Early effects of 7.5% hypertonic saline solution on splanchnic perfusion after hemorrhagic shock

PURPOSE: To evaluate the effects of SSH resuscitation on systemic and splanchnic hemodynamic variables in an experimental model of controlled hemorrhagic shock. METHODS: Ten mongrel dogs were bled (20 ml/min) to a target mean arterial pressure (MAP) of 40±5 mmHg. After 30 minutes of shock, animals received SSH infused in 5-minute and they were observed for 60 minutes thereafter. Systemic hemodynamics were evaluated through a Swan-Ganz and arterial catheters while gastrointestinal tract perfusion by a catheter inside the portal vein, an ultrasonic flowprobe around portal vein blood flow (PVBF) and a gastric tonometer. Splanchnic oxygen delivery and consumption, intramucosal pH and veno-arterial, portal-arterial and mucosal-arterial pCO2-gradients (Dap-a pCO2, Dvp-a pCO2 e Dt-a pCO2, respectively) were assessed. RESULTS: Hemorrhage (29.8±2.4ml/Kg) induced significant decreases in MAP (125±6 to 42±1 mmHg), in CO (1.9±0.2 to 0.6±0.1 L/min), and PVBF (504±73 to 126±12 ml/min) while significant increases were detected in Dap-a pCO2 (5.3±0.8 to 19.9±1.6 mmHg) Dvp-a pCO2 (5.4±1.4 to 22.6±2.1 mmHg) and Dt-a pCO2 (6.1±1.1 to 43.8±7.5 mmHg). SSH infusion promoted only partial benefits in systemic and splanchnic blood flows. Reduced pCO2 gradients but fewer effects in Dt-a pCO2 were observed. CONCLUSION: The SSH infusion promoted partial systemic and splanchnic hemodynamic benefits. Those benefits were especially poor at the splanchnic microcirculation, as evaluated by Dt-a pCO2. In addition, systemic and regional oxygen-derived variables do not reflect the regional microcirculation disturbances. Gastrointestinal tonometry clearly represents a useful tool for monitoring splanchnic perfusion in patients in hemodynamic shock.OBJETIVO: Avaliar os efeitos hemodinâmicos sistêmicos e esplâncnico da expansão volêmica inicial com SSH em modelo de choque hemorrágico controlado. MÉTODOS: Dez cães foram submetidos a sangramento controlado (20 ml/min) até uma pressão arterial média de 40±5 mmHg (PAM). Após 30 minutos de choque, receberam 4 ml/Kg de SSH em 5 minutos e posteriormente observados sem intervenções adicionais durante 60 minutos. As variáveis hemodinâmicas sistêmicas foram obtidas de um cateter arterial e de um cateter de Swan-Ganz, enquanto as regionais através da cateterização da veia porta, fluxômetro ultrassônico na veia porta e um tonômetro na cavidade. A oferta, taxa de extração e consumo esplâncnico de oxigênio, pH intramucoso e os gradientes veno-arterial, porta-arterial e mucosa-arterial da pCO2 (Dap-a pCO2, Dvp-a pCO2 e Dt-a pCO2, respectivamente), foram calculados. RESULTADOS: A hemorragia (29,8±2,4 ml/Kg) reduziu a pressão arterial média (125±6 para 42±1 mmHg), o DC (1,9±0,2 para 0,6±0,1 L/min) e o fluxo porta (504±73 para 126±12 ml/min), enquanto elevou o Dap-a pCO2 (5,3±0,8 para 19,9±1,6 mmHg), Dvp-a pCO2 (5,4±1,4 para 22,6±2,1 mmHg) e o Dt-a pCO2 (6,1±1,1 para 43,8±7,5 mmHg). A infusão de SSH resultou em recuperação parcial dos fluxos sistêmico e porta. Atenuou os gradientes de CO2 com menor impacto sobre o Dt-a pCO2. CONCLUSÃO: A SSH promoveu benefícios parciais na perfusão sistêmica e esplâncnica, os quais foram especialmente limitados na microcirculação regional, como demonstrado pelo Dt-a pCO2. Além disso, as variáveis sistêmicas e regionais dependentes de oxigênio, não refletem a adequação da perfusão da mucosa gástrica, enfatizando a importância da monitorização deste território - pela tonometria - durante os estados de choque.USP FM InCorUNIFESP-EPM Depto. de CirurgiaUSP FM Depto. de CardiopneumologiaUNIFESP, EPM, Depto. de CirurgiaSciEL

The effects of hypertonic fluid administration on the gene expression of inflammatory mediators in circulating leucocytes in patients with septic shock: a preliminary study

Contains fulltext : 98426.pdf (publisher's version ) (Open Access)ABSTRACT: OBJECTIVE: This study was designed to investigate the effect of hypertonic fluid administration on inflammatory mediator gene expression in patients with septic shock. DESIGN AND SETTING: Prospective, randomized, controlled, double-blind clinical study in a 15-bed mixed intensive care unit in a tertiary referral teaching hospital. INTERVENTIONS: Twenty-four patients, who met standard criteria for septic shock, were randomized to receive a bolus of hypertonic fluid (HT, 250 ml 6% HES/7.2% NaCl) or isotonic fluid (IT, 500 ml 6% HES/0.9% NaCl) administered over 15 minutes. Randomization and study fluid administration was within 24 hours of ICU admission for all patients. This trial is registered with ANZCTR.org.au as ACTRN12607000259448. RESULTS: Blood samples were taken immediately before and 4, 8, 12, and 24 hours after fluid administration. Real-time reverse transcriptase polymerase chain reaction (RT rtPCR) was used to quantify mRNA expression of different inflammatory mediators in peripheral leukocytes. In the HT group, compared with the IT group, levels of gene expression of MMP9 and L-selectin were significantly suppressed (p = 0.0002 and p = 0.007, respectively), and CD11b gene expression tended to be elevated (p = NS). No differences were found in the other mediators examined. CONCLUSIONS: In septic shock patients, hypertonic fluid administration compared with isotonic fluid may modulate expression of genes that are implicated in leukocyte-endothelial interaction and capillary leakage.The study was performed at the Intensive Care Department, Waikato Hospital, and at the Molecular Genetics Laboratory, University of Waikato, Hamilton, New Zealand. TRIAL REGISTRATION: Australia and New Zealand Clinical Trials Register (ANZCTR): ACTRN12607000259448

Hypertonic saline reduces inflammation and enhances the resolution of oleic acid induced acute lung injury

<p>Abstract</p> <p>Background</p> <p>Hypertonic saline (HTS) reduces the severity of lung injury in ischemia-reperfusion, endotoxin-induced and ventilation-induced lung injury. However, the potential for HTS to modulate the resolution of lung injury is not known. We investigated the potential for hypertonic saline to modulate the evolution and resolution of oleic acid induced lung injury.</p> <p>Methods</p> <p>Adult male Sprague Dawley rats were used in all experiments. <b><it>Series 1 </it></b>examined the potential for HTS to reduce the severity of evolving oleic acid (OA) induced acute lung injury. Following intravenous OA administration, animals were randomized to receive isotonic (Control, n = 12) or hypertonic saline (HTS, n = 12), and the extent of lung injury assessed after 6 hours. <b><it>Series 2 </it></b>examined the potential for HTS to enhance the resolution of oleic acid (OA) induced acute lung injury. Following intravenous OA administration, animals were randomized to receive isotonic (Control, n = 6) or hypertonic saline (HTS, n = 6), and the extent of lung injury assessed after 6 hours.</p> <p>Results</p> <p>In <b><it>Series I</it></b>, HTS significantly reduced bronchoalveolar lavage (BAL) neutrophil count compared to Control [61.5 ± 9.08 versus 102.6 ± 11.89 × 10³ cells.ml^-1]. However, there were no between group differences with regard to: A-a O2 gradient [11.9 ± 0.5 vs. 12.0 ± 0.5 KPa]; arterial PO2; static lung compliance, or histologic injury. In contrast, in <b><it>Series 2</it></b>, hypertonic saline significantly reduced histologic injury and reduced BAL neutrophil count [24.5 ± 5.9 versus 46.8 ± 4.4 × 10³ cells.ml^-1], and interleukin-6 levels [681.9 ± 190.4 versus 1365.7 ± 246.8 pg.ml^-1].</p> <p>Conclusion</p> <p>These findings demonstrate, for the first time, the potential for HTS to reduce pulmonary inflammation and enhance the resolution of oleic acid induced lung injury.</p