This study examined reflex mechanisms that mediate urinary bladder and external urethral sphincter (EUS) coordination in female Sprague-Dawley urethane-anesthetized rats under empty and distended bladder conditions. The bladder was distended either by a small balloon or a saline filled catheter inserted through the body of the bladder. Stimulation of the entire pudendal nerve elicited short latency (8-12 ms) responses in the EUS and short (3-8 ms) and long latency responses (16-20 ms) in contralateral pudendal nerve. The long latency pudendal-pudendal reflex was reduced by 36.7% in area during bladder distension with the balloon catheter. However, there was no significant change in the area of pudendal-EUS reflex during bladder distension. Peak amplitudes of both reflexes were reduced 32% by bladder distension. The effects of glutamatergic receptor antagonists on the reflexes were also examined. MK801 (0.3-5 mg/kg, i.v.), an N-methyl-D-aspartate glutamatergic receptor antagonist, markedly depressed the pudendal-pudendal reflex, but LY215490 (3 mg/kg, i.v.), an alpha-amino-5-methyl isoxazole-4-propionate antagonist, had a minimal inhibitory effect. Both glutamatergic receptor antagonists significantly suppressed the pudendal-EUS reflex. These results indicate that the EUS is innervated by multiple pathways and that glutamatergic excitatory transmission is important in the neural mechanisms underlying bladder-sphincter coordination in the rat.

Purpose: Intracranial pressure (ICP) control has long been recognized as an important requirement for traumatic brain injury (TBI) patients. Nevertheless, the long-term effect of hypertonic saline (HTS) remains unknown. The aim of this study was to elucidate the effect on clinical outcomes in TBI patients admitted to intensive care unit (ICU) settings.Methods: We retrospectively identified moderate to severe TBI patients from two public databases named Medical Information Mart for the Intensive Care (MIMIC)-IV and eICU Collaborative Research Database (eICU-CRD). A marginal structural Cox model (MSCM) was used, with time-dependent variates designed to reflect exposure over time during the ICU stay. A trajectory modeling, based on intracranial pressure evolution pattern, allowed identification of subgroups. Results: Overall, in our cohort of 1955 eligible patients, 130 (6.65%) received HTS. MSCM indicated that the HTS was significantly associated with better Glasgow coma score [(GCS): hazard ratio (HR) 1.19, 95% confidence interval (95% CI) 1.01-1.40, p = 0.041], higher infection complications [eg. urinary tract infection (HR 1.88, 95% CI 1.26-2.81, p = 0.002)], and increased ICU LOS (HR 2.02, 95% CI 1.71-2.40, p < 0.001). A protective effect from GCS by the HTS was found in the subgroup with medium and low ICP. Conclusion: Our study revealed no significant difference in the all-cause mortality rates between patients receiving HTS or not. Increased occurrence rates of infection and electrolyte imbalance were inevitable outcomes caused by continuous HTS infusion. Although the study suggested the slight beneficial effects including better neurological outcome, the results warrant further validation.

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