The potential for preoperative IV rehydration to reduce postoperative nausea and vomiting (PONV) and pain in patients undergoing ambulatory surgery remains unclear, with conflicting results reported. We sought to determine whether preoperative IV rehydration with a balanced salt solution would decrease the incidence of PONV in patients at increased risk for these symptoms. Eighty ASA grade I-III patients presenting for gynecologic laparoscopy were randomized to receive large (2 mL/kg per hour fasting) or small (3 mL/kg) volume infusions of compound sodium lactate solution over 20 min preoperatively. A standardized balanced anesthetic was used. The incidence and severity of PONV and pain, and need for supplemental antiemetic and analgesic therapy, were assessed by a blinded investigator at 0.5, 1, and 4 h postoperatively, and on the first and third postoperative days. The incidence (control 87% versus large volume 59%) and severity of PONV were significantly reduced in the large volume infusion group at all time intervals. The large volume infusion group also had decreased postoperative pain scores and required less supplemental analgesia. Preoperative correction of intravascular volume deficits effectively reduces PONV and postoperative pain in high risk patients presenting for ambulatory surgery. We recommend the preoperative administration of 2 mL/kg of compound sodium lactate for every hour of fasting to patients with an increased PONV risk presenting for ambulatory surgery.

Background: Hypercapnic acidosis exerts protective effects in acute lung injury but may also slow cellular repair. These effects may be mediated via inhibition of nuclear factor-kB (NF-kB), a pivotal transcriptional regulator in inflammation and repair. Objectives: To determine the effects of hypercapnic acidosis in pulmonary epithelial wound repair, to elucidate the role of NF-kB and to examine the mechanisms by which these effects are mediated. Methods: Confluent small airway epithelial cell, human bronchial epithelial cell and type II alveolar A549 cell monolayers were subjected to wound injury under conditions of hypercapnic acidosis (pH 7.0, carbon dioxide tension (PCO 2 ) 11 kPa) or normocapnia (pH 7.37, PCO 2 5.5 kPa) and the rate of healing determined. Subsequent experiments investigated the role of hypercapnia versus acidosis and elucidated the role of NF-kB and mitogenactivated protein kinases. The roles of cellular mitosis versus migration and of matrix metalloproteinases in mediating these effects were then determined. Results: Hypercapnic acidosis reduced wound closure (mean (SD) 33 (6.3)% vs 64 (5.9)%, p,0.01) and reduced activation of NF-kB compared with normocapnia. Buffering of the acidosis did not alter this inhibitory effect. Prior inhibition of NF-kB activation occluded the effect of hypercapnic acidosis. Inhibition of ERK, JNK and P38 did not modulate wound healing. Hypercapnic acidosis reduced epithelial cell migration but did not alter mitosis, and reduced matrix metalloproteinase-1 while increasing concentrations of tissue inhibitor of metalloproteinase-2. Conclusions: Hypercapnic acidosis inhibits pulmonary epithelial wound healing by reducing cell migration via an NF-kB dependent mechanism that may involve alterations in matrix metalloproteinase activity.

Hypercapnic acidosis attenuated ventilation-induced lung injury independent of injury severity and decreased mechanical stretch-induced epithelial injury and death, via a nuclear factor-κB-dependent mechanism.