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In this study, we applied high-performance liquid chromatography with electrochemical detection (HPLC-EC) to the measurement of acetylcholine (ACh) release from nerve endings in guinea pig tracheal smooth muscle. We also tested for muscarinic inhibitory regulation of ACh release in this species, which is widely used for studies of airway neural control. Clip-connected segments of the posterior membrane of the guinea pig trachea were mounted in organ baths between stimulating electrodes and incubated in Krebs-Henseleit buffer containing (in microM) 10 indomethacin, 1 neostigmine, 1 phentolamine, and 1 propranolol. To measure ACh, the bath was emptied and aliquots of buffer were injected directly into the HPLC-EC; the lower limit of detection was 1 pmol/200 microliters sample. Electrical field stimulation (EFS) at 5 Hz for 10 or 30 min increased ACh release from 1.8 +/- 1.4 (SE) to 6.2 +/- 1.3 pmol.mg protein-1.min-1 (n = 15). The effect of atropine was examined by comparing amounts of ACh released by EFS before and after exposure to either atropine (0.3 microM) or vehicle. Before atropine treatment, EFS-evoked ACh release was 4.9 +/- 0.6 pmol.mg protein-1.min-1; after atropine exposure, EFS-evoked release of ACh increased significantly to 15.0 +/- 2.2 pmol.mg protein-1.min-1 (n = 11; P less than 0.05). Corresponding values before and during exposure to vehicle were 9.3 +/- 4.4 and 10.7 +/- 4.7 pmol.mg protein-1.min-1, respectively. The ratios of the changes in EFS-evoked ACh release were 3.1 +/- 0.3 and 1.3 +/- 0.1 in atropine-treated and vehicle-treated groups, respectively (P less than 0.05). We conclude that HPLC-EC is a reliable and sensitive technique for the detection of EFS-evoked release of ACh from clip-connected segments of guinea pig tracheal smooth muscle.

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FUNCTIONAL RESIDUAL CAPACITY (FRC) is reduced following upper abdominal operations under general anaesthesia. The changes which have been reported <1-5) are summarized in Table I. A number of factors can be responsible for the changes observed.The reduction of FRC which follows induction of general anaesthesia may persist. The cause for this reduction is still undetermined, but the fall is not progressive with time and is related to body size. (6,7) Loss of lung volume by atelectasis or oedema will reduce FRC, as will an increase in expiratory muscle activity. Abdominal distension by pneumoperitoneum and bowel distension and incisional pain can be responsible.In all probability, all these factors play a role. The present study was undertaken to determine the role of post-operative pain in reducing FRC and vital capacity (VC) and the efficacy of epidural analgesia in reversing these changes. SUBJECT MATERIALEight patients (five females and three males) scheduled for elective upper abdominal operations were studied. They were clinically free of cardiorespiratory disease, except for patient No. 5 who had mild chronic bronchitis. The ages ranged from 34 to 67 years (mean 42.5), height varied from 145 to 183 cm (mean 159 cm), and weight from 40.9 to 88 kg (mean 67.9 kg). Consent was obtained in each case following explanation of the purpose and methods of the study. EXPERIMENTAL PROTOCOLAll subjects were studied in the supine position in the Recovery Room. Preoperative (control) measurements were made on the day of operation with the patients fasted overnight and without premedication. Measurements of FRC and VC were made following the placement of lumbar epidural and intravenous catheters by standard techniques, without injection of any anaesthetic agent. During the operation, lidocaine epidural anaesthesia was supplemented with general anaesthesia using thiopentone, endotracheal N20: 02, and meperidine. The