การเปลี่ยนแปลงทางจุลพยาธิวิทยาของกล้ามเนื้อหัวใจ ไต ตับ และกล้ามเนื้อลาย หลังการรับพิษจากงูกะปะ งูแก้วหางแดง และงูจงอาง ในหนูขาว

Abstract

Snakebite envenoming is a cause of death and disability in many tropical countries worldwild. Toxic proteins in snake venom induce a number of clinical outcomes, such as neurotoxicity, cardiotoxicity, and cytotoxicity. The objective of this study was to determine histopathological changes of cardiac muscle, kidney, liver, and skeletal muscle following the administration of Calloselasma rhodostoma venom (CRV), Trimeresurus hageni venom (THV), and Ophiophagus hannah venom (OHV). Intravenous administration (IV) of CRV (dose 1000 µg/kg) or THV (dose 800 µg/kg) significantly reduced the mean arterial pressure (MAP) and eventually killed envenomed rats within 15 seconds. Change in MAP was not observed following administration of OHV (1000 µg/kg; IV) compared with that of vehicle control. Intramuscular (IM) administration of CRV (dose 500 µg/kg) or THV (dose 1200 µg/kg) or OHV (dose 1000 µg/kg). Caused congestion of renal tubule and segmental artery, including glomerulus atrophy. Venoms also induced congestion of hepatic central vein, portal triad, and sinusoid. Moreover, inflammatory cells and Kupffer cells were also detected throughout liver tissues. In envenomed heart tissues, we found that 3 snake venoms generated rupture of cardiac myofibers. The presence of skeletal muscle damage was observed following administration of OHV (dose 1000 µg/kg; IM). However, neither CRV or THV displayed myotoxicity in experimentally envenomed rats. This finding concludes that venom coponents associated with cardiotoxicity in CRV and THV are responsible for patological changes of kidney, liver and cardiac tissues. These toxic compounds are likely to be absence in King cobra venom (OHV).