Ultrasound examination of the stomach contents of women in the postpartum period.

This study used ultrasound imaging to compare stomach contents and gastric emptying of women in the postpartum period with those of nonpregnant women. In the first part of the study, the presence or absence of solid food particles was compared between patients presenting for postpartum tubal ligation (n = 28) and those presenting for gynecological surgery (n = 24). In the second part of the study, gastric emptying of solid food in a group of women in the postpartum period (n = 20) was compared with that of a group of nonpregnant volunteers (n = 21). After a standardized meal, the subjects were not allowed any food for 4 h, and the stomach contents were examined by ultrasound. Results of the first part of the study showed that 11 of the 28 patients presenting for postpartum tubal ligation compared with none of the gynecologic patients had solid food particles in the stomach prior to surgery. In the second part of the study, 19 of 20 women in the postpartum group still had food particles in the stomach 4 h after the meal as compared with only 4 of 21 in the non-pregnant group. Both differences were statistically significant. Our results indicate that gastric contents of women in the postpartum period may include food particles and that there is delayed gastric emptying of solid food in the postpartum period.

RB 101, a purported pro drug inhibitor of enkephalin metabolism, is antinociceptive in pregnant mice.

In an earlier study, we demonstrated the enhancement of pregnancy-induced analgesia with an inhibitor of endogenous enkephalin metabolism. The purpose of the present study was to evaluate the antinociceptive effect of another inhibitor of enkephalin metabolism, RB 101, on pregnant mice. Further, since other studies have shown RB 101 to be free of opioid side effects, we examined its effect on respiratory rate. Analgesia was assessed using the hot plate test, and respiratory rate was measured by recording the output from an end-tidal carbon dioxide detector. In pregnant mice, experiments were conducted on Day 17 or Day 18 of pregnancy; mice usually deliver on Day 19. For the hot plate test, animals were tested in the following groups: Group 1, RB 101 150 mg/kg (n = 15); Group 2, RB 101 50 mg/kg (n = 15); Group 3, RB 101 vehicle (n = 15); Group 4, morphine 5 mg/kg (n = 14); and Group 5, RB 101 150 mg/kg + naloxone 5 mg/kg (n = 10). The test was repeated on the second day after delivery in animals in Groups 1 and 3 (given RB 101 150 mg/kg and RB 101 vehicle, respectively). RB 101 150 mg/kg and morphine 5 mg/kg were significantly different (mean percentage of maximum possible effect 30.0 and 37.7, respectively, at 30 min and 41.6 and 32.6, respectively, at 60 min) in their antinociceptive effect in pregnant animals from all other groups. Naloxone, when coadministered with RB 101, prevented the development of antinociception. RB 101 150 mg/kg was not antinociceptive after delivery. Depression of respiratory rate was tested in a separate set of animals in the following groups: Group 1, RB 101 150 mg/kg (n = 16); Group 2, morphine 5 mg/kg (n = 16); Group 3, RB 101 vehicle (n = 15). Morphine 5 mg/kg produced significant depression of respiratory rate at 30 min postinjection when compared with RB 101 150 mg/kg and RB 101 vehicle (mean percent change in respiratory rate was 78.5% compared with 87.7% and 92.4%, respectively, where 100% = no change). These results suggest that drugs such as RB 101 may produce antinociception with minimal effects on respiration.

Pregnancy complicated by aortic dissection: caesarean delivery during extradural anaesthesia.

We report a case where dissection of the aorta occurred in pregnancy; only medical management was undertaken. Delivery was by Caesarean section during extradural anaesthesia and was accomplished safely several weeks after the dissection. The aetiology, association with pregnancy, diagnosis and management of acute dissection of the aorta are discussed.

An enkephalinase inhibitor, SCH 32615, augments analgesia induced by surgery in mice.

BACKGROUND: Stress-induced analgesia is a well recognized phenomenon in animals and humans in which endogenous opioids have been implicated. However, analgesia induced by surgical stress has not been reported. The purpose of this study was to determine whether surgery evokes analgesia and to examine the effect of SCH 32615, an inhibitor of one of the enzymes (enkephalinase) responsible for the degradation of enkephalins, on this analgesia, in mice. METHODS: Analgesia was tested using the hot-plate test. Animals were tested before any procedure was done and then at hourly intervals thereafter. Under halothane anesthesia, the anterior abdominal wall was incised, and the abdominal aorta was compressed against the vertebral column for 1 s. This was repeated for a total of three times at 5-s intervals. At the end of the procedure, the following drug(s) were administered subcutaneously to different groups of animals: (1) no drugs, only surgery (n = 15); (2) 5 mg/kg naloxone (n = 15); (3) 150 mg/kg SCH 32615 (n = 14); (4) 150 mg/kg SCH 32615 plus 5 mg/kg naloxone (n = 15); and (5) SCH 32615 vehicle (0.9% methylcellulose; n = 13). Two more groups of animals were included as controls and were anesthetized, but no surgical procedure was performed. One control group (n = 13) received 0.9% methylcellulose and the other 150 mg/kg SCH 32615 (n = 12). RESULTS: Hot-plate latency was significantly longer after surgery (hot-plate latency at 4 h after surgery 29.3 +/- 3.2 (SE) s and at 5 h 30.7 +/- 5 s versus baseline 15.8 +/- 7 s; P < 0.05). Naloxone (5 mg/kg) inhibited this analgesic effect of surgery. SCH 32615 significantly enhanced this analgesia (percentage of maximal possible effect (%MPE) at 4 h 33.7 +/- 8.7%, at 5 h 27.5 +/- 4.7%, and at 6 h 23.2 +/- 4.7%; P < 0.05 compared to all other groups), and naloxone antagonized its effect. Anesthesia without surgery did not evoke subsequent analgesia, and SCH 32615 was not analgesic in the absence of antecedent surgery. CONCLUSIONS: Surgery activated endogenous analgesia, the development of which was prevented by naloxone. SCH 32615, an enkephalinase inhibitor, significantly enhanced this analgesia.