Autacoid and anaphylactic reactivity of pulmonary and hepatic smooth musculature of the cat

Chand, N.; Eyre, P.

doi:10.1016/0014-2999(77)90001-2

Cited by 29 publications

(26 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, we recently demonstrated that the liver and splanchnic vascular beds are involved in rat anaphylactic hypotension by showing that elimination of splanchnic circulation with total hepatectomy attenuated systemic hypotension induced by the ovalbumin antigen in anesthetized sensitized rats (23). Moreover, substantial hepatic venoconstriction is also observed in anaphylaxis of rabbits (17), guinea pigs (21), cats (4), and calves (16). On the other hand, in the mouse, although immunologic mechanisms for systemic anaphylaxis have been extensively studied (11), the hemodynamic mechanism for anaphylactic shock in mice has not been well clarified because of the technical difficulty involved in measurement of hemodynamic variables in this small animal (3).…”

mentioning

confidence: 99%

Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice

Liu¹,

Takano²,

Shibamoto³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

August 22, 2007; doi:10.1152/ajpregu.00904.2006.-Using in vivo and isolated perfused liver preparations of BALB/c mice, we determined the roles of the liver and splanchnic vascular bed in anaphylactic hypotension. Intravenous injection of ovalbumin antigen into intact-sensitized mice decreased systemic arterial pressure (Psa) from 92 Ϯ 2 to 39 Ϯ 3 (SE) mmHg but only slightly increased portal venous pressure (Ppv) from 6.4 Ϯ 0.1 cmH2O to the peak of 9.9 Ϯ 0.5 cmH2O at 3.5 min after antigen. Elimination of the splanchnic vascular beds by ligation of the celiac and mesenteric arteries, combined with total hepatectomy, attenuated anaphylactic hypotension. Ligation of these arteries alone, but not partial hepatectomy (70%), similarly attenuated anaphylactic hypotension. In contrast, isolated sensitized mouse liver perfused portally at constant flow did not show anaphylactic venoconstriction but, rather, substantial constriction in response to the anaphylaxisassociated platelet-activating factor, indicating that venoconstriction in mice in vivo may be induced by mediators released from extrahepatic tissues. These results suggest that splanchnic vascular beds are involved in BALB/c mouse anaphylactic hypotension. They presumably act as sources of chemical mediators to cause the anaphylaxisinduced portal hypertension, which induced splanchnic congestion, resulting in a decrease in circulating blood volume and, thus, systemic arterial hypotension. Mouse hepatic anaphylactic venoconstriction may be induced by factors outside the liver, but not by anaphylactic reaction within the liver. anaphylactic shock; hepatic circulation; portal hypertension; splanchnic congestion ANAPHYLACTIC HYPOTENSION appears to be caused primarily by a decrease in blood flow to the heart, because left ventricular function is relatively well preserved during anaphylactic shock (1, 2). Peripheral circulatory collapse is ascribed to hypovolemia, which results from a decrease in effective circulating blood volume. The latter could be due to vasodilation with the peripheral pooling and increased vascular permeability with a shift of intravascular fluid to the extravascular space (1, 2).In canine experimental models of anaphylactic shock, an increase in resistance to venous return is important in the pathogenesis of circulatory collapse (27): increased venous resistance decreases venous return, with a resultant decrease in stroke volume and systemic arterial pressure. Indeed, eviscerated dogs did not develop anaphylactic shock (19). In addition, Enjeti et al. (9) reported that the severity of the anaphylactic shock could be decreased by occlusion of the descending aorta. In dogs, the anaphylaxis-induced increase in venous resistance is partly caused by constriction of the hepatic veins (27, 30), which induces pooling of blood in the liver, as well as in upstream splanchnic organs. In addition, we recently demonstrated that the liver and splanchnic vascular beds are involved in rat anaphylactic hypotension by showing that elimination of splanchnic ci...

show abstract

mentioning

confidence: 99%

Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice

Liu¹,

Takano²,

Shibamoto³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

show abstract

“…The vascular effects of prostaglandins of the E series are highly variable, depending upon the concentration, species, region, blood vessels, media and spasmogen used to induce tone (Lewis & Eyre, 1972;Burka & Eyre, 1974;Joiner et al, 1975;Altura & Edgarian, 1976;Kitamura, Suzuki & Kuriyama, 1976;Chand & Eyre, 1977;Altura et al, 1980b;Chand & Altura, 1980a, c (Chand & Altura, 1980a, c Su & Bevan, 1976;Dusting et al, 1979), and variability from segment to segment of the individual (Somlyo & Somlyo, 1970;Chand & Altura, 1980a;1980c), together with the rapid pulmonary metabolism of PGE, and PGE2 (Dusting et al, 1979), it is doubtful whether either of these primary prostaglandins plays an important role. in regulating the pulmonary vasculature in either the dog or rat.…”

Section: Discussionmentioning

confidence: 99%

Differential Effects of Prostaglandins on Canine Intrapulmonary Arteries and Veins

Altura

Chand

1981

British J Pharmacology

Self Cite

View full text Add to dashboard Cite

1 The sensitivity and contractility of isolated canine intrapulmonary arteries and veins to a variety of primary prostaglandin compounds was studied.2 Intrapulmonary arteries produced no measurable contractile responses to prostaglandin A, (PGA,), PGA2, PGB,, PGD2, PGE,, PGE2 or to PGFI,. However, high concentrations of both PGB2 (> 10-7 M) and PGF2a (> 10-6 M) elicited concentrated-related, but weak, contractile responses, measuring only 5-25% of KCI-induced maximum contractions. 3 Intrapulmonary arteries, partially contracted by 5-hydroxytryptamine (5-HT), exhibited concentration-related relaxations in response to PGE,; PGE2, PGA, or PGA2 produced only weak superimposed con)actions. 4 In contrast to intrapulmonary arteries, intrapulmonary veins contracted in a concentrationrelated fashion to all prostaglandins tested, where the contractile sensitivity was (based on EC50 s and threshold concentrations): PGB2 > PGB, > PGD2 > PGF2a > PGA2 >> PGA, > PGFi, > PGE, > PGE,. 5 In terms of the ability to generate maximum contractile responses on intrapulmonary veins, the prostaglandins were also variable, with PGA2 and PGB2 being the most potent and PGD2 the least potent. 6 Intrapulmonary veins, partially contracted by 5-HT, exhibited concentration-related relaxations to PGE, at low concentrations, followed by secondary contractile responses at higher concentrations. 7 Neither PGA1 nor PGA2 (3.4 x 10-# to 3.4 x 10-5 M) inhibited or potentiated 5-HT responses of intrapulmonary arteries. 8 These data suggest that there are species, regional and major qualitative and quantitative, differences in the responsiveness of intrapulmonary arteries and veins to prostaglandin.

show abstract

“…The strips (25 x 3 x 2 mm) were dissected from the apical and cardiac lobes. Isotonic responses to drugs and antigen on paired lung strips were recorded as described by Eyre (1971) and Chand & Eyre (1977a: 1978b.…”

Section: Methodsmentioning

confidence: 99%

“…in vitro contraction of sensitized smooth muscles to antigens (Schultz, 1910;Dale, 1913) has frequently been used to demonstrate immediate hypersensitivity in a number of tissues in man and animals (Chand & Eyre, 1978a). Anaphylactic contractions to specific antigens have been demonstrated in the bronchus of guinea-pig (Grover, 1932), man (Schild, Hawkins, Mongar & Herxheimer, 1951;Brocklehurst, 1960;Dunlop & Smith, 1975;1977), cat and chicken (Chand & Eyre, 1977a;1978b); in the trachea of guinea-pig (Joiner, Wall, Davis & Hahn, 1974), cat (Lulich, Mitchell & Sparrow, 1976;Chand & Eyre, 1977a), monkey (Patterson, Miyamoto, Reynolds & Pruzansky, 1967) and dog (Antanissen, Mitchell, Kroeger & Stephens, 1978); and in the cat lung parenchymal strip (Lulich et al, 1976).…”

Section: Introductionmentioning

confidence: 99%

PHARMACOLOGY OF SCHULTZ‐DALE REACTION IN CANINE LUNG STRIP in vitro: POSSIBLE MODEL FOR ALLERGIC ASTHMA

Chand

DeRoth

Eyre

1979

British J Pharmacology

View full text Add to dashboard Cite

1 Isolated lung parenchymal strips of the dog contracted in response to histamine > carbachol > prostaglandin F2 , (PGF2#J> bradykinin (Bk) > 5-hydroxytryptamine (5-HT). The order of the relative activity of these agents on the tracheobronchial smooth muscles (TBSM) was carbachol'> 5-HT > histamine; PGF2. and Bk were inactive. Thus there are marked differences in the responsiveness of the smooth muscle of central (trachea and bronchus) and peripheral (lung strip) airways to autonomic and autacoid agents. 2 Lung strips and TBSM partially contracted by carbachol, histamine or horse plasma, were relaxed by isoprenaline, PGE1 and PGE2. 3 Lung strips from dogs sensitized to horse-plasma contracted in response to antigen (Schultz-Dale anaphylactic reaction). Tachyphylaxis or desensitization to subsequent antigen challenge was invariably observed; it was followed after 1 to 2 h of rest by partial recovery of the anaphylactic response.

show abstract

Autacoid and anaphylactic reactivity of pulmonary and hepatic smooth musculature of the cat

Cited by 29 publications

References 35 publications

Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice

Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice

Differential Effects of Prostaglandins on Canine Intrapulmonary Arteries and Veins

PHARMACOLOGY OF SCHULTZ‐DALE REACTION IN CANINE LUNG STRIP in vitro: POSSIBLE MODEL FOR ALLERGIC ASTHMA

Contact Info

Product

Resources

About