Delays in discharge are mainly due to adverse symptoms or social/system problems. Delayed discharge is associated with increased postdischarge pain, lower RNA level, and patient acceptability. Appropriate care of postoperative symptoms and system management could prevent delay in discharge and improve patient RNA level and acceptability.

We have measured the direct effects of propofol 10(-7)-10(-4) mol litre-1 on isolated canine cerebral, coronary, mesenteric, femoral and renal arteries. In arterial strips precontracted submaximally with potassium chloride or prostaglandin F2 alpha (PGF2 alpha), propofol induced further contractions at low concentrations (10(-6)-10(-5) mol litre-1) and relaxation at high concentrations (10(-4) mol litre-1). Intrafat, which contains soya bean oil, egg phosphatide and glycerol in similar concentration to the emulsion formulation of propofol, had a small relaxant effect at a concentration corresponding to propofol 10(-4) mol litre-1. In humans, clinically relevant plasma concentrations of propofol have been reported to be 1-5 x 10(-5) mol litre-1, 97-99% of which is bound to plasma proteins. Therefore, the results obtained in this study demonstrated that clinically relevant concentrations of propofol did not have direct vasodilator effects.

The findings that sevoflurane suppressed the effects of arachidonic acid, but not those of prostaglandin G2 and STA2, suggest strongly that sevoflurane inhibited TXA2 formation by suppressing cyclooxygenase activity. Halothane appeared to suppress both TXA2 formation and binding to its receptors. Sevoflurane has strong antiaggregatory effects at subanesthetic concentrations (greater than 0.13 mM; i.e., approximately 0.5 vol/%), whereas halothane has similar effects at somewhat greater anesthetic concentrations (0.49 mM; i.e., approximately 0.54 vol/%). Isoflurane at clinical concentration (0.84 mM; i.e., approximately 1.82 vol/%) does not affect platelet aggregation significantly.

Platelet aggregation is impaired during anaesthesia with sevoflurane but not with isofluranePurpose: Halothane suppresses platelet aggregation in vitro and ex vivo, and prolongs bleeding time. In a previous in vitro study we demonstrated ~ sevoflurane had a more suppressive effect on platelet aggregation than did halo~hane. The present study i~ whel~ the clinical use of sevollurane aliected plamlet al~,regation ex vivo. Methods: Thirty-eight patients undergoing minor elective surgery were divided randomly into sevoflurane and isoflurane groups. Anaesthesia was induced with thiopentone iv, and was malntainecl with sevoflurane or isoflurane with nitrous oxide. Blood was collected to measure platelet aggregation induced by adenosine diphosphate (ADP) and epinephrine. The first (control) blood collection was performed in the operating room before induction of anaesthesia, and the second 5-I 0 rain after tracheal intubation but before the start of surgery, when the end-expiratory sevoflurane or isoflurane concentrations had stabilised at I-I .S times the minimum alveolar concentration (MAC) and mean arterial pressures were between 80-I 20% of preanaesthetic values. Results: In all samples obtained during sevoflurane anaesthesia (n = 15), ADP and epinephrine could not induce secondary a~regation, although they did induce primary a~egation. In contrast, in the isoflurane group, both primary and secondary aggregation were observed in 14 out of 15 patients, and secondary aggregation was abolished in only one of the samples obtained during anaesthesia. Conclusion: Sevoflurane, but not isoflurane, alters platelet aggregation in the clinical situation, possibly by suppression of thromboxane A~ formation.Objectif: Uhalothane inhibe l'agr~tion plaquettalre in v/fro et in vivo et prolonge le temps de saignement. Nous avons antEdeurernent d~montr6 que le s(~voflurane avalt un effet inhibiteur in vitro plus important sur l'a~t~tion plaquettaire que l'halothane. La prOsente ~ude a pour but de v&ifier si l'usage clinique du s~voflurane affecte ragr~gation plaquettalre in vivo. M&hodes : Trente-huit patients soumis ~ une chirurgie Elective mineure r~partis au hasard en groupe s~voflu-rane et groupe isoflurane participaient A l'&ude, l'anesth~sie &ait induite au thiopental/v, et entretenue au s~-voflurane ou A l'isoflurane avec du protoxyde d'azote. Du sang 6tait recueilli pour la mesure de l'agr~gation plaquettaire induite par le diphosphate d'ad~nosine (ADP) et l'6pin~phrine. Le premier 6chantillon sanguin (contr61e) c~tait recueilli en salle d'op&ation avant rinduction de l'anesth~sie et le second, 5-10 rain aprEs l'intubation irachicle et avant le d~but de rintervention apr(~s stabilisation des concentrations t61&expiratoires de s~voflurane et d'isoflurane A I-1,5 lois la concentration alv~,olaire minimale (MAC) de rn~me que de la pression artErielle moyenne A 80-120% des valeurs pr~anestl~siques. R~ultats : MalgrE une agr6gation primaire, I'ADP et l'6pin6phrine n'ont induit l'agr~ation secondaire dans aucun des Echantillons rec...

Ketamine inhibits human platelet aggregation possibly by suppressed IP3 formation and subsequent suppression of cytosolic free calcium concentration. The site of action of ketamine is neither TXA2 nor thrombin binding sites but possibly receptor-coupled mechanisms, including G-protein.