Influence of laparoscopic carbon dioxide pneumoperitoneum on neonate circulation and respiration.

OBJECTIVE: This study investigated the influence of laparoscopic carbon dioxide (CO2) pneumoperitoneum on neonate circulation and respiration. METHODS: The study included neonates undergoing elective laparoscopic abdominal surgery. CO2 insufflation pressure was maintained within 8-14 mmHg for pneumoperitoneum creation. Heart rate (HR), mean arterial pressure (MAP), peripheral oxygen saturation (SpO2), partial pressure of end-tidal carbon dioxide (P ETCO2) and maximum inspiratory pressure were monitored continuously. Arterial blood samples were collected: 5 min before pneumoperitoneum creation (baseline); 5, 10, and 20 min after CO2 insufflation; 10 min after CO2 exsufflation; 10 min after surgery. pH, partial pressure of CO2 (PaCO2) and arterial oxygen saturation (SaO2) were also measured. RESULTS: Thirty-six neonates were included. HR and MAP significantly increased after pneumoperitoneum creation, then decreased to baseline after CO2 exsufflation. PaCO2 and P ETCO2 were significantly higher after pneumoperitoneum creation, whereas pH was significantly lower 20 min after pneumoperitoneum creation compared with baseline. No significant differences were observed in SpO2 and SaO2. CONCLUSION: CO2 pneumoperitoneum had a significant effect on neonatal circulation and respiration, suggesting that the pneumoperitoneal pressure should be limited within a certain range in neonates undergoing laparoscopic surgery.

[Protective effect of the cholinergic anti-inflammatory pathway against hemorrhagic shock in rats].

OBJECTIVE: To investigate the effect of the cholinergic anti-inflammatory pathway on hemodynamics in hemorrhaged rats. METHODS: Hemorrhagic shock was induced by modified Wiggers method until mean arterial pressure (MAP) was stabilized within the range of 35 to 40 mm Hg (1 mmHg=0.133 kPa). Thirty male Sprague-Dawley rats were randomly divided into six groups: sham group, hemorrhagic shock (Hem) group, vagotomy (VGX) group, vagus stimulation (STM) group, cholinergic inhibitor (THA) group and N receptor inhibitor (alpha-BGT) group. The distal end of the left vagus nerve trunk was placed on bipolar platinum electrode connected to a stimulation module and controlled by an acquisition system. Stimuli with constant voltage (5 V, 2 ms, 1 Hz) were applied to nerve for 12 minutes, starting 5 minutes after MAP stabilized at a level of 35 to 40 mmHg. Before stimulation a blood pressure transducer was implanted in the common carotid artery for continuous registration of MAP. Blood samples and liver samples were collected from animals of all groups after stimulation. Serum levels of tumor necrosis factor-alpha (TNF-alpha) and liver nuclear factor kappa-B (NF-KappaB) were determined. RESULTS: MAP was markedly lowered at the end of bleeding, and the levels of serum TNF-alpha and liver NF-KappaB markedly increased 45 minutes after the bleeding was discontinued. Bilateral cervical vagotomy did not significantly modify the changes in serum TNF-alpha, but slightly increased liver NF-KappaB activation. Application of constant electric current to the distal end of the vagus trunk significantly reduced serum TNF-alpha and blunted liver NF-KappaB activation. Tetrahydroamino-acridine (THA,1.5 mg/kg, intravenous drip administration after bilateral cervical vagotomy reversed hypotension and attenuated serum TNF-alpha and liver NF-KappaB amounts, but alpha-bungarotoxin (1.0 microg/kg intravenous drip) pretreatment reverted the inhibitory effects of vagal stimulation. CONCLUSION: The result suggest that direct electrical stimulation of the vagus nerve and its transmitter can significantly attenuate peak serum TNF-alpha amounts, inhibit the expression of liver NF-KappaB, and prevent the development of hypotension, thus it might produce a potential protective effect on hemorrhaged rats through acetylcholine (Ach) binds NAch receptor alpha 7 subunit which exists in the macrophage.