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Query: UMLS:C0278134 (anesthesia)
 110,339 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of two different anaesthetics, sodium pentobarbitone and ethyl urethane, on the enhancement of maximal bilirubin and bromosulphthalein (BSP) excretion induced by bile salts was investigated in rabbits. Two micelle-forming (glycodeoxycholate and taurocholate) and one non-micelle-forming (dehydrocholate) bile salts were used. Under urethane anaesthesia the bile flow was lower than with pentobarbitone, and this could be attributed to a smaller bile salt non-dependent fraction of secretion. The effect of bile salts on the maximal excretion of the two organic anions appeared more clearly related to some kind of micelle interaction in rabbits anaesthetized with urethane than in pentobarbitone-anaesthetized animals. Thus, under urethane, infusions of glycodeoxycholate substantially increased the maximal excretion of bilirubin and BSP, taurocholate exerted an intermediate and dehydrocholate only a small effect. Under pentobarbitone, however, the augmenting action of all three bile salts was similar. The influence of bile salts on the endogenous excretion of bile pigments in experiments in which the test anion was BSP showed corresponding differences dependent upon the anaesthetic used. Possible explanations for those results are discussed.
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PMID:A comparison of the effect of bile salts on maximal hepatic excretion of certain organic anions in the rabbit under urethane and pentobarbitone. 672 13

To determine whether salt loading increases the sensitivity of the myocardium to fatal arrhythmias induced by norepinephrine, four groups of Sprague-Dawley rats were studied. Group I received both saline (0.9%) as drinking water and deoxycorticosterone acetate (DOCA) (0.5 mg/kg, 3 times) for 14 days (DOCA high salt group); group II received only 0.9% saline as drinking water (high salt group); group III received DOCA in the same dose regime, but tap water to drink (DOCA group); and group IV received tap water (control). Under pentobarbital anesthesia, norepinephrine was infused and electrocardiogram and blood pressure were monitored. The DOCA high salt group developed arrhythmias significantly (p less than 0.05) earlier than at lower norepinephrine doses. The dose at which 50% mortality occurred was 20 micrograms . kg-1 . min-1 in DOCA high salt group, 37 micrograms . kg -1 . min-1 in high salt group, 40 micrograms . kg-1 . min-1 in the control, and 44 micrograms . kg-1 . min-1 in the DOCA group. The cumulative dose of norepinephrine associated with 50% mortality was 160 micrograms/kg in the DOCA high salt group, 370 micrograms/kg in the high salt group, 530 micrograms/kg in the control group, and 600 micrograms/kg in the DOCA group. The blood pressure after sodium loading before norepinephrine infusion was similar in all three groups. The blood pressure response to norepinephrine was not significantly different between the four groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased sensitivity to norepinephrine cardiac arrhythmias in the deoxycorticosterone acetate high salt rat before the onset of hypertension. 674 5

A double-blind comparison of carbonated bupivacaine and bupivacaine hydrochloride in extradural anaesthesia was performed in 40 patients. No significant differences in the onset times, sensory blockade, motor blockade and duration of anaesthesia were demonstrated. Carbonated bupivacaine does not appear to offer any advantage over the hydrochloride salt for extradural anaesthesia.
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PMID:Comparison of carbonated bupivacaine and bupivacaine hydrochloride for extradural anaesthesia. 676 52

Carbonated lidocaine is believed to penetrate membranes more rapidly than its hydrochloride salt and could possibly cause higher serum levels. To compare serum levels, arterial blood samples drawn at intervals were analyzed in a group of 18 patients under epidural anaesthesia with equivalent doses of lidocaine hydrochloride and lidocaine hydrocarbonate, with and without epinephrine. Results show that serum levels were significantly higher when lidocaine hydrocarbonate was used for epidural analgesia.
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PMID:Effects of carbon dioxide and epinephrine on serum levels of lidocaine after epidural anaesthesia. 678 11

The effect of indomethacin on the renal function has been surveyed by the literature and our experimental data. The primary purpose of the present paper is to discuss the various mechanisms of the prostaglandins which participate in the overall operation of the kidney. Prostaglandin has been proposed as a "natriuretic hormone" effecting the natriuresis observed with extracellular fluid volume expansion. Dogs and rabbits were volume expanded under Nembutal anaesthesia. The massive natriuresis associated with expansion ws significantly reduced in dogs by preloading injection of indomethacin (4 mg/kg) to depress prostaglandin synthesis. The indomethacin pretreatment considerably increased the diuretic and natriuretic effect of the volume expansion in the rabbit. The data are consistent with the concept that intrarenal prostaglandins play a role in adjustment of renal vascular resistance and support the concept of a physiological role of intrarenal PG-s in regulating salt and water excretion.
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PMID:The effect of indomethacin on renal function. 700 2

My study was designed to measure the effect of salt intake on secretion and catabolism of catecholamines by the kidney and renal nerve contributions to urinary catecholamine excretion. Rats with one chronically denervated (DEN) and one innervated (INN) kidney were fed either high salt (HS) or low salt (LS) diets for 5 to 14 days. Under Inactin anesthesia rats were expanded with isotonic saline while LS rats received 10% mannitol to produce the same urine flow rates. Epinephrine excretion was ten times greater from LS than from HS rats; however, epinephrine/inulin excretion was the same from INN and DEN kidneys. Norepinephrine/inulin excretion was 30% less from DEN than from INN kidneys in both HS and LS rats (P less than 0.01). Dopamine/inulin excretion was 20% less from the DEN kidney than from the INN kidney of HS rats (P less than 0.05), but the 5% lower dopamine/inulin excretion from DEN than from INN of LS rats was not significant. Norepinephrine and dopamine tubular secretions from the rats, estimated by microinjecting radioactive tracers beneath the renal capsule, were 21 and 65%, respectively. After the microinjection, 68% of radioactive norepinephrine and 65% of radioactive dopamine were secreted unchanged. Catecholamine secretion rates and catabolism were not altered by denervation or different salt intakes. Estimated neural NE release was 1 ng/min in INN kidneys of both HS and LS rats; dopamine release 0.6 ng/min in kidneys of HS rats. Thus, when anesthesized, renal nerves contribute 30% to urinary NE and up to 21% to urinary dopamine excretion. Salt intake did not influence NE release from renal nerves or catecholamine secretion and catabolism by the kidney, but salt depletion decreased the renal nerve contribution to urinary dopamine excretion.
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PMID:Effects of salt intake and renal denervation on catecholamine catabolism and excretion. 706 96

The anticholinesterase activity of the unsymmetric bisquaternary 6-aminoquinoline salt NSC-176319 (QB) was studied in vitro. QB proved to be a noncompetitive inhibitor of both acetylcholinesterase (or true cholinesterase) and butyrylcholinesterase (or pseudocholinesterase) having a KI = 0.5 X 10(-6) M for acetylcholinesterase and 1.5 X 10(-6) M for butyrylcholinesterase. Further, QB inhibited esterase activity of murine plasma in a noncompetitive manner (KI = 4.2 X 10(-6) M). The inhibition was instantaneous in onset and did not diminish with prolonged incubation of the drug and enzyme. All mice treated intravenously with 2 mg QB/kg died within 5 min. Prior to death, mice developed severe parasympathomimetic effects and convulsions. Although the parasympathomimetic effects were diminished by atropine sulfate pretreatment, death could only be prevented by barbiturate anesthesia.
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PMID:Anticholinesterase activity of the unsymmetric bisquaternary 6-aminoquinoline salt NSC-176319. 707 62

A combination of autoradiography of water-soluble compounds and normal and retrograde perfusions was used to study whether there was a heterogeneity in bile salt transport between zone 1 and zone 3 hepatocytes of the rat and, if so, whether such a heterogeneity was due to the localization of these cells in the liver blood-stream, to intrinsic cellular differences, or to both. When a low dose of [3H]taurocholate was administered under pentobarbital sodium anesthesia in vivo or to normally perfused livers, the label was localized primarily in zone 1; in livers perfused in a retrograde direction, it appeared predominantly in zone 3. High doses of [3H]taurocholate administered in vivo and in normal and retrograde perfusions resulted in a more homogeneous labeling of the acini. The plasma disappearance of [3H]taurocholate was similar in normal and retrograde perfusions, but in the latter biliary excretion occurred at a considerably slower rate. From these results it is concluded that at low doses bile salts are primarily transported by zone 1 cells. Zone 3 cells appear to be able to take up taurocholate with ease, but their biliary excretion is slower compared with zone 1 cells.
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PMID:Autoradiographic and kinetic demonstration of acinar heterogeneity of taurocholate transport. 714 29

It was shown in acute experiments on mice and dogs that aspartic acid and its sodium salt administered 15-30 minutes prior to ether and hexenal anesthesia prolong the animals' life span by 42.2-99.9% compared to control given an isotonic solution of sodium chloride. The stabilizing action of the aspartate is accounted for by its effect on the reactive properties of the central nervous system, particularly on the new cortex, old cortex, archicortex and circulation. This effect is also associated with the increased oxygen tension in brain tissues, with increased heart contractions and slowing down of their rhythm.
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PMID:[Changes in the reactive properties of the body under anesthesia against a background of aspartic acid premedication]. 744 65

Since hemorrhagic events represent a major safety concern associated with the use of new antithrombotic therapies such as glycoprotein (GP) IIb/IIIa receptor blockade, we evaluated the ability of a monoclonal antibody recognizing DMP 728 (cyclic [D-2-aminobutyryl-N2-methyl-L-argininyl-glycyl-L-aspartyl-3- aminomethyl-benzoic acid] methanesulfonic acid salt), a potent GPIIb/IIIa receptor antagonist, to reverse the pharmacological actions of DMP 728 in the dog. DC11 was chosen for in vivo evaluation based on its ability to inhibit the binding of [3H]DMP 728 to activated platelets and to attenuate the inhibition of ADP-induced aggregation on platelet-rich plasma ex vivo by DMP 728. After anesthesia mongrel dogs were given DMP 728 (20 micrograms/kg body wt IV) infused into the femoral vein, bleeding times were determined using a Simplate device from incisions on the backside of the tongue, and platelet aggregation was determined ex vivo. Nearly complete inhibition of platelet aggregation was observed for the dogs treated with DMP 728 (20 ug/kg IV) for up to 210 minutes, and bleeding times were prolonged > 15 minutes for 2 hours and remained elevated for more than 4 hours. DC11 (0.2 or 1.0 mg/kg body wt IV) given to dogs 10 minutes after DMP 728 resulted in 50% attenuation of the effect of DMP 728 on aggregation at 3 hours. Approximately 34% inhibition of the DMP 728-mediated bleeding time was achieved at 1 hour with the 0.2 mg/kg dose, whereas approximately 50% inhibition of the bleeding time was observed for the 1 mg/kg dose at 1 hour.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A monoclonal antibody that recognizes the GPIIb/IIIa antagonist DMP 728. Reversal of the effects of DMP 728 on platelet aggregation and bleeding time in the dog. 748 42


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