Spinal cord injury (SCI)-induced diabetes insipidus (DI) presents a unique therapeutic challenge due to concurrent autonomic hypotension unresponsive to conventional desmopressin. This study evaluates the clinical efficacy of Pituitrin, a synthetic vasopressin analog with dual V1a/V2 receptor agonism, designed to simultaneously address antidiuretic hormone deficiency and hemodynamic instability in acute SCI-related DI. In this retrospective propensity-matched cohort study, 317 consecutive acute SCI patients (2010 -2021) were screened, with 60 (18.9%) developing DI. Patients were stratified into a Pituitrin-treated group (2014 - 2021, n = 30) and historical controls (2010 - 2013, n = 30). Propensity score matching (1:1 nearest-neighbor, caliper = 0.2 standard deviation) adjusted for age, American Spinal Injury Association (ASIA) grade, injury level (cervical/thoracic), concurrent mild brain injury (Glasgow coma scale 13 - 15), and treatment era covariates, yielding 23 matched pairs. Post-matching groups demonstrated balanced baseline characteristics with cervical injury prevalence 95.7% and ASIA grade A/B injuries 100%. The intervention group received protocolized Pituitrin infusion (initial 1 U/h, titrated 0.5 - 5 U/h based on urine output) with fluid restriction (<2000 mL/day), while controls received standard care including desmopressin and vasopressors as needed. Primary outcomes included DI duration (days to urine output <3000 mL/day concurrent with serum sodium ≥135 mmol/L), in-hospital mortality, and hospitalization length. This study of 317 acute SCI patients (84% male) revealed DI developed in 18.9% (60/317), with striking cervical predominance (57 (31.0%) cervical vs. 3 (4.9%) thoracic SCI; χ2 = 21.4, p < 0.001). In propensity score-matched cohorts (23 pairs balanced for age, ASIA grade, injury level, and era). Early Pituitrin therapy demonstrated transformative efficacy: DI duration reduced by 7.6 days (4.4 ± 1.5 vs. 12.0 ± 2.6 days; 95% confidence interval (CI): 6.4 - 8.8, p < 0.001), 26% absolute mortality reduction (number needed to treat (NNT) = 3.85; p = 0.014), and shortened median hospitalization by 5 days (14 vs. 19 days, p = 0.008). Cervical ASIA A/B patients exhibited maximal benefit with 24% mortality reduction (NNT = 4.17, p = 0.014) and universal hemodynamic stabilization-Pituitrin eliminated vasopressor need in 87% of cases (vs. 23/30 controls requiring norepinephrine; risk difference = 0.63, NNT = 1.59). Notably, 100% of DI cases demonstrated autonomic hypotension preceding hyponatremia, with treatment initiation within 24 h of diagnosis accelerating recovery (r = -0.818, p < 0.001). The intervention proved exceptionally safe, with only 1 (3.3%) experiencing transient headaches. This study establishes the first evidence-based protocol for dual V1a/V2 receptor targeting in SCI-induced DI, demonstrating that early Pituitrin administration achieves rapid antidiuresis (median 8-day resolution) while stabilizing hemodynamics (87% vasopressor independence). The 26% absolute mortality reduction (NNT = 3.85) and shortened hospitalization (Δ5 days) suggest promising therapeutic potential, especially for cervical complete injuries, and warrant further validation in larger prospective cohorts. These findings establish a novel treatment paradigm addressing the pathophysiological triad of arginine vasopressin deficiency, autonomic hypotension, and hyponatremia unique to acute SCI.

The human brain maintains intricate interconnections with various peripheral organs. Recent scientific inquiry has substantiated the existence of the gut-brain axis; nevertheless, emerging evidence suggests that the brain and lungs engage in bidirectional communication through multiple pathways, thereby giving rise to the conceptualization of a brain-lung axis. Studies indicate the presence of crosstalk between the central nervous system and the lungs, mediated by the lung microbiome, neural pathways, metabolite signaling, and immune pathways. This bidirectional communication between the brain and lungs is further implicated in the pathogenesis of several diseases: traumatic brain injury, stroke, and other cerebral disorders can precipitate pulmonary injury; conversely, severe pulmonary conditions, such as acute respiratory distress syndrome and chronic obstructive pulmonary disease, can exacerbate neuroinflammation, intensify brain damage, impair neurological function, and contribute to adverse prognoses. Exploring the brain-lung axis not only facilitates a multifaceted understanding of disease progression, but also unveils critical targets for therapeutic intervention. Research into the brain-lung axis provides novel perspectives for deciphering underlying pathological mechanisms, developing diagnostic methodologies, and formulating treatment strategies. It further establishes a theoretical foundation for cross-organ targeted therapies, holding promise for ameliorating patient outcomes and promoting the advancement of integrated diagnostic and therapeutic approaches for respiratory and neurological disorders.