Effect of l-Epinephrine and l-Arterenol on Egg White Edema in the Rat.

Clark, William G.; Kay, Eaton M. Mac

doi:10.3181/00379727-71-17090

Cited by 20 publications

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“…An in crease in extracellular fluid volume may result from an increase in vas cular permeability. However, evidence presented by Boizzi [3] and Clark and MacKay [6] suggest that epinephrine inhibits the increase in vascular permeability that is normally caused by other substances.…”

Section: Discussionmentioning

confidence: 99%

Action of Epinephrine on the Distribution of Two Model Amino Acids in the Diabetic Rat

Sanders¹,

Jacob²

1971

Pharmacology

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The injection of epinephrine (1.0 mg/kg) into alloxan-diabetic, fasted rats depressed the serum concentration of previously administered α-aminoisobutyric acid (AIB) and 1-aminocyclopentanecarboxylic acid (ACPC) within 2 h and simultaneously increased the concentration of these amino acids in the liver. The increase of ACPC and AIB concentrations in the liver following epinephrine injection was nearly 3 times as great in the alloxan-diabetic rats as in normal intact rats. The levels of the two amino acids in skeletal muscle, heart, and diaphragm of the alloxanized rats were unchanged following epinephrine injection, but the distribution ratios in these tissues were raised because the serum concentration decreased 20%.Further studies were carried out employing rats that were treated 1 h before epinephrine injection, with mannoheptulose, a compound which blocks insulin release. The concentration of ACPC and AIB in the serum 2 h after epinephrine injection were lowered. At the same time the concentrations of ACPC in liver and heart were raised, as was the concentration of AIB in heart. The levels of the two amino acids in skeletal muscle and diaphragm were unaltered. However, distribution ratios were raised in the four tissues. These results demonstrate that epinephrine enhances AIB and ACPC transport into the tissues of the insulin-deficient rats in vivo and suggest that epinephrine-stimulated amino acid transport is not due indirectly to insulin.

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Section: Discussionmentioning

confidence: 99%

Action of Epinephrine on the Distribution of Two Model Amino Acids in the Diabetic Rat

Sanders¹,

Jacob²

1971

Pharmacology

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“…Recently, 2-deoxyglucose has been found to be a potent diuretic and removal of oedema fluid from the reactive sites represents a possible inhibitory mechanism; this is unlikely, however, because other potent diuretics such as hydrochlorothiazide and theophylline do not inhibit the dextran reaction (Ankier, unpublished results). 2-Deoxyglucose may be potent in inhibiting the anaphylactoid response, as it is an efficient releaser of catecholamines from the adrenal medulla (Brown & Bachrach, 1959;Hokfelt & Bydgeman, 1961), and catecholamines are known to be active in antagonizing the reactions of rats to egg-white (Clark & MacKay, 1949) and dextran (Briot & Halpern, 1952).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of the Anaphylactoid Reaction in Rats

Ankier¹,

West²

1968

British Journal of Pharmacology and Chemotherapy

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) into rats produces an acute inflammatory response termed the anaphylactoid reaction. Some rats of the Wistar albino strain are genetically resistant to dextran and do not exhibit the reaction. Selective breeding experiments have since shown that the character of " non-reactivity " is associated with an autosomal recessive gene (Harris, Kalmus & West, 1963).It was recently found that relatively high intravenous doses of egg-white elicit an anaphylactoid reaction in dextran-resistant rats (termed non-reactors) and that dextrin is equally active in both reactor (that is, sensitive) and non-reactor rats (Ankier & West, 1964a, b). In the present work, the effects of some antagonists of histamine and 5-hydroxytryptamine (5-HT) and of some carbohydrates on the anaphylactoid reaction elicited in both types of rat by egg-white and dextrin and in reactor rats by dextran have been studied. A preliminary note of part of this work has already been published (Ankier & West, 1965). METHODS Test for reactivity to dextranMale Wistar albino rats (body weight 120-150 g) obtained from the Agricultural Research Council's Field Station (Compton) were injected with a single intraperitoneal dose of dextran 240 mg/kg (Intradex, Glaxo) once a week on three occasions. Animals showing peripheral oedema were classed as " reactors " and those failing to react to any of three injections were classed as " non-reactors." Rats were used subsequently after a period of time of not less than one week. Measurement of the anaphylactoid reactionAzovan blue dye (18 mg/kg) was injected intravenously immediately before the intraperitoneal or intravenous injection of fresh hens' egg-white (12 ml/kg), dextran (240 mg/kg) or dextrin (Astra, 1,250 mg/kg). The extent of oedema formation and colloidal dye accumulation in the extremities were estimated visually every half an hour over a period of 4 hr, using an arbitrary shock-score (with values of 0, 1, 2 or 3) for each of twelve areas (nose and bristle area, eyelids, lips, tongue, ear *Present address:

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“…a prolonged circulatory depressor action of egg-white in the non-sensitized cat was noted by Edmunds (1914). Also, it has been shown that parenteral egg-white causes such histamine-like effects as hyperaemia, pruritus, increased capillary permeability and oedema in the skin of rats (Parker & Parker, 1924;Selye, 1937; Leger, Masson & Prado, 1947), and that the effects are greatly reduced by the antihistamine drugs Halpern & Briot, 1949;Clark & MacKay, 1949;Gross, 1950). Leger & Masson (1948) further demonstrated that this syndrome in the rat is produced by the ovomucoid protein fraction of egg-white.…”

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confidence: 99%