Endothelial dysfunction in patients with bronchial asthma

Abstract

Background. To estimate interrelation of clinical and functional parameters and vessel tome regulating function of endothelium in patients with bronchial asthma. Methods. 126 patients with bronchial asthma have been examined, including 29 patients with mild bronchial asthma (the first group), 32 persons with moderate bronchial asthma (the second group), 40 respondents with severe asthma (the third group) and 25 patients with steroiddependent asthma (fourth group). The control group included 27 healthy volunteers. We have assessed the parameters of external respiration, vasodilatation function, and the levels of TNFa, IL4, sCD31 in the plasma. Results. The results of the research of vessel tome regulating function in patients with bronchial asthma are presented. The existence of endothelial function of an endothelium are characterized by disturbance of vasomotor activity of endothelium, rising of sCD31 and levels of cytokines (Il-4, TNFa) in plasma was revealed. These changes deteriorate within the ages and the course of bronchial asthma. Conclusion. We have demonstrated that endothelial dysfunction is developed even at the early stages of bronchial asthma.

Adenosine diphosphate ribose cyclase: An important regulator of human pathological and physiological processes

“…This indicated that the ratio of estrogen to progesterone determines the expression of CD38 and the activity of ADPRC. The effects of estrogen and other steroid superfamily hormones on specific cell functions and hormone-induced gene expression in target cells are mediated by the cADPR-Ca 2+ release pathway (Dogan et al, 2002;Poltronieri et al, 2021;Sobko et al, 2013).…”

“…This indicated that the ratio of estrogen to progesterone determines the expression of CD38 and the activity of ADPRC. The effects of estrogen and other steroid superfamily hormones on specific cell functions and hormone‐induced gene expression in target cells are mediated by the cADPR‐Ca 2+ release pathway (Dogan et al, 2002; Poltronieri et al, 2021; Sobko et al, 2013). l ‐thyroxine regulates the expression of proapoptotic biomarkers by regulating calcium mobilization, mediated by calmodulin, thus protecting renal cells from ischemia‐reperfusion injury and changing renal toxicity (El‐Hamoly et al, 2017).…”