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

The alpha-adrenergic blocking agent phenoxybenzamine (PBA) was administered intravenously (10 mug kg-1 min-1) during a steady state water diuresis under pentothal anesthesia to six normal dogs, six dogs with chronic throacic inferior vena cava constriction and ascites (caval dogs) and seven dogs chronically salt depleted by sodium restriction and furosemide administration. In normal dogs urinary sodium excretion increased significantly from 265+/56 (SEM) to 370+/65 muequiv./min, whereas no increase in sodium excretion was noted in either caval dogs or salt depleted animals after PBA. In all three groups urine volume, fractional free water clearance and distalsodium load did not change significantly. In normal dogs, tubular sodium reabsorption decreased significantly from 73.4+/2.8% to 63.1+/4.0%, whereas no change was noted in caval or salt depleted dogs. Blood pressure and renal hemodynamics were not significantly altered by PBA administration in any group. These data demonstrate a natriuretic effect of alpha-adrenergic blockade in normal dogs with the major effect in the water clearing segment of the nephron. The absence of any effect in chronic caval or salt depleted dogs suggests that increased alpha-adrenergic activity does not play a significant role in the sodium retention of these animals.
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PMID:Effects of alpha-adrenergic blockade on sodium excretion in normal and chronic salt retaining dogs. 0 99

Clonidine s.c. (0.01-0.3 mg/kg), in unanesthetized rats, caused an initial rise (+20 mm Hg), followed by a continuous fall of BP and a dose-dependent natriuresis and diuresis for up to 2 h. Glomerular filtration rate (GFR) (CIn) increased during the first 20 min, while effective renal plasma flow (ERPF) (CPAH) remained normal. Subsequently, between 20 and 60 min after injection, ERPF (CPAH) decreased considerably while GFR had reverted to its normal value. In saline-infused rats clonidine diuresis was accompanied by an "inappropriate" positive free water clearance. Pentobarbital anesthesia suppressed the initial BP peak and the diuresis. Phenoxybenzamine (1 mg/kg i.v.) was antinatriuretic in saline diuresis; the effect of phenoxybenzamine + clonidine on diuresis and salt excretion represented the sum of the effects of both drugs, but phenoxybenzamine enhanced the clonidine-induced increase of GFR. Neither haloperidol (1 mg/kg i.v.) nor bulbocapnine (3 mg/kg i.v.) interfered with the renal effects of clonidine. Clonidine s.c. caused hyperglycemia and glucosuria which did not account for the natriuresis. Clonidine thus appears to increase the GFR and "filtration fraction" (FF) by a phenoxybenzamine-insensitive rise of glomerular ultrafiltration, to depress ERPF by alpha-adrenergic afferent vasoconstriction, to induce natriuresis by a tubular action not blocked by phenoxybenzamine and to exert an antivasopressin effect, either by depressing pituitary vasopressin secretion or the renal response to vasopressin.
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PMID:The renal effects of clonidine in unanesthetized rats. 4 24

In rats, the sleeping time induced by overdosage with eight steroid anesthetics--alfathesin, 3-(3-oxo-17beta-hydroxy-19-nor-4-androsten-17alpha-yl)-propionic acid-lactone (SC-8109), 21-hydroxy=5alpha-pregnane-3,20-dione (P-234), 4-pregnene-3,11,20-trione (Bio.66), 17-hydroxy-3-oxo-4-androstene-17alpha-propionic acid-gamma-lactone(SC-5233),3alpha-hydroxy-5beta-pregnane-11,20-dione, 5beta-pregnane-3,11,20-trione (U-1373), and hydroxydione--was abolished or considerably reduced by a variety of catatoxic compounds, particularly 3beta-hydroxy-20-oxo-5-pregnene-16alpha-carbonitrile (PCN), 9alpha-fluoro-11beta,17-dihydroxy-3-oxo-4-androstene-17alpha-propionic acid potassium salt (CS-1), prednisolone, ethylestrenol and spironolactone. Phenobarbital and diphenylhydantoin, two non-steroidal stimulators of hepatic microsomal drug metabolism, were also highly effective. In contrast, triamcinolone, estradiol,progesterone, desoxycorticosterone and hydroxydione, which exert little or no catatoxic activity, failed to significantly diminish anesthesia or sedation.
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PMID:Inhibition of the effects of alfathesin and other steroid anesthetics by catatoxic steroids in rats. 5 71

Earlier studies had demonstrated that in Lymnaea stagnalis thyrotropin releasing factor (TRF) may be the secretory product of the so-called dark green neurosecretory cells. The dark green cells are believed to serve an osmoregulatory function. If TRF is the secretory product of the dark green cells, it should be capable of controlling the salt and water balance in L. stagnalis. In this study, the effect and fate of synthetic TRF injected in vivo into L. stagnalis was assessed. It was found that TRF caused an increase in the rate of loss of body water which normally occurs after anaesthesia. TRF also increased the loss of body water when it was administered to unanaesthetized animals. The peptide was accumulated and degraded by the tissues of the foot, mantle, and head regions, tissues which are believed to be the targets of the hormone of the dark green cells. Our results support the hypothesis that TRF may be the secretory product of the dark green cells and may be involved in osmoregulation in L. stagnalis.
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PMID:Effect of thyrotropin releasing factor on body weight of the pond snail Lymnaea stagnalis. 11 15

The effect of ouabain and atropine on bile flow and bile iodine concentration in intravenous cholangiography was investigated in 4 cholecystectomized dogs (20 experiments) with complete bile diversion under general anesthesia and compared to the effect of sodium taurocholate. Iodipamide was administered intravenously with an initial priming dose of 50 mg per kg followed by a constant infusion of 2 mg per min per kg. Ouabain in stepwise increasing infusion rates, .0625 to .25 microgram per min per kg, had no significant effect. Atropine infusion rates from 1 to 8 microgram per min kg increased the bile iodine concentration up to 19% but already a 14% increase with a 5% reduction in bile flow was found with the smallest atropine dose. The lowest taurocholate infusion rate resulted in the highest bile iodine concentration and lowest bile flow. It is suggested that atropine premedication and low bile salt plasma levels might improve the opacification of the biliary tree particularly in hepatic dysfunction by reducing selectively specific fractions of the basal bile flow.
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PMID:Pharmacocholangiography. 14 7

Salt deprivation has been shown to cause fluid volume contraction and marked renin release; it is not clear whether angiotensin-induced vasoconstriction adds to low volume in compromising circulatory function or whether there are additional facets to the salt-deprived state. Mature Wistar rats were fed a low-salt diet for 1 mo and then, under pentobarbital anesthesia, compared to normals. Arterial pressure (is congruent to 125 mmHg), cardiac output (is congruent to 200 ml/min per kg), and total peripheral resistance were nearly identical in both groups. The influence of angiotensin was estimated by injecting converting enzyme inhibitor (SQ 20881, 1 mg/kg), and then observing the immediate hemodynamic response. Salt-deprived rats responded with a large (-47 mmHg) fall in pressure and total peripheral resistance indicating that, although total peripheral resistance was normal in salt deprivation, an increased fraction (30% vs. 11%) of the resistance was supported by angiotensin. Cardiac output decreased (-8%) in contrast to the increase that would be expected during marked arterial dilation; elevated angiotensin levels may have caused a moderate, beneficial decrease in venous compliance. These results suggest that circulatory function is adequately maintained during salt deprivation by a combination of normal total peripheral resistance and decreased venous compliance.
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PMID:Angiotensin and the hemodynamics of chronic salt deprivation. 16 93

The percutaneous penetration of the local anaestetic lidocaine was investigated in the guinea-pig. Three different types of composition were employed: lidocaine hydrochloride in aqueous solution, lidocaine base in an aqueous alcoholic solvent mixture and lidocaine base in aqueous solutions of dipolar aprotic solvents. The latter solvents included simple tertiary aliphatic amides, amides related to dimethylacetamide, some cyclic amides as well as a number of miscellaneous compounds. The degree of dermal anaesthesia was noted in each case. In addition, the uptake and distribution of lidocaine in the skin and its absorption into the blood were studied using tritium-labelled drug. The results show that the percutaneous penetration of lidocaine is dependent on the concentration of the agent, the time of epicutaneous application of the composition, whether the agent was used as salt or free base, and the nature of the solvent medium. Lidocaine base in aqueous dimethylacetamide was most effective in producing percutaneous local anaesthesia.
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PMID:Penetration enhancers and other factors governing percutaneous local anaesthesia with lidocaine. 47 60

Plasma catecholamine levels have been used experiemtally and clinically as the indices of the sympathetic nerve activity. We measured plasma catecholamines using high pressure liquid chromatography in rats to assess the significance of plasma catecholamines as an index of the sympathetic nerve activity and its role in hypertension. Pentobarbital anesthesia depressed plasma catecholamine levels, especially plasma adrenaline. Sodium loading for 5 weeks suppressed plasma noradrenaline, while administration of furosemide (1 mg/kg) produced the elevation of plasma noradrenaline. Experimental hypertension, one-kidney and two-kidney types of Goldblatt hypertension and DOCA-salt hypertension, raised plasma noradrenalines both in acute and chronic phases. The infusion of pressor doses of angiotensin II suppressed plasma noradrenaline by the reflex mechanism. Sar1, Ile8-angiotensin II and SQ 14,225 did not suppress plasma cathecholamine elevation due to hemorrhage. L-Hydroxyldopamine produced elevation of plasma catecholamines in experimental nypertension and controls in rats. After adrenal demedullation, plasma noradrenaline was decreased by the administration of 6-hydroxy-dopamine. Acute reduction of circulating blood volume and blood pressure fall produced the elevation of plasma catecholamine, especially plasma adrenaline. In rats, the adrenal medulla plays an important role in the regulation of blood pressure.
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PMID:Plasma catecholamines determination using high pressure liquid chromatography and their roles in blood pressure regulation and experimental hypertension in rats. 50 4

Rapid administration of intravascular volume expanders is often necessary during anesthesia. Significant controversy still exists on the relative values of different volume expanders. Fifteen hypoxemic patients (Pao2 less than 70 torr on room air) were studied preoperatively. They were randomized into three groups. One group received 1.5 ml/kg of 25% salt-poor human albumin, a second group, 7 ml/kg of fresh frozen plasma; a third group, 7 ml/kg of 0.9% NaCl in water (normal saline). The infusions were given intravenously and completed in 20 minutes. Changes in hemodynamic pressures and flows, blood chemistries, and oxygen uptake and transport variables were studied. It was concluded that fresh frozen plasma afforded the greatest increase in cardiac output and oxygen availability with the least increase in left ventricular stroke work. Colloid osmotic pressure was more significantly increased by fresh frozen plasma than by salt-poor human albumin. Normal saline caused both a decrease in oxygen availability and colloid osmotic pressure. Pulmonary venous admixture increased to some extent in all patients receiving fresh frozen plasma or normal saline. In three patients, this increase was very marked and accompanied by severe arterial hypoxemia.
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PMID:Rapid volume expansion in patients with interstitial lung diseases. 57 Dec 16

The cardiovascular responses of aortic cross-clamping and declamping with normal and high ventricular filling pressures were compared during epidural and nitrous oxide-morphine anesthesia in 32 male patients undergoing reconstructive aortic surgery. The patients were divided into four groups. Groups I and II had lumbar epidural blocks with bupivacaine and received nitrous oxide in oxygen to breathe; groups III and IV were anesthetized with morphine (2 mg/kg) and nitrous oxide. During aortic occlusion groups I and III received Ringer's lactate at a rate which maintained mean pulmonary capillary wedge pressure (PCWP) 3 to 4 torr above pre-anesthetic values whereas groups II and IV were given Ringer's lactate rates which kept PCWP similar to pre-anesthetic values. Prior to cross-clamping mean arterial blood pressure and systemic vascular resistance were lower in groups I and II than in groups III and IV but cardiac output, PCWP, and pulmonary vascular resistance were similar in the four gropus. Cross-clamping of the aorta produced no significant change in any cardiovascular variable measured in any group. Declamping did not significantly alter any variable in groups I and III but produced moderate hypotension in group IV and severe hypotension in group II as well as significant decreases in PCWP in both groups. Our data demonstrate that aortic cross-clamping and release result in little change in cardiovascular dynamics in patients anesthetized with epidural or morphine-nitrous oxide and given balanced salt solutions intravenously in amounts adequate to increase left ventricular filling pressures prior to release of the aortic cross-clamp. Our findings also indicate that hypotension can occur in patients in whom left ventricular filling pressures are maintained at normal levels prior to cross-clamp release, especially in patients given epidural anesthesia.
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PMID:Cardiovascular responses to clamping of the aorta during epidural and general anesthesia. 57 60


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