Interaction of beta Adrenergic Blockade and Certain Vasodilators in Dextran-Induced Rat Paw Edema

McKinney, Gordon B.; Lish, Paul M.

doi:10.3181/00379727-121-30813

Cited by 17 publications

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“…The almost universally inhibitory effect of cyclic AMP on leukocyte function (8) (26,27). The impressive interweaving of inflammatory and immune responses in both host defenses and the causation of many diseases suggests, however, that servomechanisms might exist.…”

Section: Discussionmentioning

confidence: 99%

Hemolytic Plaque Formation by Leukocytes in Vitro CONTROL BY VASOACTIVE HORMONES

Melmon¹,

Bourne²,

Weinstein³

et al. 1974

J. Clin. Invest.

212

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A B S T R A C T Histamine, beta-adrenergic amines, and prostaglandins inhibited hemolytic plaque formation by splenic leukocytes from immunized mice. The same agents had previously been shown to prevent both the IgE-mediated release of histamine from human basophils and the immunologically specific cytolytic activity of murine lymphocytes, through stimulation of the production of cyclic AMP in leukocytes. We therefore tested the hypothesis that cyclic AMP might mediate an inhibitory effect of these drugs by comparing the ability of these agents to inhibit plaque formation with their effects on cyclic AMP accumulation in leukocytes. In splenic cells from three mouse strains, the dose-dependent effects of these agents on cyclic AMP correlated with their inhibition of plaque formation. Beta-but not alpha-adrenergic agonists were effective in both systems, and the effects of isoproterenol were inhibited by propranolol. Histamine was approximately equipotent with isoproterenol in both systems. Two prostaglandins (Ei and E2) were effective in both systems, but prostaglandin F2. was not. Dibutyryl cyclic AMP, a lipid-soluble analog of the endogenous nucleotide, inhibited plaque formation by cells of all three strains. Theophylline, an inhibitor of cyclic AMP degradation, inhibited plaque formation slightly, but potentiated the effects of histamine, isoproterenol, and the prostaglandins on both cyclic AMP accumulation and plaque formation. Finally, cholera enterotoxin, a potent activator of adenyl cyclase, produced a delayed inhibition of plaque formation and a parallel increase in leukocyte cyclic AMP content; both effects of the toxin were blocked by canine antitoxin. These results suggest that leukocyte cyclic AMP may act as a "second messenger" to suppress plaque formation in vitro. The inhibitory effects of hormones and

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Section: Discussionmentioning

confidence: 99%

Hemolytic Plaque Formation by Leukocytes in Vitro CONTROL BY VASOACTIVE HORMONES

Melmon¹,

Bourne²,

Weinstein³

et al. 1974

J. Clin. Invest.

212

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“…Secondly, while there is less evidence to link catecholamines with the type of non-chronic infectious diseases reported in this study, anti-inflammatory properties of catecholamines have been described [35,36]. Qualliotine [37,38] reported that catecholamines reduced the bactericidal activity of leukocytes, and Ignarro and Colombo [39] have shown that catecholamines and cyclic-AMP inhibit the osmotic release of /3-glucuronidase from leukocyte lysosomes.…”

Section: Resultsmentioning

confidence: 73%

Catecholamine activity and reported morbidity

Gruchow

1976

Journal of Chronic Diseases

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Abstract:Urinary VMA levels were measured in relation to the reporting of morbidity in an attempt to determine whether altered catecholamine activity is related to specific disease syndromes, or is a general characteristic of morbidity. The cross-sectional data show elevated VMA levels to be associated with the reporting of chronic disease conditions; non-chronic conditions and affective disorders were associated with lower VMA values, Although these findings are interpreted as supporting the hypothesis that psycho-social stimuli acting through the sympathetic-adrenal medullary system may be important in the etiology of chronic disease conditions, alternative explanations are discussed and the need for further longitudinal studies indicated. Article:INTRODUCTION DURING the past several decades, the study of relationships between psychosocial factors and disease has led to better understanding of both the psychosocial events which may trigger or enhance disease processes, and the physiological mechanisms involved. Investigators are now in substantial agreement that psychosocial events can play an etiological role in a variety of different diseases. However, despite this progress, it is still unclear how these events are translated into disease states.Two different approaches have generally been taken to study this problem. One approach holds that there is a degree of specificity in these relationships, with certain types of psychosocial events more often associated with one type of pathophysiologic condition than other types. This approach is illustrated by numerous studies which have successfully demonstrated that specific disease entities such as tuberculosis [1,2], hypertension [3][4][5], coronary heart disease [6], cancer [7,8], rheumatoid arthritis [9,10], and even complications of pregnancy [11, 12] can be related to certain psychosocial events or to certain individual behavior patterns.Other investigators have taken a second approach, in which the general nature of a person's interactions within the social environment is related to overall morbidity [13][14][15][16][17], and increased morbidity of all types has been related to perception of `...life situations as demanding, threatening and frustrating ' [18].A way to begin resolving this question of causality is to evaluate both the morbidity and the presumed psychosocial risk factors for a common physiological link. One such physiological intermediary appears to be the sympathetic-adrenal medullary system, Elevated levels of the catecholamines and their metabolites have been reported in experimental subjects associated with exposure to various types of psychosocial stimuli [19]. Furthermore, increased catecholamine levels have been reported for several disease states including angina [20], hypertension [21,22] and gastric and duodenal ulcers [23,24]. In addition, elevated catecholamine activity has been suggested as a possible factor in the etiology of diabetes [25,26], and a beta adrenergic mechanism has been proposed as a central element in the develo...

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“…Fassina May et al (26) have shown that cyclic 3', 5'-AMP inhibits the release of lysosomal p-glucuronidase. Other investigators (27)(28)(29) have shown that epinephrine exhibits antiinflammatory action. Ascorbic acid may potentiate this effect.…”

Section: Control Tb Injected (G-c)mentioning

confidence: 98%

Some Anti-Inflammatory Properties of Ascorbic Acid

Dolbeare

Martlage

1972

Experimental Biology and Medicine

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Vascular and cell membrane permeability increases, the immune (allergic) response, and lysosomal hydrolase activity are interrelated in the inflammatory process. Ascorbic acid has been shown to play a stabilizing role in several of these processes indirectly in scorbutic animals. Ascorbic acid deficiency leads to separation of the cells in the vascular endothelium (1). A similar effect has been observed after histamine injection ( 2 ) . The evidence for ascorbate stabilization of cellular membranes is not well documented (3). The anti-allergic effect of ascorbic acid has been demonstrated through its ability to reduce anaphylaxis in the guinea pig (4), mouse ( 5 ) , and rat ( 6 ) ; but not in the dog ( 7 ) . We have shown previously that ascorbic acid can inhibit lysosomal P-glucuronidase (8). These results led us to investigate the effect of ascorbic acid in several animal models of inflammation. This report compares the inhibitory actions of ascorbic acid, aspirin, and phenylbutazone against rat liver lysosomal P-glucuronidase (in vitro), UV erythema in guinea pigs, carrageenan edema in rats, adjuvant arthritis and peritonitis-polyarthritis in rats.Materials and Methods. Animals used in these studies were (1) male, Cox/Holtzman rats for lysosomal P-glucuronidase and PPA, (2) female, Harlan/Holtzman rats for carrageenan edema and adjuvant arthritis, and (3) female albino guinea pigs for UV erythema. L-Ascorbic acid (Eastman), aspirin, and phenylbutazone (Geigy) were made up in stock solutions 2 0 x final concentration in ethanol/isotonic saline ( 1 / 1 ) for in vitro studies and five-fold concentration in carboxymethylcellulose for animal studies. Lysosomes were prepared by the method of deDuve et al. (9). The lysosomal pellets from five grams of rat liver were suspended in 200 ml of Mg-free Krebs-Ringer-Phosphate buffer, pH 7.4. Fifty p1 of stock solution of drug was added to 1 ml of lysosomal suspension. Control tubes contained 1 ml of lysosomal suspension and 50 pl of ethanol/saline. The tubes were incubated for 60 min at 37'. Then, 250 p1 of 5 mM p henolph t hale in-p-glucur onide ( sodium salt ) (Sigma) in 0.5 M acetate buffer, pH 5.0, was added to each tube. Incubation was continued for an additional 10 min. The enzyme reaction was stopped by the addition of 2.0 ml of 0.4 M glycine buffer, pH 10.7, containing 0.2 5 % sodium dodecyl sulfate to clear the suspension. Phenolphthalein was determined with a Zeiss PMQ I1 spectrophotometer at 560 nm.UV erythema was induced on guinea pigs by a modification of the method of Winder et al. ( 10). A Hanovia lamp (Kromayer model 10) was placed in contact with the skin on the back of a guinea pig for seven seconds. The animals were dosed Po 15 min before UV exposure. The erythemas were examined at 1 hr then half hour intervals until two and one-half hours after irradiation. The severity of the burn was rated 0-3. The rating was multiplied by 4 at 1 hr, 3, 2, 1 for each of the successive intervals. Control irradiated animals rated 120 by this technique.Edema was produced ...

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Interaction of beta Adrenergic Blockade and Certain Vasodilators in Dextran-Induced Rat Paw Edema

Cited by 17 publications

References 0 publications

Hemolytic Plaque Formation by Leukocytes in Vitro CONTROL BY VASOACTIVE HORMONES

Hemolytic Plaque Formation by Leukocytes in Vitro CONTROL BY VASOACTIVE HORMONES

Catecholamine activity and reported morbidity

Some Anti-Inflammatory Properties of Ascorbic Acid

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