Enterohepatic haemodynamics in calves during acute systemic anaphylaxis

Holroyde, Martin C.; Eyre, P.

doi:10.1016/0014-2999(75)90200-9

Cited by 5 publications

(3 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the other hand, we have been proposing that anaphylactic hypotension is accompanied by hepatic venoconstriction, possibly beyond the species differences, and that the liver and splanchnic vascular beds play significant roles in anaphylactic hypotension. Actually, anaphylactic hepatic venoconstriction is observed in dogs (27,30), rats (23), rabbits (17), guinea pigs (21), cats (4), and calves (16). The anaphylactic portal hypertension may increase the intravascular volume (blood pooling) and the capillary pressure of the upstream splanchnic vascular beds.…”

Section: Perspectives and Significancementioning

confidence: 99%

“…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%

See 1 more Smart Citation

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

Section: Perspectives and Significancementioning

confidence: 99%

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

“…More recently, the sheep has been employed as a potential model of allergic bronchospasm associated with human asthma (Wanner e t al., 1979). In studies of anaphylactic shock to E. coli (Wray & Thomlinson, 1972) and to certain antigens (Wells e t al., 1973;Alexander e t al., 1970;Holroyde & Eyre, 1975a) gastrointestinal lesions have been observed. Most prominent among these are mesenteric and hepatic engorgement and the accumulation of fluid in the abdominal cavity.…”

Section: Introductionmentioning

confidence: 99%

Preliminary pharmacological characterization of ovine mesenteric vasculature

Mirbahar

Eyre

1984

Vet Pharm & Therapeutics

View full text Add to dashboard Cite

Spirally cut strips of ovine mesenteric vein and artery were studied in isolated organ baths. No qualitative differences were observed in the autonomic and autacoid reactivity of these blood vessels. Both arterial and venous preparations responded in a dose-related manner to 5HT greater than or equal to adrenaline greater than phenylephrine greater than histamine. The responses of venous and arterial strips to 5HT were antagonized by methysergide while mepyramine inhibited histamine-induced contractions. Phentolamine competitively inhibited adrenaline on arteries. Vascular preparations, incubated with mepyramine (2 X 10(-7) M) and contracted half-maximally with 5HT, responded with relaxations to the higher doses of histamine. Specific H2-agonists, impromidine and dimaprit also caused relaxations of half-maximally contracted venous and arterial strips. Impromidine was approximately 500-5000 times more potent than histamine and dimaprit. Trimetaquinol effectively relaxed both venous and arterial preparations while isoproterenol had either no effect or produced weak contractions/relaxations. This investigation suggested the presence of (i) both excitatory and inhibitory receptors for histamine, (ii) D-tryptaminergic receptors mediating contractile effects of 5HT, and (iii) a predominance of alpha-adrenergic receptors, in the mesenteric vasculature of sheep.

show abstract

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

Chand

Eyre

1977

European Journal of Pharmacology

View full text Add to dashboard Cite

Enterohepatic haemodynamics in calves during acute systemic anaphylaxis

Cited by 5 publications

References 13 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

Preliminary pharmacological characterization of ovine mesenteric vasculature

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

Contact Info

Product

Resources

About