Peritoneal absorption of CO 2 during abdominal insufflation in laparoscopy may disrupt the acid-base equilibrium and alter the physiological response to stress. Current nonventilated rodent models of laparoscopy do not manage the CO 2 load of pneumoperitoneum, but ventilated surgical rodent models are invasive (tracheotomy) and may independently induce the inflammatory response. A comprehensive rodent model of laparoscopy was developed. Rats were randomized to receive anesthesia alone, anesthesia plus CO 2 pneumoperitoneum, or anesthesia plus CO 2 pneumoperitoneum with videoendoscopic intubation and mechanical ventilation. Arterial blood-gas analysis was performed at baseline and after 30 min of intervention. Baseline pH, pCO 2, and HCO 3 - arterial blood gas parameters were normal for all rats. After 30 min, pCO 2 and pH changed slightly but remained normal among rats receiving anesthesia alone (pCO 2 = 46.5 ± 1.9; pH = 7.365 ± 0.009) whereas animals receiving anesthesia plus CO 2 pneumoperitoneum that were dependent on spontaneous respiration for ventilation developed significant hypercarbic acidosis (pCO 2 = 53.2 ± 1.9, P < 0.05; pH = 7.299 ± 0.011, P < 0.001). This acidosis was completely corrected with increased minute ventilation in intubated rats receiving mechanical ventilation (pCO 2 = 36.8 ± 1.5, P < 0.001; pH = 7.398 ± 0.011, P < 0.001). CO 2 pneumoperitoneum induces significant hypercarbic acidosis in nonventilated rats. Noninvasive endotracheal intubation is feasible in the rat with videoendoscopic assistance. Our noninvasive rodent model of laparoscopic surgery controls for anesthesia- and capnoperitoneum-related acid-base changes and provides an environment in which the biological response to pneumoperitoneum can be studied precisely.
- animal models
- carbon dioxide
- endotracheal intubation
- minimally invasive surgical procedures
ASJC Scopus subject areas