治療性體溫調控對腹腔內高壓造成器官損傷之影響：以新型指數評估腎臟、肝臟與肌肉損傷模式

何宣緯

嘉義長庚紀念醫院 泌尿科

Therapeutic Hypothermia in Intra-abdominal Hypertension: Distinct Organ Injury Phenotypes and Renal Protection Mechanisms

Hsuan-Wei Ho

Chang Gung Memorial Hospital, Urology, Chiayi, Taiwan

Purpose:

Abdominal compartment syndrome (ACS) impairs renal perfusion and leads to acute kidney injury (AKI). While therapeutic hypothermia (HypoT) is a potential renal-protective strategy, its systemic, multi-organ effects are poorly characterized. We used a novel clinical index analysis to differentiate the temperature-dependent patterns of renal, hepatic, and muscular injury in a rat ACS model.

Materials and Methods:

Sprague-Dawley rats (n=27) were randomized into five groups: Control, ACS (Normal Temp, ~37°C), ACS+HypoT (32°C), ACS+HyperT (42°C), and ACS+Extreme HyperT (47°C). ACS was induced via intraperitoneal gelatin infusion to maintain IAP at 30 mmHg for 4 hours. Systemic injury was assessed by measuring a panel of 10 serum parameters before and after the IAP intervention: Renal function: Blood Urea Nitrogen (BUN), Creatinine. Hepatic injury: Aspartate Aminotransferase (AST/GOT), Alkaline Phosphatase (ALP). Muscular/systemic damage: Creatine Kinase (CK), Lactate Dehydrogenase (LDH). Metabolic: Amylase, Calcium, Sodium, Potassium (K). Statistical significance was assessed using one-way ANOVA (p<0.05).

Results:

Traditional renal markers (BUN, Cre) and the BUN/Cre ratio did not differ significantly among groups (p=0.2947), indicating that the 4-hour ACS duration was insufficient to produce measurable AKI. However, systemic injury indices demonstrated significant, temperature-dependent organ injury patterns. The AST/CK ratio (p=0.0343) differentiated the dominant source of injury: HypoT

induced a liver-predominant pattern (mean ratio = 4.34), while HyperT induced a muscle-predominant pattern (mean ratio = 0.58). Thus, HypoT mitigated muscular damage (low CK) but induced a unique hepatic stress response, whereas HyperT caused extensive muscle-dominant systemic injury.

Conclusion:

Temperature modulation in ACS alters not only the magnitude but also the pattern of organ vulnerability. Conventional renal markers were insensitive within this short-term model, whereas novel biochemical indices uncovered distinct temperature-dependent injury profiles. Hypothermic therapy demonstrated protective effects against muscle injury but may shift stress toward hepatic pathways. Conversely, hyperthermia produced severe, muscle-dominant systemic damage. These findings suggest that clinicians exploring therapeutic hypothermia for ACS should monitor hepatic function, with the AST/CK ratio serving as a potential clinical indicator of organ-specific stress.