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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Baroreflex sensitivity (BS) was used to quantitatively assess the effects of halothane and isoflurane on the heart rate/arterial pressure relationship during steady-state (10 minutes) and dynamic pressure changes in adult horses. Arterial pressure was decreased in response to nitroglycerin or sodium nitroprusside and increased in response to phenylephrine HCl. Mean (+/- SEM) BS in awake horses was 28.9 +/- 2.6 and 13.2 +/- 2.0 ms/mm of Hg during steady-state decreases and increases in systolic arterial pressure (SAP), respectively. Halothane and isoflurane either significantly (P less than 0.05) decreased or eliminated BS during steady-state decreases in SAP, with no significant differences detected between anesthetic agents. During steady-state decreases in SAP, significant (P less than 0.05) correlation between R-R interval and arterial pressure was not observed for 6 of 10 and 4 of 11 halothane and isoflurane anesthesia periods, respectively. Halothane significantly (P less than 0.05) decreased BS during steady-state increases in SAP to 7.9 +/- 0.6 and 6.5 +/- 1.1 ms/mm of Hg during low and high minimal alveolar concentration (MAC) multiples, respectively. Isoflurane decreased BS during steady-state increases in SAP to 9.6 +/- 1.5 and 6.6 +/- 1.1 ms/mm of Hg during low and high MAC anesthesia, respectively, with high MAC of isoflurane decreasing BS significantly (P less than 0.05), compared with awake and low MAC values. Plasma catecholamine (epinephrine and norepinephrine) concentrations increased significantly (P less than 0.05), compared with baseline values during steady-state vasodilator infusions in halothane- and isoflurane-anesthetized horses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of halothane and isoflurane on baroreflex sensitivity in horses. 261 Apr 41

We compared the vitamin B-6 status of 12-wk-old rats (n = 12) fed excess (1400 mg/kg diet) or the recommended level (7 mg/kg diet, control) of pyridoxine (PN) hydrochloride to test if excess vitamin B-6 would cause tissue depletion of pyridoxal phosphate (PLP), the active coenzyme form of vitamin B-6. Plasma PLP, tryptophan-load test results, food intake, and tissue and body weights were not different at wk 6. Red blood cell endogenous alanine aminotransferase activity and PLP concentration were elevated (P less than 0.01) in rats fed 1400 mg PN.HCl/kg diet. In contrast, PLP concentration in muscle was significantly lower (P = 0.01) in rats fed excess vitamin B-6 (9.7 +/- 0.8 nmol/g, mean +/- SEM) than in controls (14.9 +/- 1.4). PLP concentration in other tissues, including plasma, was not affected. In rats fed excess vitamin B-6, pyridoxal was increased in all tissues examined (P less than 0.05), and total vitamin B-6 was increased in plasma, red blood cells and kidneys (P less than 0.05). Total glycogen phosphorylase (a + b) activity in the gastrocnemius was not affected, but phosphorylase a activity was increased in rats fed excess vitamin B-6 (P = 0.025). Concentrations of dopamine and metabolites in the caudate nucleus of the basal ganglia were not affected. A transient, but significant, elevation in acoustic startle response, a central nervous system reflex, was observed in rats fed excess vitamin B-6. The depletion in muscle PLP could not hae been predicted by either plasma or red blood cell PLP concentration, although the latter did reflect vitamin B-6 intake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of vitamin B-6 status and function of rats fed excess pyridoxine. 268 1

The aim was to determine whether cholecystokinin-octapeptide (CCK-OP), bethanechol Cl, or metoclopramide HCl would increase the antidumping effect of intestinal pacing in five dogs with truncal vagotomy and Roux gastrectomy. While recording electrical activity from the conscious animals, the amount of a 100-ml, 25% dextrose gastric instillate emptied in 20 min was determined during control tests, during tests with CCK-OP (500 ng/kg/hr), bethanechol (80 micrograms/kg/hr), or metoclopramide alone (600 micrograms/kg/hr) given intravenously or during tests using combinations of pacing and drugs. In other tests, intraluminal gastrointestinal pressure was measured during control and drug infusions. CCK-OP, which relaxed the proximal stomach, slowed emptying of the dextrose instillates (mean +/- SEM emptied, no pacing, no drug = 74 +/- 5 ml; CCK-OP alone = 34 +/- 5 ml; P less than 0.05). CCK-OP also enhanced the slowing effect produced by pacing (pacing alone = 41 +/- 7 ml; pacing plus CCK-OP = 19 +/- 8 ml; P less than 0.05). In contrast, bethanechol and metoclopramide, which did not alter proximal gastric motility, did not alter emptying or augment or diminish the effect of pacing. The conclusion was that the combination of pacing and CCK-OP slowed gastric emptying of the dextrose more than pacing alone and thus had a greater antidumping effect. In contrast, neither bethanechol nor metoclopramide enhanced the pacing effect.
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PMID:Increasing antidumping effect of intestinal pacing with motor-active agents. 286 25

We report a method for the extraction of angiotensin peptides from plasma with a mixture of acetone, 1 mol/L HCl, and water (40/1/5 by vol). The method is highly reproducible for the measurement of angiotensin I and angiotensin II in small sample volumes, with analytical recoveries of about 80% for both peptides. We investigated the influence of sample handling and found a standard procedure for blood collection, plasma preparation, and extraction was essential. The method was used to measure angiotensin I and II in rat and human plasma. In rat plasma, the mean (+/- SEM) concentrations of angiotensin I and angiotensin II were determined to be 67 (+/- 8) and 14 (+/- 1) pmol/L (n = 10), respectively. Neither angiotensin I nor angiotensin II was detectable 24 h after bilateral nephrectomy. Acute oral administration of the converting-enzyme inhibitor ramipril caused a significant increase of angiotensin I from 85 (+/- 6) to 257 (+/- 33) pmol/L (n = 10; P less than 0.001) and a significant decrease of angiotensin II from 12 (+/- 1) to 7 (+/- 0.4) pmol/L in rat plasma (n = 9; P less than 0.001). In human plasma, angiotensin I and angiotensin II values of 21 (+/- 1) and 6.6 (+/- 0.5) pmol/L (n = 10) were found. A single oral dose of the diuretic furosemide increased angiotensin I significantly from 21 (+/- 1) to 32 (+/- 1.7) pmol/L (n = 5); P less than 0.001), whereas angiotensin II remained unchanged, 6.6 (+/- 0.5) vs 6.4 (+/- 0.4) pmol/L (n = 5). Extracted peptides could be identified as [IIe5]-angiotensin I and [IIe5]-angiotensin II by HPLC in combination with specific radioimmunoassays for angiotensin I and angiotensin II.
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PMID:Measurement and characterization of angiotensin peptides in plasma. 296 40

To determine whether the stimulatory effect of CO2 on the peripheral chemoreceptors is due to molecular CO2, H+ or both we measured steady-state ventilation (Ve) during normoxia in 9 and during hypoxia in 5 chloralose-urethane anaesthetized cats using the artificial brain stem perfusion technique. This technique allows one to manipulate independently the PaCO2, PaO2 and the pHa of the blood in the systemic circulation (peripheral) and the blood perfusing the brain stem (central). Keeping the central conditions constant the H+ and CO2 concentrations in the systemic circulation were changed by i.v. infusion of 0.3 M HCl or 0.6 M NaHCO3 and by giving the animal different CO2 mixtures to inhale. The peripheral H+ concentration ([H+]p) range covered was from 27 to 103 nmol X 1(-1); the peripheral arterial CO2 tension (PaPCO2) ranged from 2.3 kPa to 8.4 kPa. Fitting the data with the function VE = a[H+]p + bPaPCO2 + c revealed that the coefficient b was not significantly different from zero at the 0.05 level during normoxia and hypoxia. The mean value (+/- SEM) found for the coefficient a was 33.0 +/- 3.6 at normoxia and 36.0 +/- 15.4 ml X min-1 X nM-1 at hypoxia. We conclude that the steady-state ventilatory response due to the stimulation of the peripheral chemoreceptors with CO2 is mediated by H+. The effects of molecular CO2 are negligible.
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PMID:Effects of CO2 and H+ on the ventilatory response to peripheral chemoreceptor stimulation. 308 87

Ketamine HCl [2-(o-chlorophenyl)-2-(methylamino) cyclohexanone HCl] concentrations in whole blood were used to study the pharmacokinetics of i.v., i.m., and rectal administrations, at a dose of 25 mg/kg, in normal domestic cats. Absorption was rapid with both the i.m. and rectal routes. Systemic availability was 51% (SEM 10) for the i.m. dose and 43.5% (SEM 6.1) for the rectal dose. The first-pass effect had a minimal influence on the metabolism of ketamine HCl administered rectally. The elimination rate constant (beta) of the drug was statistically similar in the i.v., i.m., and rectal groups, at a 95% level of significance (P less than 0.05). At the dosage rates studied, ketamine HCl produced an anesthetic effect in the cat following i.v., i.m. and rectal administration.
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PMID:Pharmacokinetics of ketamine HCl and metabolite I in the cat: a comparison of i.v., i.m., and rectal administration. 337 68

Antihypertensive medications currently used in the treatment of hypertensive urgencies are limited due to deleterious side effects or requirements for sophisticated monitoring techniques. Labetalol HCl (Trandate) is a unique adrenergic blocking agent that can smoothly lower blood pressure following bolus injection without increasing heart rate or cardiac output. This study evaluates the efficacy and safety of intravenous boluses of labetalol HCl in the treatment of patients presenting to the hospital with a diagnosis of hypertensive urgency (diastolic blood pressure greater than or equal to 110 mm Hg). After baseline blood pressure and heart rate were recorded, 20 consecutive patients were treated with an initial 20-mg bolus of labetalol. Additional boluses of 40, 80, and 160 mg were administered at least 10 minutes apart in a step-wise fashion until control of blood pressure (diastolic blood pressure less than 100 mm Hg) was achieved or a total of 300 mg had been given. Blood pressures and heart rates were recorded at the time of response or following the last dose of labetalol. Mean (+/- SEM) supine systolic blood pressure decreased from 185 +/- 3 to 155 +/- 4 mm Hg (P less than 0.05) following labetalol therapy, and mean supine diastolic pressure decreased from 120 +/- 2 to 98 +/- 2 mm Hg (P less than 0.05). Mean heart rate did not change significantly. Eighteen of the 20 patients exhibited a therapeutic response; nine patients received a total of 20 mg, six required 60 mg, two required 140 mg, one received 300 mg. Of the two patients who did not respond, one received the maximum dose (300 mg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical evaluation of intravenous labetalol for the treatment of hypertensive urgency. 341 4

This paper investigates acid disposal by gastric and duodenal mucosa with particular reference to the mechanisms of acid-stimulated luminal alkalinization in the duodenum. The bulk of solute flux across duodenal epithelium occurs by paracellular permeation, and passive diffusion of HCO3 via shunt pathways contributes substantially to luminal alkalinization by this tissue in vitro. Effects on epithelial permeability of two treatments which stimulate mucosal alkaline secretion (PGE2 and low luminal pH) were studied in vivo by measuring transmucosal fluxes of radiolabeled urea (mol wt 76) and inulin (mol wt approximately 5000). Rats were anesthetized and rates of alkalinization in segments of distal duodenum perfused with saline were monitored by continuous titration. PGE2 (10 microM, topically) increased alkaline secretion from 1.63 +/- 0.34 to 3.07 +/- 0.54 microeq/cm/hr (mean +/- SEM, N = 5). Luminal acid exposure (10 mM HCl for 10 min) increased alkalinization rate from 1.54 +/- 0.43 to 2.69 +/- 0.76; subsequent addition of PGE2 induced a further rise to 3.27 +/- 0.54. Recovery of inulin in the luminal perfusate following intravenous injection was less than 10% of that of urea. Topical PGE2 had little or no effect on recovery of either marker. Luminal acidification increased the rate of appearance of urea by 130 +/- 30% (P less than 0.01, N = 6); recovery of inulin rose slightly but did not achieve statistical significance compared with control. Thus stimulation of mucosal alkaline secretion by luminal PGE2 or acid are associated with differential effects on mucosal permeability.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of acid disposal and acid-stimulated alkaline secretion by gastroduodenal mucosa. 342 26

A combined HCl-collagenase digestion technique and scanning electron microscopy were used to isolate the enamel organ and to confirm the presence of maturation ameloblasts of both ruffle-ended (RA) and smooth-ended (SA) types on maturing enamel in kitten permanent tooth germs. EDTA perfusion of animals fixed with aldehyde produced two or three belt-like shallow grooves (from 30 to 100 micron wide) running horizontally through the maturing enamel surface, coinciding closely with the SA distribution pattern. In animals that had been perfusion-fixed with unbuffered osmium tetroxide containing 2.5% potassium pyroantimonate, SEM-EDX analysis detected K in a superficial enamel layer overlaid by the SA layer. Potassium concentration decreased gradually toward the deeper layers. Very little K penetrated the enamel under the RA layer. Energy-dispersive x-ray analysis of Ca and P concentrations in the enamel revealed an even distribution of these elements throughout the superficial layer of maturing enamel. These results suggest that the SA layer forms an access route for K and EDTA and that, in spite of the obvious morphological and functional differences between RA and SA, the maturing enamel surfaces overlaid by these two cell types show similar degrees of mineralization.
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PMID:Correlated observations and analysis of maturation-ameloblast morphology and enamel mineralization. 345 21

The purpose of the present study was to investigate the relationship of the gastroesophageal pressure gradient (GEPG) to lower esophageal sphincter pressure (LESP) in normal and in severely obese subjects. Eight lean volunteers with no clinical evidence of gastroesophageal reflux and eight asymptomatic severely obese patients (at least 80% over their ideal weight) underwent esophageal manometric studies with measurements of the LESP and GEPG in both inspiration and expiration. The LESP/GEPG ratio was also calculated in both inspiration and expiration. Acid sensitivity was assessed by means of infusion of 0.1 N HCl subsequent to the baseline motility study. There was no significant difference between the LESP in obese patients (O.P.) and normal subjects (N.Sb.) in either inspiration (mean +/- SEM in mm Hg: N.Sb. = 16.4 +/- 1.6, O.P. = 18.7 +/- 2.5), or expiration (N.Sb. = 16.6 +/- 1.5, O.P. = 20.6 +/- 2.6). However, the GEPG in both inspiration (N.Sb. = 13.3 +/- 1.6, O.P. = 23.1 +/- 2.0; p less than 0.001) and in expiration (N.Sb. = 2.1 +/- 0.5, O.P. = 8.1 +/- 1.1; p less than 0.001) was significantly higher in obese patients than in controls. As a result, the GEPG/LESP ratios were also higher (expiration N.Sb. = 0.15 +/- 0.03, O.P. = 0.46 +/- 0.10; p less than 0.01) in obese patients; and for inspiration (N.Sb. = 0.86 +/- 0.13, O.P. = 1.33 +/- 0.12; p less than 0.01) in the obese patients the ratio was greater than 1. None of the normal subjects exhibited acid sensitivity, but 6 of the 7 obese patients tested developed heartburn during acid infusion. In conclusion, the GEPG/LESP ratio in inspiration was greater than unity for obese patients inspite of normal LESP. Such a change in the ratio could facilitate reflux in obese patients.
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PMID:Lower esophageal sphincter pressure and gastroesophageal pressure gradients in excessively obese patients. 348 Sep 30


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