Severity: Warning
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Filename: helpers/my_audit_helper.php
Line Number: 197
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 197
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
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Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
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Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
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Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
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Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
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Function: require_once
Objective: This study was performed to evaluate the effects of 0.9% saline (SAL), 0.9% saline + sodium bicarbonate + mannitol (SAL/BIC/MAN), and hypertonic saline-dextran (HSD) on hemodynamic variables, tissue blood flow, and oxidant injuries in experimental traumatic rhabdomyolysis (TR) in rats subjected allogeneic muscle extract infusion.
Design: Prospective, randomized, experimental.
Setting: Physiology experiment laboratory.
Subjects: Male Sprague-Dawley rats, weighing 250-300 g.
Interventions: All groups (n = 8 each) underwent femoral artery and vein catheterization. The animals in the TR, SAL, SAL/BIC/MAN, and HSD groups received an infusion of 2 mL of autologous muscle extract for 60 mins. After autologous muscle extract infusion, the SAL and HSD groups received 30 mL/kg 0.9% saline for 30 mins or 4 mL/kg HSD for 5 mins, respectively. The SAL/BIC/MAN group received 30 mL/kg 0.9% saline for 30 mins plus a bolus of 1 g/kg mannitol and a bolus of 2 mEq/kg sodium bicarbonate diluted in 1 mL of saline. At 2 hrs of autologous muscle extract infusion, erythrocyte flows in liver and kidney were measured by using a laser Doppler flowmeter. Then, blood samples and kidney and liver biopsies were taken to measure levels of glutathione and malondialdehyde.
Measurements And Main Results: TR caused decreases in mean arterial pressure, tissue blood flow, and tissue glutathione and an increase in malondialdehyde. Rats in the HSD group had significant metabolic acidosis. SAL resuscitation did not correct tissue blood flow and prevent oxidant injury. HSD increased tissue blood flow, mean arterial pressure, and liver and kidney glutathione and decreased serum, liver, and kidney malondialdehyde. SAL/BIC/MAN resuscitation corrected all oxidant damage variables but did not increase tissue blood flow. SAL/BIC/MAN preserved serum malondialdehyde and liver glutathione better than the HSD did.
Conclusions: HSD prevented oxidant injury and restored tissue blood flow but increased metabolic acidosis that followed autologous muscle extract infusion. SAL/BIC/MAN seems to be more effective than HSD in decreasing oxidant injury. Further research on the effects of the solute overload and metabolic acidosis due to HSD resuscitation on renal function in experimental rhabdomyolysis is warranted.
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http://dx.doi.org/10.1097/01.ccm.0000186767.67870.8c | DOI Listing |
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