Methods: Sixty-six severe TBI patients who required emergency craniotomy or craniectomy and were planned for post-operative ventilation were randomised into NS (n = 33) and BF therapy groups (n = 33). The calculation of maintenance fluid given was based on the Holliday-Segar method. The electrolytes and acid-base parameters were assessed at an 8 h interval for 24 h. The data were analysed using repeated measures ANOVA.
Results: The NS group showed a significant lower base excess (-3.20 versus -1.35, P = 0.049), lower bicarbonate level (22.03 versus 23.48 mmol/L, P = 0.031), and more hyperchloremia (115.12 versus 111.74 mmol/L, P < 0.001) and hypokalemia (3.36 versus 3.70 mmol/L, P < 0.001) than the BF group at 24 h of therapy. The BF group showed a significantly higher level of calcium (1.97 versus 1.79 mmol/L, P = 0.003) and magnesium (0.94 versus 0.80 mmol/L, P < 0.001) than the NS group at 24 h of fluid therapy. No significant differences were found in pH, pCO2, lactate, and sodium level.
Conclusion: BF therapy showed better effects in maintaining higher electrolyte parameters and reducing the trend toward hyperchloremic metabolic acidosis than the NS therapy during prolonged fluid therapy for postoperative TBI patients.
METHODS: Orchidectomized, adult male rats were given 125 and 250 μg/kg/day testosterone subcutaneously, with or without flutamide and finasteride for seven consecutive days. At the end of the treatment, rats were anesthetized and vas deferens were perfused. Changes in vas deferens fluid secretion rate, pH, HCO3-, Cl- and Na+ concentrations were recorded in the presence of amiloride and Cftr inh-172. Rats were then sacrificed and vas deferens were harvested and subjected for molecular biological analysis.
RESULTS: Testosterone treatment caused the fluid pH and HCO3- concentrations to decrease but secretion rate, Cl- and Na+ concentrations to increase, where upon amiloride administration, the pH and HCO3- concentration increased but Cl- and Na+ concentrations further increased. In testosterone-treated rats, administration of Cftr inh-172 caused all fluid parameters to decrease. In testosterone-treated rats co-administered with flutamide or finasteride, pH and HCO3- concentration increased but fluid secretion rate, Cl- and Na+ concentrations decreased and these parameters were not affected by amiloride or Cftr inh-172 administration. Under testosterone influence, CFTR and γ-ENaC were highly expressed at the apical membrane while NHE-1 and 4 were highly expressed at the basolateral membrane of vas deferens epithelium. Meanwhile, NHE-2 and 3 were highly expressed at the apical membrane.
CONCLUSIONS: Differential expression of ENaC, CFTR and NHE in vas deferens under testosterone influence indicated the important role of these transporters in creating optimal fluid microenvironment that is essential for preserving male fertility.