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Role of some vasoactive mediators in scorpion envenomed children: Possible relation to envenoming outcome

Research Authors
Sahar E.M. El-DeeK a, Ayat A. Sayed a, Ahmed Y. Nassar a, Zeynab M. Mohey-Eldeen b,
Hussein M. Eldeeb c, Abdel-Raheim M.A. Meki a, *
Research Department
Research Journal
Toxicon
Research Member
Research Publisher
NULL
Research Rank
1
Research Vol
Vol. 127
Research Website
NULL
Research Year
2017
Research_Pages
pp. 77 - 84
Research Abstract

Scorpion envenomation causes an autonomic storm resulting in changes in the vasoactive mediators’
levels which lead to myocardial damage, cardiovascular disturbances, peripheral circulatory failure,
pulmonary edema, multi-system-organ-failure and death. The study aimed to determine the circulating
levels of adrenaline, noradrenaline, angiotensin converting enzyme (ACE), Angiotensin II (Ang II), kallikrein
enzyme, nitric oxide (NO), aldosterone, and electrolytes Naþ, Kþ and Caþ2 in scorpion envenomed
children and to evaluate the potential relation between these vasoactive mediators, the severity of
scorpion envenoming and the clinical outcome of envenomed children. Forty envenomed children (22
mild and 18 severe cases) along with 10 healthy control children were enrolled in the study. The
circulating levels of adrenaline, noradrenaline, Ang II, ACE, kallikrein enzyme, and NO were determined
by ELISA, and spectrophotometric assays on admission and 24 h later. On admission, serum aldosterone,
and electrolytes; Naþ, Kþ and Caþ2 were determined by RIA, Flame photometer and Flame atomic absorption
respectively. All envenomed children showed significant surge of adrenaline, noradrenaline,
ACE, Ang II, aldosterone, NO and Naþ, that concomitantly faced by significant reduction in kallikrein, Kþ
and Caþ2 on admission. Twenty four hours later, all envenomed children continued to show significant
elevation of ACE, Ang II and NO. The severely envenomed children showed considerable reduction in
circulating levels of adrenaline, noradrenaline, ACE and Ang II, while dramatic increase in kallikrein
activity was reported in comparison to mildly envenomed children after 24 h of medical care. Also, NO
exhibited considerable accumulation in non survivors, on admission, that was persistent for the subsequent
24 h and was accompanied by high kallikrein, low catecholamines and Ang II levels compared to
survivors. Finally, the hypertensive cases showed substantial higher levels of catecholamine, ACE and Ang
II, 24 h after admission. These findings indicated that, disturbances of the studied vasoactive mediators
were common in scorpion envenomed children and may account for several inflammatory manifestations
and clinical outcome. ACE inhibitors could be considered as possible therapeutic agent in victims
with prominent increase in ACE and Ang II while kallikrein inhibitor and antioxidants may be effective in
the treatment of late hypotensive ones.