ABSTRACT
Activation of the sympathetic nervous system aggravates the course of myocardial infarction. Semax peptide moderated the degree of this activation and prevented the increase in the density of sympathetic endings in rat caudal artery in 28 days after ischemia or ischemia/reperfusion. The peptide reduced the density of α-adrenoreceptors in the caudal artery of rats with myocardial infarction. Semax produced no effect on ß-adrenoreceptors in both experimental models. The experiments on isolated segments of the caudal artery revealed reduced vascular responsiveness to electrical stimulation and norepinephrine infusion in rats treated with Semax after ischemia/reperfusion injury.
Subject(s)
Adrenocorticotropic Hormone/analogs & derivatives , Myocardial Infarction/drug therapy , Myocardial Infarction/metabolism , Peptide Fragments/pharmacology , Peptide Fragments/therapeutic use , Sympathetic Nervous System/drug effects , Sympathetic Nervous System/metabolism , Adrenocorticotropic Hormone/pharmacology , Adrenocorticotropic Hormone/therapeutic use , Animals , Electric Stimulation , Male , Neuroprotective Agents/pharmacology , Neuroprotective Agents/therapeutic use , Norepinephrine/pharmacology , Norepinephrine/therapeutic use , Rats , Receptors, Adrenergic, beta/metabolismABSTRACT
The described case illustrates difficulties in diagnosing atypical hemolytic-uremic syndrome (aHUS) in incomplete thrombotic microangiopathy (TMA) in the absence of thrombocytopenia, one of the signs of the classic triad of aHUS, which has resulted in the delayed verification of its diagnosis and in progressive kidney injury. The paper discusses the need to carry out kidney biopsy and to include sHUS in both the presence of a complete set of symptoms of this disease and in the absence of one of them into a range of diagnostic search.
