Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Propofol was used for 1,350 sessions of electro-convulsive therapy (ECT). After 0.5 mg of intravenous atropine, patients received 1 to 1.5 mg.kg-1 bolus of propofol over a period of 20 seconds or less. This was convenient for loss of the eye-lash reflex. A bolus of 15 to 20 mg suxamethonium was given, in non allergic patients, to prevent trauma from the seizure. The patient was hyperventilated with pure oxygen through a facial mask. The electric shock was delivered bitemporally after a dental protection had been inserted. For each patient, the following data were noted: sex, use of tricyclic antidepressant drugs, atopy, amount of administered propofol and the effective intensity of the electric shock. The 99 patients were given 16.27 +/- 14 ECT sessions. Among them 26 took antidepressant drugs and 34 were atopic. There was no difference, except for weight, between the 25 men and 74 women. The mean dose of propofol was 1.37 +/- 0.3 mg.kg-1. The dose decreased with increasing age. There was no statistical relationship between the amount of propofol and intensity of the electric shock required to set off a seizure. The use of antidepressant drugs, and atopy did not influence the required amount of propofol. Speed of injection seemed to be the determining factor for narcosis with low doses of propofol. Hyperoxia and hypocapnia induced by hyperventilating with pure oxygen seemed to facilitate occurrence and duration of seizures. Although propofol has been said to reduce the length of seizures, there is controversy concerning the ECT efficacy criteria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Use of propofol in 1350 anesthetized patients for electroconvulsive therapy]. 200 69

We have investigated the effects of a continuous infusion (18 mg kg-1 h-1) of the aqueous emulsion formulation of propofol on mean pulmonary arterial (PAP)/cardiac output (O) and mean systemic arterial pressure (SAP)/Q relationships in 15 intact pentobarbitone-anaesthetized dogs subjected to hyperoxia (F/O2 0.4) and hypoxia (F/O2 0.1). Five-point PAP/Q and SAP/Q plots were obtained by opening an arterio-venous femoral fistula or by stepwise inflations of an inferior vena cava balloon. Over the range of Q studied (2-5 litre min-1), hypoxia increased PAP in eight dogs ("responders") and did not affect PAP in seven others ("non-responders"). Hypoxic pulmonary vasoconstriction (HPV) was restored in non-responders by the administration of acetylsalicylic acid (ASA) 1 g i.v. Hypoxia did not affect SAP over the range of Q studied in the responders or in the non-responders treated with ASA. Propofol had no effect on hyperoxic or on hypoxic PAP at all values of Q either in responders or in non-responders with HPV restored by ASA. Propofol did not change Q at uncontrolled flow, but decreased SAP at the lowest Q (2 and 3 litre min-1) during hyperoxia and at all values of Q during hypoxia. The systemic vascular effects were the same in animals of both groups, treated with ASA or not. We conclude that propofol does not influence pulmonary vascular tone and does not inhibit HPV, but reduces systemic vascular tone when venous return or oxygenation is decreased. The haemodynamic response to propofol was not affected by cyclo-oxygenase inhibition.
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PMID:Effects of propofol on pulmonary and systemic arterial pressure-flow relationships in hyperoxic and hypoxic dogs. 278 23

We have investigated the effect of inhaled oxygen tension on lipid metabolism during propofol infusion. Propofol is supplied as a lipid emulsion containing 10% soybean oil, which is rich in triglycerides (TG). Infused TG are metabolized via three pathways in the liver cell; Krebs cycle, ketogenesis and release as very low density lipoproteins (VLDL) into the blood. For this reason, we measured TG and the products of the three pathways; carbon dioxide, ketone bodies and VLDL. Thirty-two rabbits were anaesthetized under four different conditions: propofol under hyperoxia, normoxia, hypoxia and isoflurane anaesthesia under hyperoxia. Our results indicated that hyperoxia produced more ketone bodies, normoxia more PaCO2 and hypoxia more free fatty acids (FFA) and TG compared with the other propofol infusion groups. We conclude that hyperoxia during propofol infusion facilitated fat metabolism through ketogenesis, while normoxia did so via the Krebs cycle. Also, hypoxia suppressed utilization of TG and VLDL production in the liver.
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PMID:Effects of inhaled oxygen concentration on fat metabolism during propofol infusion in rabbits. 1043 35