3x shed blood volume. Twenty-four hours post-HS/R, animals were submitted to cecal ligation and puncture and, 24 h thereafter, to REL. Leukocyte-endothelium interactions were assessed by intravital microscopy and intercellular adhesion molecule (ICAM) 1 and P-selectin expression by immunohistochemistry. Lungs were observed for ICAM-1 expression and neutrophil infiltration. Single and double injury induced significant increases in rolling (approximately 2-fold), adherent (approximately 5-fold), and migrated leukocytes (approximately 7-fold); ICAM-1 expression (approximately 1/2-fold), and P-selectin expression (approximately 1/2-fold) at the mesentery compared with control-HS group. REL normalized leukocyte-endothelium interactions at the mesentery in single-injured animals. However, in double-injured rats, adherence and migration of leukocytes decreased but did not normalize. Similar results were observed on ICAM-1 expression and neutrophil infiltration in the lungs from these animals. In conclusion, the current in vivo observation of the mesenteric microcirculation after a double injury followed by REL is a suitable model for the systematic evaluation of the inflammatory reaction at local and distant sites. In addition, data presented herein emphasized the importance of surgical removal of the septic focus in controlling the otherwise lethal sepsis-induced multiple organ dysfunction syndrome.

Ischemic preconditioning prevents apoptotic cell death and necrosis in early and intermediate phases of liver ischemia-reperfusion injury in rats.

Ischemic preconditioning (IPC) may be useful in attenuating the hepatic ischemia reperfusion (IR) syndrome by means of improving cell resistance to anoxia and reoxygenation and preventing cell death. Since there are insufficient data available regarding the chronology of preconditioning effects, we investigated the role of IPC, to test the hypothesis that liver protection would occur during the early and intermediate phases of the reperfusion period. Wistar rats (n = 72) were randomly assigned into six experimental groups, 12 animals each. A 40-min ischemia to the left lateral and median liver lobes was induced by selective hepatic pedicle clamping followed by 30 min or 240 min of reperfusion (IR30 and IR240). IPC groups (IPC30 and IPC240) underwent a 10 min of ischemia followed by 10 min of reperfusion preceding the definitive 40-min ischemic period. Sham-operated animals were followed for 30 and 240 min. Hepatic enzymes and histological evaluation were performed after the reperfusion period. Hepatic ischemia-reperfusion (IR30 and IR240) induced marked increases in liver enzymes levels after 30 min and particularly after 240 min. IPC effectively attenuated those enzymatic increases. Microvesicular steatosis was observed after 30 min, but not 240 min, of reperfusion in both IPC and IR livers. Necrosis was detected in 66.7% of IR240 and only in 8.3% of IPC240. Both hepatocyte and sinusoidal apoptosis were markedly attenuated by IPC. We conclude that IPC provided protection against hepatic ischemia reperfusion injury in early and intermediate phases of the reperfusion period, reducing hepatic enzymatic leakage and ameliorating hepatic apoptosis and necrosis.

Small volume of hypertonic saline as the initial fluid replacement in experimental hypodynamic sepsis.

INTRODUCTION: We conducted the present study to examine the effects of hypertonic saline solution (7.5%) on cardiovascular function and splanchnic perfusion in experimental sepsis. METHODS: Anesthetized and mechanically ventilated mongrel dogs received an intravenous infusion of live Escherichia coli over 30 minutes. After 30 minutes, they were randomized to receive lactated Ringer's solution 32 ml/kg (LR; n = 7) over 30 minutes or 7.5% hypertonic saline solution 4 ml/kg (HS; n = 8) over 5 minutes. They were observed without additional interventions for 120 minutes. Cardiac output (CO), mean arterial pressure (MAP), portal and renal blood flow (PBF and RBF, respectively), gastric partial pressure of CO2 (pCO2; gas tonometry), blood gases and lactate levels were assessed. RESULTS: E. coli infusion promoted significant reductions in CO, MAP, PBF and RBF (approximately 45%, 12%, 45% and 25%, respectively) accompanied by an increase in lactate levels and systemic and mesenteric oxygen extraction (sO2ER and mO2ER). Widening of venous-arterial (approximately 15 mmHg), portal-arterial (approximately 18 mmHg) and gastric mucosal-arterial (approximately 55 mmHg) pCO2 gradients were also observed. LR and HS infusion transiently improved systemic and regional blood flow. However, HS infusion was associated with a significant and sustained reduction of systemic (18 +/- 2.6 versus 38 +/- 5.9%) and mesenteric oxygen extraction (18.5 +/- 1.9 versus 36.5 +/- 5.4%), without worsening other perfusional markers. CONCLUSION: A large volume of LR or a small volume of HS promoted similar transient hemodynamic benefits in this sepsis model. However, a single bolus of HS did promote sustained reduction of systemic and mesenteric oxygen extraction, suggesting that hypertonic saline solution could be used as a salutary intervention during fluid resuscitation in septic patients.

Outcome after surgical repair of sealed rupture abdominal aortic aneurysms: a case-control study.

OBJECTIVE: To establish, in a case-control study, the early mortality and long-term survival after surgical correction of sealed rupture abdominal aortic aneurysm, compared to controls who underwent standard, nonruptured abdominal aortic aneurysm repair. PATIENTS AND METHODS: From January 1992 to December 2002, 465 patients underwent infrarenal abdominal aortic aneurysm repair. Of those, 13 had sealed rupture abdominal aortic aneurysm (2.8%). These cases were compared to 26 controlsin which surgical repair was performed immediately preceding or succeeding each one of the sealed rupture abdominal aortic aneurysm surgeries. RESULTS: Age, sex, risk factors for atherosclerosis, associated disease, and cardiac ischemia were similar between groups. Patients with sealed rupture abdominal aortic aneurysm presented a higher incidence of lumbar pain than controls (92.3% versus 3.9%; P < .001); fever and weight loss were detected in 5 (38.5%) patients with SAAA and in none of controls (P = .0022). Mean red blood cell transfusion was greater for sealed rupture abdominal aortic aneurysm than controls (1,516 +/- 697 vs. 773 +/- 463 mL (P = .0003). Postoperative complications were similar between groups. Early mortality was 7.7% for sealed rupture abdominal aortic aneurysm and 0% for controls. Five-year survival was significantly lower for sealed rupture abdominal aortic aneurysm (68.4%) than for controls (84.4%, P = .04). CONCLUSION: We conclude that sealed rupture abdominal aortic aneurysm presents diagnostic and surgical challenges that can be adequately managed, achieving early postoperative mortality and complication rates that are similar to standard abdominal aortic aneurysm. However, patients with sealed rupture abdominal aortic aneurysm present higher mortality in the long term compared with patients having standard abdominal aortic aneurysm.

Sustained gastric mucosal acidosis after hemorrhage in spite of rapid hemodynamic restoration with blood or hypertonic/hyperoncotic solution.

Splanchnic hypoperfusion has been implicated as the motor of multiple organ dysfunction. Hypertonic saline has shown to benefit microcirculatory blood flow. In hemorrhaged animals, we tested the hypothesis that small-volume 3% NaCl/10% dextran 40 (3%HSD) promotes global and regional improvements, including gastric mucosal acidosis reversal. Seventeen dogs (18.8 +/- 1.2 kg) were bled (20 mL/min) to a mean arterial pressure of 40-45 mm Hg, which was maintained at these levels for 15 min. They were randomly assigned to two groups: Blood (n = 9), total shed blood retransfused at 40 mL/min; or a 4-min bolus injection of 3%HSD (n = 8), in a volume equivalent to 25% of total shed blood. All animals were followed for 30 min thereafter. Gastric mucosal PCO2 (gas tonometry), portal vein PCO2, superior mesenteric artery blood flow (SMA, ultrasonic flowprobes), and systemic and regional O2-derived variables were evaluated throughout the protocol. Hemorrhage induced significant reductions of arterial pressure, cardiac output, and SMA blood flow, while portal-arterial and gastric-arterial PCO2 gradients increased. Total shed blood transfusion, as well as 3%HSD bolus injection, promptly restored all parameters, except for the increased gastric-arterial PCO2 gradient. We conclude that persistent gastric mucosal acidosis cannot be adequately predicted by global and splanchnic O2 derived variables in following hemorrhage and resuscitation with total shed blood transfusion or small-volume hypertonic-hyperoncotic solution.