Original Article - Basic Research Archives - Critical Care Science (CCS)
Abstract
Rev Bras Ter Intensiva. 2012;24(4):326-333
DOI 10.1590/S0103-507X2012000400006
OBJECTIVE: Liver failure can occur as a consequence of the systemic inflammation after acute pancreatitis. We assessed the effect of volume repositioning with hypertonic saline solution or normal saline on hepatic cytokine production and the expression of heat-shock proteins and apoptotic proteins after acute pancreatitis. METHODS: Wistar rats were divided in four groups: C - control animals that were not subjected to insult or treatment; NT - animals that were subjected to acute pancreatitis and received no treatment; normal saline - animals that were subjected to acute pancreatitis and received normal saline (NaCl 0.9%); and HS - animals that were subjected to acute pancreatitis and received hypertonic saline solution (NaCl 7.5%). Acute pancreatitis was induced by retrograde transduodenal infusion of 2.5% sodium taurocholate into the pancreatic duct. At 4, 12 and 24 h following acute pancreatitis induction, TNF-alpha, IL-1-beta, IL-6 and IL-10, caspase-2 and -7, Apaf-1, AIF and HSP60 and 90 were analyzed in the liver. RESULTS: Casp2 decreased in the normal saline and hypertonic saline groups (p<0.05 versus. C) at 12 h. Apaf-1, AIF and HSP90 remained unchanged. At 4 h, Casp7 increased in the NT group (p<0.01 versus C), although it remained at the baseline levels in the reperfused groups. HSP60 increased in all of the groups at 4 h (p< 0.001 vs. C). However, the hypertonic saline group showed lower expression of HSP60 than the normal saline group (p<0.05). Hypertonic saline solution maintained the production of cytokines at normal levels. Volume reperfusion with normal or hypertonic saline significantly modulated the expression of Casp7. CONCLUSION: Volume replacement with hypertonic or normal saline was effective in reducing caspase 7. However, only hypertonic solution was capable of regulating cytokine production and HSP60 expression at all time points.
Abstract
Rev Bras Ter Intensiva. 2012;24(4):326-333
DOI 10.1590/S0103-507X2012000400006
OBJECTIVE: Liver failure can occur as a consequence of the systemic inflammation after acute pancreatitis. We assessed the effect of volume repositioning with hypertonic saline solution or normal saline on hepatic cytokine production and the expression of heat-shock proteins and apoptotic proteins after acute pancreatitis. METHODS: Wistar rats were divided in four groups: C - control animals that were not subjected to insult or treatment; NT - animals that were subjected to acute pancreatitis and received no treatment; normal saline - animals that were subjected to acute pancreatitis and received normal saline (NaCl 0.9%); and HS - animals that were subjected to acute pancreatitis and received hypertonic saline solution (NaCl 7.5%). Acute pancreatitis was induced by retrograde transduodenal infusion of 2.5% sodium taurocholate into the pancreatic duct. At 4, 12 and 24 h following acute pancreatitis induction, TNF-alpha, IL-1-beta, IL-6 and IL-10, caspase-2 and -7, Apaf-1, AIF and HSP60 and 90 were analyzed in the liver. RESULTS: Casp2 decreased in the normal saline and hypertonic saline groups (p<0.05 versus. C) at 12 h. Apaf-1, AIF and HSP90 remained unchanged. At 4 h, Casp7 increased in the NT group (p<0.01 versus C), although it remained at the baseline levels in the reperfused groups. HSP60 increased in all of the groups at 4 h (p< 0.001 vs. C). However, the hypertonic saline group showed lower expression of HSP60 than the normal saline group (p<0.05). Hypertonic saline solution maintained the production of cytokines at normal levels. Volume reperfusion with normal or hypertonic saline significantly modulated the expression of Casp7. CONCLUSION: Volume replacement with hypertonic or normal saline was effective in reducing caspase 7. However, only hypertonic solution was capable of regulating cytokine production and HSP60 expression at all time points.
Abstract
Rev Bras Ter Intensiva. 2012;24(3):219-223
DOI 10.1590/S0103-507X2012000300003
OBJECTIVE: Antioxidants are widely used in animal models to prevent renal injury after ischemia/reperfusion, but it is unknown if the benefits of antioxidants are additive. In this study, we aimed to investigate the protective effects of N-acetylcysteine plus deferoxamine in an animal model of kidney ischemia/reperfusion injury. METHODS: Bilateral kidney ischemia was mastintained for 45 minutes. N-acetylcysteine, deferoxamine or both were administered into the aorta above the renal arteries immediately prior to induction of ischemia. Five rats from each group were sacrificed 1, 6 or 12 hours after reperfusion for the determination of blood creatinine, kidney oxidative damage parameters and myeloperoxidase activity. RESULTS: The combination of N-acetylcysteine and deferoxamine, but not their isolated use, prevented the increase in creatinine after ischemia/reperfusion. This prevention was followed by a consistent decrease in myeloperoxidase activity and oxidative damage parameters both in the kidney cortex and medulla. CONCLUSION: Treatment with N-acetylcysteine and deferoxamine was superior to the isolated use of either compound in an animal model of kidney ischemia/reperfusion.
Abstract
Rev Bras Ter Intensiva. 2012;24(3):219-223
DOI 10.1590/S0103-507X2012000300003
OBJECTIVE: Antioxidants are widely used in animal models to prevent renal injury after ischemia/reperfusion, but it is unknown if the benefits of antioxidants are additive. In this study, we aimed to investigate the protective effects of N-acetylcysteine plus deferoxamine in an animal model of kidney ischemia/reperfusion injury. METHODS: Bilateral kidney ischemia was mastintained for 45 minutes. N-acetylcysteine, deferoxamine or both were administered into the aorta above the renal arteries immediately prior to induction of ischemia. Five rats from each group were sacrificed 1, 6 or 12 hours after reperfusion for the determination of blood creatinine, kidney oxidative damage parameters and myeloperoxidase activity. RESULTS: The combination of N-acetylcysteine and deferoxamine, but not their isolated use, prevented the increase in creatinine after ischemia/reperfusion. This prevention was followed by a consistent decrease in myeloperoxidase activity and oxidative damage parameters both in the kidney cortex and medulla. CONCLUSION: Treatment with N-acetylcysteine and deferoxamine was superior to the isolated use of either compound in an animal model of kidney ischemia/reperfusion.
Abstract
Rev Bras Ter Intensiva. 2011;23(3):283-290
DOI 10.1590/S0103-507X2011000300005
OBJECTIVES: Although fluid resuscitation guided by central venous oxygen saturation (SvcO2) is currently considered the gold standard in sepsis therapy, few studies have described hemodynamic and perfusion parameters during this procedure. This study aims to describe these parameters during septic shock without resuscitation and after 12 hours of goal-directed resuscitation. METHODS: Thirteen anesthetized pigs (35-45 kg) had peritonitis caused by fecal inoculation (0.75 g/kg). After developing persistent hypotension, both groups were given antibiotics and randomized either to the control group (n=7) or the experimental group (n=6). In the control group, hemodynamic control was optimized to maintain a central venous pressure of 8-12 mmHg, a urinary output above 0.5 mL/kg/hour and a mean arterial blood pressure above 65 mmHg. The experimental group received the above target therapy in addition to maintaining a SvO2 above 65%. The interventions included lactated Ringer's solution and norepinephrine for both groups and dobutamine in the SvO2 group. The animals were treated for 12 hours or until death. RESULTS: Untreated sepsis was associated with significant reductions in SvO2, PvO2, cardiac output and central venous pressure in addition to increased arteriovenous oxygen saturation and veno-arterial CO2 differences. Following resuscitation, these parameters were corrected in both groups. Goal-directed resuscitation was associated with a better hemodynamic profile, characterized by higher SvO2, cardiac output and central venous pressure. CONCLUSIONS: Non-resuscitated sepsis showed a hemodynamic profile suggesting hypovolemia, with worsened perfusion and hemodynamics, which is reversed upon fluid resuscitation. Goal-directed resuscitation is associated with significantly improved hemodynamic and perfusion parameters
Abstract
Rev Bras Ter Intensiva. 2011;23(3):283-290
DOI 10.1590/S0103-507X2011000300005
OBJECTIVES: Although fluid resuscitation guided by central venous oxygen saturation (SvcO2) is currently considered the gold standard in sepsis therapy, few studies have described hemodynamic and perfusion parameters during this procedure. This study aims to describe these parameters during septic shock without resuscitation and after 12 hours of goal-directed resuscitation. METHODS: Thirteen anesthetized pigs (35-45 kg) had peritonitis caused by fecal inoculation (0.75 g/kg). After developing persistent hypotension, both groups were given antibiotics and randomized either to the control group (n=7) or the experimental group (n=6). In the control group, hemodynamic control was optimized to maintain a central venous pressure of 8-12 mmHg, a urinary output above 0.5 mL/kg/hour and a mean arterial blood pressure above 65 mmHg. The experimental group received the above target therapy in addition to maintaining a SvO2 above 65%. The interventions included lactated Ringer's solution and norepinephrine for both groups and dobutamine in the SvO2 group. The animals were treated for 12 hours or until death. RESULTS: Untreated sepsis was associated with significant reductions in SvO2, PvO2, cardiac output and central venous pressure in addition to increased arteriovenous oxygen saturation and veno-arterial CO2 differences. Following resuscitation, these parameters were corrected in both groups. Goal-directed resuscitation was associated with a better hemodynamic profile, characterized by higher SvO2, cardiac output and central venous pressure. CONCLUSIONS: Non-resuscitated sepsis showed a hemodynamic profile suggesting hypovolemia, with worsened perfusion and hemodynamics, which is reversed upon fluid resuscitation. Goal-directed resuscitation is associated with significantly improved hemodynamic and perfusion parameters
