Abstract
This study investigated possible implication of nitric oxide and prostanoids in anaphylactic reaction in small mesenteric and coronary arteries. MATERIAL AND METHODS. Isolated arteries from guinea pigs, sensitized with 0.5 mL of horse serum or sham-sensitized, were challenged with 1% of horse serum in vitro. Contractile responses of arteries (normalized diameter, 350-450 microm) were recorded by a small blood vessel wire myograph. For inhibition of the release of NO or prostanoids, vessels were pretreated with N(G)-nitro-L-arginine methyl ester (30 microM) or indomethacin (10 microM), respectively. RESULTS. Antigen challenge was followed by contraction of both coronary and mesenteric vessels. Two patterns of contraction were observed: 1) peak contraction - an immediate transient contraction of relatively high amplitude; this was the most common pattern; 2) biphasic: the initial peak contraction was followed by a slow growing contraction with low amplitude. Biphasic pattern was observed in 60% of the mesenteric vessels and 40% of the coronary vessels. Inhibition of NO synthase significantly increased the peak contraction in the coronary vessels and the second-phase contraction in the mesenteric vessels. Inhibition of cyclooxygenase caused a decrease in the peak and second-phase contraction of both the coronary and mesenteric vessels. CONCLUSIONS. Despite anaphylactic contraction, nitric oxide seems to be released from the endothelium following antigen challenge in the small coronary and mesenteric arteries. This may contribute to the development of hypotension during anaphylaxis. Prostanoids are playing a different role - the contracting products of cyclooxygenase pathway are important for the development of anaphylactic contraction of the small isolated arteries.
Highlights
Anaphylactic shock is a generalized form of IgE hypersensitivity and is characterized by complex cardiovascular disorders including severe arterial hypotension
Nitric oxide seems to be released from the endothelium following antigen challenge in the small coronary and mesenteric arteries
According to our results, antigen challenge in the small isolated mesenteric and coronary arteries from the sensitized guinea pig is followed by anaphylactic contraction but not relaxation
Summary
Anaphylactic shock is a generalized form of IgE hypersensitivity and is characterized by complex cardiovascular disorders including severe arterial hypotension. The main possible cause of hypotension is the release of mediators of anaphylaxis, following the IgE hypersensitivity reaction. Vasoactive substances such as histamine [1,2,3,4], serotonin [5,6,7], and bradykinin [5, 8] are well-recognized mediators of cardiac anaphylaxis. Following stimulation of the receptors, endothelial NO synthase (NOS) converts L-arginine into NO [18,19,20]; NO may produce relaxation by decreasing Ca2+ levels in smooth muscle cells through a cGMP-dependent pathway or through hyperpolarization due to increased conductance of K+ channels [21].
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