[Evolution of plasma histamine after midazolam in patients at risk of histamine liberation]. / Evolution de l'histamine plasmatique après midazolam chez les sujets à risque d'histaminolibération.

Changes in plasma histamine levels 2 min (t1) and 10 min (t2) after the intravenous injection of 0.2 mg X kg-1 midazolam were measured in 10 subjects at risk of releasing histamine (group I) and compared with those of 15 other subjects free from any risk of releasing histamine (group II). There was mean increases in plasma histamine levels of 0.78 ng X ml-1 between t0 and t1 (p less than 0.01), and of 0.41 ng X ml-1 between t0 and t2 (p less than 0.01) in group I; they only rose by 0.18 ng X ml-1 between t0 and t2 (p less than 0.01) in group II. The only statistically significant variation between the two groups was that at t1 (p less than 0.03): plasma histamine levels rose higher at the second minute in those cases at risk. This was a rather small increase, within physiological limits, and without any clinical or haemodynamic manifestation.

[Analgesia after laparoscopic cholecystectomy by intraperitoneal administration of bupivacaine]. / Analgésie après cholécystectomie par voie coelioscopique par administration intrapéritonéale de bupivacaïne.

OBJECTIVES: The aims of this study were to assess the analgesic effect of the intraperitoneal topical administration of 0.375% bupivacaine in patients undergoing laparoscopic cholecystectomy and to carry out a pharmacokinetic study of bupivacaine administered topically by intraperitoneal route. STUDY DESIGN: Randomized, double-blind controlled trial. PATIENTS AND METHODS: Twenty-four patients of ASA physical status 1 or 2, undergoing elective laparoscopic cholecystectomy, were included. Anaesthesia technique was the same for all patients. At the end of surgery, they were randomly assigned to one of two groups. Patients in group bupivacaine were administered 0.375% bupivacaine, 0.6 mL.kg-1 intraperitoneally in both subdiaphragmatic areas and the cholecystectomy wound, those of the control group were given the same volume of NaCl 0.9%. Analgesia was provided by morphine PCA. Postoperative pain, assessed on a 100 mm visual analogue pain scale (VAS), and administered morphine were recorded 30 min after extubation, and 0.5, 1, 2, 3, 6, 12, 24, 36 and 48 hours later. Blood samples were collected 2, 5, 15, 30, 60, 90, 120, 180, 300 and 480 min after the intraperitoneal administration of bupivacaine to measure bupivacaine plasma concentration. Statistics included Student t test and Chi square test. P < 0.05 was considered significant. RESULTS: There was no significant difference between the two groups with regard to VAS scores during the first 48 postoperative hours. Morphine requirements (total and at each point) were also similar. Plasma bupivacaine concentrations reached a plateau at 10-20 min, and then decreased slowly. The median plasma peak concentration was 0.94 +/- 0.47 microgram.mL-1. In one patient toxic concentrations (> 1.6 micrograms.mL-1) during the first 60 min after intraperitoneal administration were obtained, while in another patient a concentration of 1.58 micrograms.mL-1 was reached twice. CONCLUSIONS: Intraperitoneal administration of 0.6 mL.kg-1 of 0.375% bupivacaine is ineffective in reducing postoperative pain after laparoscopic cholecystectomy. Furthermore these high doses of bupivacaine may result in toxic plasma concentrations. This technique is not safe and cannot be recommended.

Haemodynamic and respiratory effects of post-operative doxapram and almitrine in patients following pneumonectomy.

Respiratory analeptics have been shown to give important increases in pulmonary vascular resistance and pulmonary arterial pressure in hypoxaemic respiratory failure patients, but no studies have been carried out in the post-operative recovery period. The aim of this study was to compare the haemodynamic and respiratory effects of doxapram and almitrine infusion given over 1 h in patients who had just undergone pneumonectomy. Two hours after the end of anaesthesia, three groups of randomly selected patients were therefore given 3 mg kg-1 doxapram (n = 10), 1 mg kg-1 almitrine (n = 10) or placebo (n = 10). Measurements were made before and 15, 30, 60, 90, 120 and 180 min after the beginning of the infusion. There was an immediate 15-20% fall (P less than 0.01) in PaCO2 and a 20% rise in PaO2 (P less than 0.005), identical for both drugs; the variations in the placebo group became significant only after 60 min. Heart rate and cardiac index did not change. Mean arterial pressure did not change with doxapram, but decreased by 20% during the infusion of almitrine (P less than 0.01), remaining low until the 90th min (P less than 0.05). This hypotension was due to a decrease in peripheral arterial resistance (P less than 0.05) and a small decrease in right atrial pressure (P less than 0.05). The mean pulmonary arterial and wedge pressures were increased before starting the infusion, and did not vary significantly. Pulmonary arterial resistance increased with both analeptics but only significantly with the doxapram (P less than 0.05) at 5, 60 and 90 min; however, there was no significant difference between doxapram and almitrine. The post-operative respiratory efficiency of these drugs has been confirmed, there being no difference between almitrine and doxapram. The haemodynamic effects were moderate, especially with almitrine. Both of these drugs, therefore, may be recommended for use after lung surgery.