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Biomedical subjects

E B Weiss

Publications and source records attributed to E B Weiss.

12 recordsLinked to original sources
PubMed1979

Calcium hypersensitivity in airways smooth muscle. Isometric tension responses following anaphylaxis.

The isometric tension of anaphylactic guinea pig trachealis muscle preparation was examined at subphysiologic extracellular calcium concentrations, in vitro. Paired observations of control to passively sensitized (egg albumin antiserum) and antigen-challenged muscles (anaphylaxis) were made to exposure to trace Ca++ followed by cumulative Ca++ replacement. Following anaphylaxis, a leftward shift of the Ca++ concentration-tension responses was found at 0.25--0.5 mM Ca++ (p less than 0.001); EC50 was 1.5 x greater than control. A greater maximal tension was also noted at 2.52 mM Ca++. Passively sensitized muscles did not exhibit this heightened response. Subthreshold tissue chemical mediators are tentatively excluded as causative. An increased sensitivity to extracellular Ca++ exists in resting smooth muscle following anaphylaxis.

Anaphylaxis↗
PubMed1978

T3 thyrotoxicosis in a child.

We report the case of a 5-year-old hyperthyroid boy with normal serum T4 levels are elevated serum T3 levels. The findings are diagnostic of T3 thyrotoxicosis, a condition that has been very infrequently reported in childhood. We postulate that low dietary iodine intake may be an etiologic factor in some cases of T3 thyrotoxicosis.

Child, Preschool↗
PubMed1978

The inhibitory action of lidocaine in anaphylaxis.

The action of lidocaine, a local anesthetic, was investigated during anaphylaxis in guinea pigs after passive sensitization in vitro of lung tissue and trachealis muscle. Pretreatment of the trachealis muscle with 8.54 mM lidocaine resulted in the total inhibition of anaphylactic isometric tension. Full reversal of anaphylactic-induced contractures was rapidly achieved with concentrations of 4.27 mM lidocaine. Release of histamine from both lung tissue and trachealis muscle was inhibited by 73 to 82 per cent, respectively, over concentration ranges of 2.13 to 8.54 mM lidocaine. A bimodal effect on sensitized tissues was noted, with lidocaine causing a slight release of histamine in the trachealis muscle of 1.6 per cent at a concentration of 8.54 mM. Lidocaine did not impair the initial passive sensitization process, nor did it appear to elute antibody once it was cell bound. The dual inhibitory effect on mast-cell release of mediators and on muscle contraction by lidocaine may be related in part to common processes involving the binding or flux of calcium.

Amines↗
PubMed1978

Allopurinol-induced arteritis in partial HGPRTase deficiency. Atypical seizure manifestation.

A 17-year-old boy with partial hypoxanthine-guanine phosphoribosyl transferase deficiency developed a hypersensitivity reaction to allopurinol. The reaction was manifested by the development of bizarre, atypical seizures. The patient had been neurologically normal prior to the reaction. Seizures disappeared following discontinuation of allopurinol therapy. Allopurinol apparently can cause a diffuse vasculitis involving cerebral vessels after many year of therapy, resulting in atypical seizures.

Adolescent↗
PubMed1977

Effect of histamine on the length-tension properties of guinea pig trachealis muscle.

The isotonic length-tension properties of excised live guinea pig trachealis muscle have been determined as a function of histamine concentration. Over the range of histamine concentrations studied, a family of curves corresponding to the total and active tensions were obtained. Reciprocal plots of the tension-concentration data revealed a length dependence of the affinity constant of histamine for its receptor The tensions and lengths below resting were considered to be of special importance because of the role of muscle contraction in airway closure. A mechanochemical model for shortening and reelongation of the trachealis muscle during anaphylaxis has been proposed on the basis of this data. By comparing the force-length properties of the muscle at the lowest histamine concentration, it was suggested that the formation of a histamine-Ca++ receptor complex causes an increase in the rigidity of the muscle membrane. The complete range of lengths, tensions, and concentrations must be employed in order to propose a mechanism of action from mechanical data alone.

Animals↗
PubMed1977

Effect of propranolol on normal human erythrocytes.

The present study was undertaken to standardize the effect of propranolol on normal human red cells and thus establish certain parameters enabling us to evaluate propranolol's effect on pathological cells. Normal human erythrocytes lost 40 MEq. of potassium, decreased the intracellular pH by 0.06 units, and shifted the oxyhemoglobin dissociation curve 6.0 mm. Hg to the right in the presence of propranolol. The series of events and magnitude of the response induced by propranolol was time dependent and sensitive to temperature, pH, drug concentration, and erythrocyte concentration. Calcium was an absolute requirement for maximal propranolol action with simultaneous incorporation of trace amounts of radioactive calcium into the cell. Chelation of calcium with EDTA or EGTA inhibited the response to propranolol.

Calcium↗
PubMed1977

Folic acid nonresponsive homocystinuria due to methylenetetrahydrofolate reductase deficiency.

Four siblings from a family with 11 children of Irish ancestry were observed to suffer from an essentially identical clinical illness, consisting of delayed psychomotor development in infancy and childhood, severe mental retardation, and upper motor neuron dysfunction. Death occurred at an early age in three siblings. In cases in which detailed physical examinations were performed, ectopia lentis, marfanoid features, and severe bony deformities were absent. Homocystinuria, homocystinemia, relatively normal concentrations of methionine and cystine in tissue fluids, and absence of methylmalonic aciduria were found. A deficiency of methylenetetrahydrofolate reductase was demonstrated in cultured skin fibroblasts from two siblings. Postmortem examination of two of the three patients who died showed extensive vascular thrombosis. No biochemical improvement was observed in the surviving child following treatment with large doses of folic acid.

Adolescent↗
PubMed1976

Hormonal therapy and cholelithiasis.

This report is to alert the abdominal surgeon to a new factor responsible for a rising incidence of cholelithiasis in the younger woman. The cause of cholelithiasis has been explained on the basis of biochemical changes with mechanical obstruction. The role of estrogen-progesterone elevation in pregnancy with associated hypercholesteremia is well-known. Little known are reports (more common in non-American literature) that female hormones effect a sluggishness of gallbladder function. Thus, a chemical change with a functional type of obstruction in the biliary tree predisposes toward cholelithiasis. A survey of 1346 cholecystic operations from 1969 through 1973 showed the expected greater incidence in women. Women under 40 years of age who received hormonal medication were younger when operated upon than a comparable group not receiving hormonal therapy. The incidence of gallbladder disease in young women using hormonal therapy should be expected to increase in the coming years. Cholelithiasis should be suspected in the young female taking birth control medication. X-ray study is indicated and early surgery is desirable to prevent morbidity, mortality and the complications of cholecystic disease.

Adult↗
PubMed1975

The effect of local anesthetic, lidocaine, on guinea pig trachealis muscle in vitro.

The effect of lidocaine was studied in guinea pig trachealis muscle by dose-response reversal and protection of agonist-induced contractures in a superfusion system. Lidocaine reversed histamine, acetylcholine, and depolarizing hypertonic potassium contractures with the median effective doses of 2.8, 6.0, and 3.2 mg. Lidocaine presuperfusion shifted in a nonparallel fashion (P less than 0.05) the dose-response of histamine, acetylcholine, depolarizing potassium, and supramaximal electrical stimulation by contact electrodes. Pretreatment with 7 x 10(-6) M atropine did not modify lidocaine's inhibition of the hypertonic potassium contractions. These findings and the decrease in maximal response indicated noncompetitive antagonism. In contrast to isoproterenol, the action of lidocaine was not influenced by beta-blockade induced by superfusate propranolol, 1.0 mug per ml (P = 0.2). Lidocaine's effect on trachealis smooth muscle was facilitated by a decrease in hydrogen ion activity from pH 6.71 to 7.90, consistent with enhanced penetration of the free base. Low bolus dose lidocaine-induced contractures were noted in many studies. The potency of isoproterenol in comparison to lidocaine, as indexed by median effective doses, was 10(5) greater for reversal of histamine contractures and 10(4) greater for acetylcholine. The data were consistent with a nonspecific, reversible antagonism on the smooth muscle cell and may involve an effect on calcium activity.

Acetylcholine↗