P Pu ur rp po os se e: : t has been suggested that long-medium chain triglyceride (LCT/MCT) emulsive propofol causes less injection pain than long chain triglyceride (LCT) emulsive propofol because of the decreased propofol concentration in the aqueous phase. Alternatively, LCT propofol generates bradykinin causing the injection pain and activates complement, but these effects when using LCT/MCT propofol have not been examined. To identify the mechanism for reduced pain with LCT/MCT propofol, injection pain, bradykinin generation and complement activation with use of both propofol products were compared.M Me et th ho od ds s: : Two hundred adult patients randomly allocated to two groups were given 1.5 mg·kg -1 iv of either LCT propofol or LCT/MCT propofol at a rate of 200 mg·min -1 in a double-blind manner and were asked to grade pain scores. In another study, bradykinin and activated complement 3 (C3a) concentrations were measured using blood obtained from 13 healthy volunteers mixed with saline, LCT propofol or LCT/MCT propofol.R Re es su ul lt ts s: : There was a significant difference in pain scores between groups, showing a lower incidence of injection pain in the LCT/MCT propofol group. The bradykinin concentrations in blood mixed with LCT and LCT/MCT propofol were significantly higher than in blood mixed with saline. The C3a concentrations showed similar results.C Co on nc cl lu us si io on ns s: : LCT/MCT propofol causes less pain on injection compared with LCT propofol. Bradykinin generation and complement activation are similar with both LCT and LCT/MCT propofol. Thus, the reason for less pain on injection with LCT/MCT propofol may be attributed to a decreased concentration of propofol in the aqueous phase. Objectif : On a pensé qu'une émulsion de propofol avec une chaîne mi-longue de triglycéride (CLT/CMT) cause moins de douleur à l'injection qu'une émulsion à chaîne longue (CLT) parce que la concentration de propofol diminue pendant la phase aqueuse. Aussi, le propofol avec CLT génère de la bradykinine, causant de la douleur à l'injection, et active le complément, mais ces effets n'ont pas été étudiés avec le propofol CLT/CMT. Pour définir le mécanisme qui réduit la douleur avec le propofol CLT/CMT, nous avons comparé la douleur à l'injection, la génération de bradykinine et l'activation du complément avec l'usage des deux produits de propofol. Méthode : Deux cents patients adultes ont été répartis au hasard en deux groupes et ont reçu 1,5 mg·kg -1 iv de propofol CLT ou CLT/CMT

Twelve elderly patients undergoing total knee arthroplasty received lumbar epidural anaesthesia and propofol infusion at 5 mg.kg(-1).h(-1) following a 1.5-2.0 mg.kg(-1) bolus dose with preservation of spontaneous respiration via a laryngeal mask airway. Circulatory, respiratory and metabolic variables were measured before and 1, 3, 5, 15 and 30 min after release of a pneumatic thigh tourniquet. The blood pressure was decreased at all time-points and the respiratory rate increased at 1 min. The P(a)CO(2) was increased only at 1 min. Arterial blood pH and base excess were decreased at 1 and 3 min and 1, 3 and 5 min, respectively. Arterial blood lactate levels were increased at all times. These characteristics were considered to be identical to those under regional anaesthesia with conscious spontaneous respiration, showing that spontaneous respiration under this anaesthetic regimen has a similar respiratory capacity to that of conscious spontaneous respiration.

Inspired O(2)(-) attenuates blood lactate concentrations. This may be attributed, in part, to the systemic stimulatory effect on superoxide dismutase activity, which accelerates oxidative phosphorylation in the mitochondria, thus attenuating lactate generation.

We have examined whether propofol activates complement. In the first study, blood was mixed with saline, propofol or the lipid solvent for propofol, and the activated complement 3 (C3a) and 4 (C4a) concentrations in the supernatant were assayed. In the second study, blood and propofol were mixed with various levels of nafamostat mesilate (anti-complement agent) up to 0.3 mmol/l and the C3a was assayed. In the third study, the time course of plasma C3a concentration in patients during propofol anaesthesia was examined. The results showed that the lipid solvent activated complement and produced similar levels of C3a to propofol, probably via both the classical and alternative pathways. This activation was not inhibited by any of the nafamostat concentrations used. There was no significant change in plasma C3a concentration during propofol anaesthesia. These results suggest that C3a is generated by the lipid solvent, but its accumulation during propofol anaesthesia is minimal.

bilization but it is still unclear which situations are prone to favour PA. Risk factors for PA include peripheral circulatory failure, such as hypotension secondary to dehydration or massive blood loss. Endotracheal intubation and intraoperative Trendelenburg position have also been implicated. [2][3][4][5] However, none of these risk factors were present in our patients.In summary, we describe three LDLT donors who developed occipital PA. Clinicians should be aware that LDLT surgery may be associated to PA. However, the reasons for this potential association remains obscure.