Cardiovascular aspects of anaphylaxis: implications for treatment and diagnosis

Brown, Simon G A

doi:10.1097/01.all.0000174158.78626.35

Cited by 149 publications

(99 citation statements)

References 32 publications

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“…19 A recent single-center trial described successful initial management with intravenous epinephrine infusions for anaphylaxis with hypotension, suggesting that this might be a viable strategy. 10,20 Detailed procedures for the preparation and administration of epinephrine infusions have been published. 5 It is important to recognize the potential for lethal arrhythmias when administering intravenous epinephrine, and therefore continuous cardiac monitoring is recommended.…”

Section: Epinephrinementioning

confidence: 99%

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Second symposium on the definition and management of anaphylaxis: Summary report—Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium

Sampson

Muñoz-Furlong²,

Campbell

et al. 2006

Journal of Allergy and Clinical Immunology

1,931

1,114

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Section: Epinephrinementioning

confidence: 99%

“…20 Recent case reports and animal studies have demonstrated that vasopressin is useful when treating hemorrhagic and septic shock. The effect of vasopressin on systemic anaphylaxis has not been investigated, except in clinical case reports.…”

Section: Vasopressorsmentioning

confidence: 99%

Second symposium on the definition and management of anaphylaxis: Summary report—Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium

Sampson

Muñoz-Furlong²,

Campbell

et al. 2006

Journal of Allergy and Clinical Immunology

1,931

1,114

View full text Add to dashboard Cite

“…During an anaphylactic reaction, serious cardiovascular or pulmonary dysfunction often leads to acute death, with severe hypotension as the cardinal clinical feature. Intravenous fluids and parenteral adrenaline administration are considered the only effective treatment; unfortunately, severe cardiovascular collapse during anaphylaxis is often resistant to this treatment (1,3).…”

Section: Introductionmentioning

confidence: 99%

Anaphylactic shock depends on PI3K and eNOS-derived NO

Cauwels¹

2006

Journal of Clinical Investigation

123

117

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Anaphylactic shock is a sudden, life-threatening allergic reaction associated with severe hypotension. Platelet-activating factor (PAF) is implicated in the cardiovascular dysfunctions occurring in various shock syndromes, including anaphylaxis. Excessive production of the vasodilator NO causes inflammatory hypotension and shock, and it is generally accepted that transcriptionally regulated inducible iNOS is responsible for this. Nevertheless, the contribution of NO to PAF-induced shock or anaphylactic shock is still ambiguous. We studied PAF and anaphylactic shock in conscious mice. Surprisingly, hyperacute PAF shock depended entirely on NO, produced not by inducible iNOS, but by constitutive eNOS, rapidly activated via the PI3K pathway. Soluble guanylate cyclase (sGC) is generally regarded as the principal vasorelaxing mediator of NO. Nevertheless, although methylene blue partially prevented PAF shock, neither 1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one (ODQ) nor sGCα1 deficiency did. Also, in 2 different models of active systemic anaphylaxis, inhibition of NOS, PI3K, or Akt or eNOS deficiency provided complete protection. In contrast to the unsubstantiated paradigm that only excessive iNOS-derived NO underlies cardiovascular collapse in shock, our data strongly support the unexpected concept that eNOS-derived NO is the principal vasodilator in anaphylactic shock and define eNOS and/or PI3K or Akt as new potential targets for treating anaphylaxis.

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“…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.…”

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

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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...

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Cardiovascular aspects of anaphylaxis: implications for treatment and diagnosis

Cited by 149 publications

References 32 publications

Second symposium on the definition and management of anaphylaxis: Summary report—Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium

Second symposium on the definition and management of anaphylaxis: Summary report—Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium

Anaphylactic shock depends on PI3K and eNOS-derived NO

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

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