Postoperative pain treatment after cholecystectomy with epidural sufentanil at lumbar or thoracic level

The difference in analgesic activity following lumbar (group I) or thoracic (group II) epidural administration of 50 ug sufentanil was studied after cholecystectomy. Fifteen patients in each group were evaluated for pain relief using a linear analog scale (LAS), heart rate (HR), mean arterial pressure (MAP), respiratory rate (RR), peak expiratory flow (PEF), forced vital capacity (FVC), forced expiratory volume (FEV,) and arterial CO₂ tension (Paco₂). In five additional patients in each group 75 μg sufentanil was injected for determination of serum levels. Pain scores were lower than three in both groups after 10 min, while mean pain scores remained below one from 20 min until 2 h following injection in both groups. Satisfactory pain relief lasted for 4 h. RR was significantly decreased from two until 360 min. in the lumbar group and from five until 120 min in the thoracic group. Paco₂ was raised in both groups only during the first hour. PEF and FVC were significantly improved compared to control 1, 2 and 4 h following injection. Serum sufentanil levels reached a maximum of 0.299 ±0.052 ng.ml^-1 in the lumbar group and 0.377 ± 0.076 ng–ml^-1 in the thoracic group after 5 min. There were no significant differences between the two groups in the variables studied.     

HAEMODYNAMIC CHANGES DURING ANAESTHESIA INDUCED AND MAINTAINED WITH PROPOFOL

The haemodynamic effects of propofol, given as a single doseof 2 mg kg^–1 immediately followed by a continuous infusionof 6 mg kg^–1 h^–1, were studied in 10 elderly patientspremedicated with lorazepam 1 mg i.v. All patients breathedroom air spontaneously. Unconsciousness was successfully inducedin all patients and persisted during the 60 min of the infusion.Statistically significant decreases in systolic and diastolicarterial pressures were observed 2 min after induction (28%and 19% respectively) and during infusion (30% and 25% respectively)and were related to decreases in systemic vascular resistance(21% following induction and 30% during infusion). Cardiac outputwas not affected at any time nor were stroke volume and heartrate. We conclude that the arterial hypotension associated withthe induction and infusion of propofol is mainly a result ofa decrease in afterload without compensatory increases in heartrate or cardiac output.     

Vasostatins,N-terminal products of chromogranin A,are released from the stimulated calf spleen in vitro

Vasostatins are the N-terminal chromogranin A peptides 7 ? 22 kDa. They have been shown to be present in several endocrine tissues and exhibit vasoinhibitory activity in vitro. In a first series of experiments, we investigated the presence and subcellular localization of vasostatins in the bovine splenic nerve. Experimental results, obtained using gradient centrifugation, showed that noradrenaline was enriched 25-fold in the large dense core vesicle fraction, compared with the original homogenate. In the latter fraction, the 7 and 18 kDa peptides were observed following immunodetection with antiserum to chromogranin A_{1, 4o} and laser densitometric scanning revealed these two fragments as the major N-terminal fragments. Subsequently, we examined the release of the 7 and 18 kDa peptides from perfused calf spleen during veratridine (20 μM) or 1,1-dimethyl-4-phenylpiperazinium iodide (20 μM) stimulation. In the prestimulatio samples, we were not able to detect these peptides, however, following stimulation, the 7 and 18 kDa chromogranin A fragments became apparent. The vasostatin-immunoreactivity, in both bovine chromaffin granule lysate and calf spleen perfusate, elutes at the same retention time on reversed-phase high performance liquid chromatography. The present study demonstrated that vasostatins are present in the large dense core vesicles of sympathetic axons and are released from the nerve terminals in response to stimulation. The release of vasostatins from sympathetic nerves in the spleen suggest an in vivo function for N-terminal chromogranin A products of neuronal origin.