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Biomedical subjects

J E Mack

Publications and source records attributed to J E Mack.

11 recordsLinked to original sources
PubMed1992

Acute cardiovascular effects of methyl methacrylate monomer: characterization and modification by cholinergic blockade, adrenergic stimulation and calcium chloride infusion.

1. Methyl methacrylate monomer (MMA) given by i.v. infusion to anesthetized dogs caused a sustained hypotension, bradycardia, reduction of cardiac output and stroke volume, and increased peripheral resistance. 2. Epinephrine i.v. could reverse the hypotension but not the bradycardia; isoproterenol i.v. could reverse the bradycardia but not the hypotension. 3. Bilateral cervical vagotomy prevented bradycardia but not other cardiovascular effects of MMA, and prevented all respiratory effects except hypoxemia. 4. Calcium chloride i.v. reversed all circulatory changes except bradycardia; a combination of atropine and calcium reversed all cardiovascular changes from MMA.

Animals↗
PubMed1991

Effect of polyethylene glycol on lipid peroxidation in cold-stored rat hepatocytes.

A mechanism suggested to cause injury to preserved organs is the generation of oxygen free radicals either during the cold-storage period or after transplantation (reperfusion). Oxygen free radicals can cause peroxidation of lipids and alter the structural and functional properties of the cell membranes. Methods to suppress generation of oxygen free radicals of suppression of lipid peroxidation may lead to improved methods of organ preservation. In this study we determined how cold storage of rat hepatocytes affected lipid peroxidation by measuring thiobarbituric acid reactive products (malondialdehyde, MDA). Hepatocytes were stored in the UW solution +/- glutathione (GSH) or +/- polyethylene glycol (PEG) for up to 96 h and rewarmed (resuspended in a physiologically balanced saline solution and incubated at 37 degrees C under an atmosphere of oxygen) after each day of storage. Hepatocytes rewarmed after storage in the UW solution not containing PEG or GSH showed a nearly linear increase in MDA production with time of storage and contained 1.618 +/- 0.731 nmol MDA/mg protein after 96 h. When the storage solution contained PEG and GSH there was no significant increase in MDA production after up to 72 h of storage and at 96 h MDA was 0.827 +/- 0.564 nmol/mg protein. When freshly isolated hepatocytes were incubated (37 degrees C) in the presence of iron (160 microM) MDA formation was maximally stimulated (3.314 +/- 0.941 nmol/mg protein). When hepatocytes were stored in the presence of PEG there was a decrease in the capability of iron to maximally stimulate lipid peroxidation. The decrease in iron-stimulated MDA production was dependent upon the time of storage in PEG (1.773 nmol/mg protein at 24 h and 0.752 nmol/mg protein at 48 h).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Comparison of the effects of hydrochlorothiazide and furosemide on lithium disposition.

OBJECTIVE: This study examined the interaction between lithium and diuretics, comparing both the pharmacokinetic and the pharmacodynamic variable of hydrochlorothiazide, furosemide, and placebo. METHOD: The study, which took place in an outpatient research clinic of a university hospital, used a double-blind, placebo-controlled crossover design. The subjects were normal, healthy male volunteers who responded to recruitment announcements. Thirteen subjects entered and completed the study. All subjects took lithium, 300 mg b.i.d., for 6 weeks. Hydrochlorothiazide, 25 mg b.i.d.; furosemide, 20 mg b.i.d.; and placebo were given during weeks 2, 4, and 6 in a random order of assignment. Serum lithium levels and indices of diuretic activity were measured during each week. RESULTS: The subjects' serum lithium levels after 5 days of taking hydrochlorothiazide were significantly higher than after 5 days of taking furosemide and placebo. At the doses studied, hydrochlorothiazide was also more potent than furosemide in increasing plasma renin activity, increasing sodium excretion, and decreasing lithium excretion. CONCLUSIONS: The observed differences between diuretics in effects on serum lithium may have been due to differences in the potency of the diuretics at the doses studied as well as in the site of action of the diuretic effect. The results must be interpreted cautiously, however, because the effects were small and of questionable clinical significance, and the study used healthy volunteers and low doses of lithium instead of psychiatric patients and the usual therapeutic levels of lithium.

Adult↗
PubMed1989

Alcoholics Anonymous and contemporary psychodynamic theory.

AA's success rests on its ability to establish and maintain abstinence. This basic and essential accomplishment has tended to detract from the fact that AA is successful in good part because it is a sophisticated psychosocial form of treatment that addresses human psychological vulnerabilities that alcoholics and others share related to problems of self-regulation. The "character defects" that AA addresses are related to attitudes about self and others that are embodied in character traits and styles that make interdependence, experience, and expression of feelings and self-care problematical and difficult. AA confronts these "defects" by effectively advocating surrender, acceptance of a Higher Power, and challenging human self-centeredness. In its insistence on openness, support, sharing of experiences, and mutual concerns, AA imaginatively employs group psychology to address vulnerabilities in self-governance and problems in regulating feelings and self-care.

Alcoholics Anonymous↗
PubMed1988

The enemy system.

Explore the source record for details and available documents.

Attitude↗
PubMed1987

Influence of veratridine on [3H]-L-quinuclidinyl benzilate ([3H]QNB) binding in mouse hindbrain.

The neurotoxin veratridine is well known for its ability to open sodium channels in neuronal and muscle tissues in micromolar concentrations. It has also been shown that veratridine is an inhibitor of the potent muscarinic receptor antagonist L-quinuclidinyl benzilate (QNB) at these concentrations. These findings prompted us to examine the relationships between action potential sodium channels and muscarinic receptors in a glass-fiber filtration assay for [3H]QNB binding to mouse hindbrain membranes using agents known to affect interconversion of the affinity states in some muscarinic receptor populations, i.e. guanosine triphosphate (GTP) and magnesium (Mg2+). The actions of the sodium channel antagonist tetrodotoxin (TTX) were also examined. Veratridine inhibited [3H]QNB binding with a Ki value of approximately 2.5 microM. This inhibition exhibited a competitive mechanism at higher concentrations (5-10 microM), while showing an apparent non-competitive action at low concentrations (1 microM). Magnesium caused a parallel shift to the right in the inhibition curve with a 32% increase in the veratridine Ki. GTP caused a non-parallel shift to the left with the greatest displacement occurring at lower veratridine concentrations (2-5 microM). The addition of magnesium to GTP did not alter the action of GTP significantly. TTX (5 microM) caused a parallel shift of the veratridine inhibition curve to the right. In addition, TTX alone inhibited the binding of [3H]QNB. Therefore, it appears that there may be more than one binding site for veratridine which may be linked to the muscarinic system and that these may be action potential sodium channels.

Animals↗
PubMed1986

The effects of sodium channel ligands on muscarinic receptor binding in mouse forebrain.

The neurotoxins veratridine and aconitine are best known for their abilities to open action potential sodium channels in neuronal and muscle cells. These neurotoxins were tested for their abilities to influence the binding of 3H-QNB in mouse forebrain employing a glass-fiber filtration assay. Veratridine and aconitine produced approximately 95% and 77% inhibition of muscarinic receptor specific 3H-QNB binding with IC50 values of 11 and 20 microM, respectively. Further analysis revealed that both veratridine and aconitine were competitive inhibitors of 3H-QNB binding. Tetrodotoxin, an antagonist of the actions of veratridine and aconitine on sodium channels, at 10 microM inhibited the binding of 3H-QNB by 9% in the presence of 10 microM veratridine while having no effect when used in combination with aconitine. These data indicate that there may be a relationship between muscarinic receptors and action potential sodium channels.

Aconitine↗