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Biomedical subjects

M Maze

Publications and source records attributed to M Maze.

At least 127 records · Page 7Linked to original sources
PubMed1985

Postcountershock myocardial damage after pretreatment with adrenergic and calcium channel antagonists in halothane-anesthetized dogs.

Transthoracic electric countershock can cause necrotic myocardial lesions in humans as well as experimental animals. The authors investigated the effect on postcountershock myocardial damage of pretreatment with prazosin (0.1 mg/kg), an alpha-1 antagonist; L-metoprolol (0.5 mg/kg), a beta-1 antagonist, and verapamil (0.5 mg/kg), a calcium channel-blocking agent. Twenty dogs were anesthetized with halothane and given two transthoracic countershocks of 295 delivered joules each after drug or vehicle treatment. Myocardial injury was quantitated 24 h following countershock by measuring the uptake of technetium-99m pyrophosphate in the myocardium. Elevated technetium-99m pyrophosphate uptake occurred in visible lesions in most dogs regardless of drug treatment. For each of four parameters of myocardial damage there was no statistically significant difference between control animals and those treated with prazosin, metoprolol, or verapamil. These data suggest that adrenergic or calcium channel-mediated mechanisms are not involved in the pathogenesis of postcountershock myocardial damage.

Anesthesia, Inhalation↗
PubMed1985

Alpha 1-adrenergic blockade raises epinephrine-arrhythmia threshold in halothane-anesthetized dogs in a dose-dependent fashion.

The authors determined whether increasing alpha 1-adrenergic blockade resulted in progressively less arrhythmic activity in the canine halothane-epinephrine arrhythmia model. Dogs (n = 7) were anesthetized with halothane (1.5%) in oxygen. Stepwise increases in steady-state plasma levels of either of two alpha 1-adrenoceptor antagonists (droperidol, doxazosin) were produced by applying Wagnerian principles to the known pharmacokinetic parameters of these drugs. At each steady state plasma level of these antagonists, the extent of the alpha 1-adrenergic blockade produced was assessed by defining a phenylephrine (PE) dose pressor response curve. The degree of alpha 1-blockade produced was quantitated as the dose of PE that caused a 25-mmHg increase in mean arterial pressure (ED25) as derived by polynomial regression analysis. By analysis of variance (ANOVA) the ED25 increased significantly for each targeted steady state plasma level of either droperidol (P less than 0.001) or doxazosin (P less than 0.001). For an assessment of the antiarrhythmic activity of these alpha 1-antagonists, the arrhythmogenic dose of epinephrine (ADE) was determined at each of the states of alpha 1-adrenergic blockade previously defined. By ANOVA there was a significant increase in the ADE over the range of alpha blockade produced for either droperidol (P less than 0.001) or doxazosin (P less than 0.001). A close correlation (r2) existed between the ED25 and the ADE for the target steady state levels that were achieved for either droperidol (0.99) or doxazosin (0.74).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1985

Prolonged hyporesponsiveness of vascular smooth muscle contraction after halothane anesthesia in rabbits.

Halothane diminishes smooth muscle contractility in vascular tissue. In order to further characterize this phenomenon we undertook a series of in vivo and ex vivo experiments. Pressor dose-response curves to the selective alpha 1-adrenergic agonist, phenylephrine, were constructed in groups of rabbits before, during and 2 hr after halothane anesthesia and the dose of phenylephrine that induced a 25 torr increase in mean arterial pressure (ED25) was derived by polynomial regression analysis. ED25 torr increased significantly during halothane anesthesia, and rabbits remained in this insensitive state when the ED25 was assessed 2 hr after anesthesia. The halothane-induced loss of responsiveness was corroborated by ex vivo experiments utilizing aortic rings from halothane-anesthetized rabbits. The maximal contraction to norepinephrine (NE) was significantly lower in halothane-treated aortic rings and only slowly returned to normal by 4 hr. The EC50 (the dose causing a 50% maximal contraction) for NE was significantly greater in aortic rings from halothane-anesthetized rabbits. This loss of sensitivity, reflected by the higher EC50 was not restored by 4 hr of ex vivo incubation in a halothane-free medium. We conclude that halothane induces loss of sensitivity to adrenergic agonists that persists for several hours after termination of the halothane anesthetic.

Anesthesia↗
PubMed1985

[Adrenoreceptors].

With the development of techniques for the qualitative and quantitative assessment of receptor function and knowledge of the biological responsiveness of neurotransmitter-mediated pathways, it is now quite clear that the response of a patient to a drug does not only involve the concentration of the drug in blood and tissue. Number and function of receptors are also important factors. A perturbation in which the receptor number is elevated is called "up-regulation", whereas "down-regulation" refers to the uncoupling between receptor and effector and the consecutive decrement in the receptor concentration. In general, there is an inverse relationship between the ambient concentration of the agonist and the number of its receptors and, therefore, the sensitivity of the target organ. The demarcation between alpha- and beta-adrenergic receptors has long been appreciated. Recent advances in the understanding of adrenergic receptors have led to the subdivision of beta-receptors; beta 1-adrenoceptors mediate the stimulation of rate and force of cardiac contraction and stimulate lipolysis. beta 2-adrenoceptors mediate smooth muscle relaxation and facilitate glycogenolysis and the release of insulin, glucagon and renin. The alpha-adrenergic receptors may also be divided into two subgroups. The alpha 1-adrenoceptors are postsynaptic located and facilitate smooth muscle constriction. Presynaptic located alpha 2-adrenoceptors mediate feedback inhibition of norepinephrine-release, while postsynaptic alpha 2-adrenoceptors facilitate smooth muscle contraction in selected vascular beds and stimulate the inhibition of various metabolic processes (insulin and renin secretion, lipolysis). The stage is now set for the application of the new knowledge of receptor function and regulation to the advancement of the practice of anaesthesia and intensive care.

Adrenal Cortex Hormones↗
PubMed1985

Effects of volatile anesthetics or fentanyl on hepatic function in cirrhotic rats.

Halothane, enflurane, isoflurane, and fentanyl were examined for their potential to exacerbate liver dysfunction in rats with preexisting cirrhosis. Male Wistar rats given sodium phenobarbital for 2 weeks are assigned randomly to two groups. One group (cirrhotic) was exposed by inhalation to carbon tetrachloride (CCl4) in air at weekly intervals for 12 weeks to induce cirrhosis. The other group (noncirrhotic) was handled similarly but received air only. Five weeks after the last exposure to CCl4, cirrhotic and noncirrhotic rats were given three hours of 1 MAC halothane, enflurane, or isoflurane in 50% oxygen, or 350 micrograms fentanyl per kg of body weight and 50% oxygen, or 50% oxygen only. Blood gas tensions and blood glucose levels were measured before, during, and at the end of exposure. Forty-eight hours after exposure, serum chemistries were measured in each rat for comparison with preexposure values. Rats were then killed by CO2 overdose, and liver, kidney, and testis were prepared for microscopic examination. Enflurane, isoflurane, and halothane, but not fentanyl, produced mild respiratory acidosis and no change in serum glucose levels. All anesthetics resulted in a mild but similar degree of acute liver dysfunction as indicated by small increases in SGOT or SGPT in both cirrhotic and noncirrhotic rats. Liver histology revealed mild to moderate portal cirrhosis with fibrosis and well-developed micronodules in rats exposed to CCl4, but no superimposed acute hepatocellular damage was noted. It is concluded that all the anesthetics used in this study were associated with the same minimal degree of postanesthetic hepatic dysfunction and that the dysfunction was similar in both cirrhotic and noncirrhotic rats.

Alanine Transaminase↗
PubMed1984

Alpha-adrenergic responsiveness correlates with epinephrine dose for arrhythmias during halothane anesthesia in dogs.

The dose of epinephrine required to elicit ventricular arrhythmias during halothane anesthesia may depend on end-organ sensitivity. We determined whether the arrhythmogenic dose for epinephrine (ADE) could be correlated with either alpha- or beta-adrenergic responsiveness. After ADE was determined in 26 dogs anesthetized with 1.2 MAC halothane, an in vivo assessment of adrenergic responsiveness was made. The alpha-adrenergic responsiveness was defined as the dose of phenylephrine required to increase mean arterial pressure by 75% (alpha 75), while the dose of isoproterenol causing a 75% increase in heart rate was a measure of beta-adrenergic responsiveness (beta 75). The correlation coefficients for alpha 75 and beta 75 vs ADE then were determined by multiple linear regression analysis. There was a highly significant correlation with the alpha 75 (F = 9.06; P less than 0.01), while no relationship existed with beta 75 (F = 0.52; P greater than 0.05). Thus the alpha-adrenergic responsiveness in individual patients may be used to predict the threshold for epinephrine-induced arrhythmias during halothane anesthesia.

Anesthesia, General↗
PubMed1984

A multicenter study of the prevalence of hepatitis B viral serologic markers in anesthesia personnel.

Health care workers with frequent blood contact are at high risk of infection with hepatitis B virus. We surveyed 154 physician anesthesiologists (MD) and certified registered nurse anesthetists (CRNA) at four university-affiliated medical centers to determine the prevalence of serologic markers of hepatitis B virus (HBV). Questionnaires were used to ascertain historical and demographic information, nonoccupational risk factors, and characteristics of the participants' anesthesia practice. The overall prevalence of seropositivity was 18.8% (range 10.2-30.3%), and there were no statistically significant differences among the four centers, MD and CRNA groups, or males and females. In contrast to other studies, the prevalence of seropositive markers did not increase with an increase in the participants' age or length of time in the specialty. For the groups sampled in this study, geographic location or type of practice did not influence the increased prevalence of HBV seropositivity in anesthesia personnel. The current methods of HBV infection control were not associated with a decreased prevalence of serum markers. The majority of the susceptible anesthesia personnel at these four institutions did not plan to receive the hepatitis B vaccine when surveyed at the time of this study.

Anesthesiology↗
PubMed1984

Halothane-epinephrine arrhythmias and adrenergic responsiveness after chronic imipramine administration in dogs.

The incidence of halothane-epinephrine arrhythmias increases after the short-term administration of imipramine, probably because of enhanced noradrenergic transmission. To determine whether this effect persists after long-term imipramine treatment, we have studied the arrhythmogenicity and adrenergic responsiveness in halothane anesthetized dogs after six weeks of imipramine administration, 150 mg X day-1, orally. The mean (+/- SD) arrhythmogenic dose of epinephrine (ADE) in nine dogs anesthetized with 1.2 MAC halothane was 2.57 (+/- 1.04) micrograms X kg-1 X min-1. The alpha-adrenergic responsiveness, assessed as the dose of phenylephrine that caused a 75% increase in mean arterial pressure (alpha 75), was 5.78 +/- 2.39 micrograms X kg-1 X min-1. The dose of isoproterenol that increased heart rate by 75% (beta 75) was 309 +/- 180 ng X kg-1 X min-1. After imipramine treatment, the ADE (2.63 +/- 1.26), alpha 75 (5.16 +/- 2.05), and beta 75 (386 +/- 266) were not statistically different from the pre-imipramine values (P greater than 0.05), despite a fivefold increase in circulating norepinephrine. We conclude that chronic imipramine does not alter arrhythmogenicity and adrenergic responsiveness, since compensatory mechanisms, at the sympathetic nerve terminal, may revert the initial hyper-responsiveness to normal.

Anesthesia↗
PubMed1983

Identification of receptor mechanism mediating epinephrine-induced arrhythmias during halothane anesthesia in the dog.

The adrenergic receptor mechanism by which halothane sensitizes the myocardium to the ventricular arrhythmogenic properties of catecholamines is unknown. The new generation of selective adrenergic receptor antagonists have been used to determine which receptor blockade causes the greater increase in the dose of epinephrine needed to achieve a threshold for ventricular arrhythmias. Dogs anesthetized with 1.2 MAC halothane had an arrhythmogenic dose of epinephrine (ADE) of 2.2 micrograms X kg X min-1 that significantly increased (P less than 0.01) to 27 micrograms X kg-1 X min-1 after alpha 1 blockade with prazosin. beta 1 blockade with metoprolol also significantly increased the ADE to 12 micrograms X kg-1 X min-1 (P less than 0.05) but was less than the effect noted after prazosin treatment (P less than 0.05). The dramatic increase in the threshold for arrhythmias noted after prazosin could not be ascribed solely to its hemodynamic properties because treatment with sodium nitroprusside did not change the ADE (2.7 micrograms X kg-1 X min-1) significantly; yet nitroprusside treatment resulted in a similar drop in mean arterial pressure (59 mmHg) to that of prazosin treatment (51 mmHg) when compared with the control group. Thus postsynaptic myocardial alpha 1 adrenergic receptors mediate most of the sensitization by halothane to the ventricular arrhythmogenic effects of catecholamines, while a lesser contribution is conferred by the beta 1 adrenoceptors. These results have implications for the treatment and identification of patients particularly at risk from halothane-epinephrine interactions.

Adrenergic alpha-Antagonists↗
PubMed1983

Verapamil decreases MAC for halothane in dogs.

Verapamil hydrochloride is a calcium entry blocking drug that is being prescribed with increasing frequency for cardiovascular disorders in the perioperative setting. Verapamil's calcium channel blocking effect is not selective, because it also exerts activity on the sodium channel. Because of the well-described effects of sodium channel blockers on anesthetic requirements, the authors studied the MAC for halothane in dogs before and after a therapeutic dose of verapamil 0.5 mg . kg-1. There was a 25% reduction in halothane MAC from 0.97-0.72% (P less than 0.01) when a therapeutic plasma level of verapamil (64 ng . ml-1) was present. Anesthetic requirements for halothane are reduced by dl-verapamil possibly on the basis of its local anesthetic-like sodium channel blocking properties. Adjustments in anesthetic dosage may be necessary in patients receiving verapamil.

Anesthesia, Inhalation↗
PubMed1982

Prednisolone enhances aminopeptidase turnover in adult rat small intestine.

In adult male rats, fed prednisolone (0.75 mg/kg/day) for 7 days, brush border aminopeptidase activity was increased (P less than 0.001) by 106% compared to pair-fed controls. [14C]Tyrosine was injected intraperitoneally 16 h and [3H]tyrosine 6 h before death. The 3H/14C ratio was 1.79 +/- 0.21 (S.D.) in purified microvillus membranes from treated rats compared to 1.30 +/- 0.16 (P less than 0.01) in controls. Polyacrylamide gel electrophoresis of brush border membranes under denaturing conditions showed that the increased double-isotope ratio in membranes from treated rats was mainly in the high molecular weight protein subunits (greater than 80 kDa). Detergent-solubilized aminopeptidase was purified after in vivo labeling by protein A-Sepharose-antiaminopeptidase affinity chromatography. The 3H/14C ratio in aminopeptidase was 2.42 +/- 0.15 (P less than 0.05) in treated rats compared to 1.63 +/- 0.13 in controls. Over the experimental period steady-state isotope reutilization and protein labeling was demonstrated and there was no isotope metabolism. Total microvillus membrane lipid content was unaffected by prednisolone. We conclude that prednisolone increases brush border aminopeptidase activity by increasing enzyme turnover. Other high molecular weight brush border proteins were similarly affected.

Aminopeptidases↗
PubMed1978

Clinical trial of four pancreatic scanning agents.

Four 75Se-labelled amino acids have been tested in 22 patients. In 11 of the patients pancreatic function was estimated by the Lundh test. Scans at varying time intervals up to 30 hours from isotope administration were assessed by blind marking. Pancreatic visualization with all four agents was markedly poorer than would have been expected with 75Se-selenomethionine. Whole-body retention was estimated for all four agents; two showed faster 75Se clearance than selenomethionine. Radioactivity in duodenal aspirate was measured for two of the agents.

Amino Acids↗
PubMed1976

Pancreatic scanning.

The 75Se-selenomethionine pancreas scan cannot differentiate between chronic pancreatitis and carcinoma of the pancreas and may--although chiefly in certain defined clinical conditions--give a false-positive result. It is also rather more time-consuming than other radioisotopic scanning procedures. Its value in clinical practice stems from the fact that all the other methods currently available for studying the pancreas have their own disadvantages. Because a normal scan is only rarely seen in patients with carcinoma of the pancreas, pancreatic scanning can be particularly useful in helping to decide which patients should, and which should not, be subjected to other procedures involving greater discomfort or risk.

Chronic Disease↗