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眼镜王蛇(Lesson,1831年)对高环境温度暴露的生理反应,包括毒液分泌。

Physiological responses of the monocled cobra ( Lesson, 1831) including venom production, to high ambient temperature exposure.

作者信息

Vasaruchapong Taksa, Chaiyabutr Narongsak, Nampimoon Thanida, Thammacharoen Sumpun

机构信息

Department of Physiology, Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand.

Queen Saovabha Memorial Institute, The Thai Red Cross Society, Bangkok, Thailand.

出版信息

J Venom Anim Toxins Incl Trop Dis. 2025 Feb 14;31:e20240058. doi: 10.1590/1678-9199-JVATITD-2024-0058. eCollection 2025.

DOI:10.1590/1678-9199-JVATITD-2024-0058
PMID:39963263
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11832193/
Abstract

BACKGROUND

Temperature regulation is essentially important for survival of poikilotherms such as snakes. Body temperature is regulated by snakes through behavioral and physiological responses. The global-warming crisis, combined with the need to house large population of snakes in limited spaces, increases the likelihood of exposing snakes to high ambient temperature (HTa), requiring it reliance on physiological responses. This study aimed to study the effect of HTa exposure on physiological responses and venom production, which have rarely been studied.

METHODS

Eleven adult monocled cobras ( Lesson, 1831) were divided into two groups. The concurrent control group was housed in a temperature-controlled room, and the heat exposed group was housed in the same room with gradually increasing temperatures (25°C-35°C) for 4 h on four consecutive days. Data were collected 3 days before the experiment as the baseline and then compared with day 1 and day 4 after HTa exposure data representing immediate and prolonged effects. Body temperature, body weight, water intake, heart rate, hematology, plasma biochemistry, body-fluid compartments, hormonal response, heat shock protein expression and venom production were measured.

RESULTS

In response to HTa exposure, body temperature and heart rate increased, plasma volume significantly decreased, but water intake increased. Hematocrit and plasma protein progressively decreased in the latter stages of experimentation, but HTa diminished this effect. HTa only increased plasma corticosterone on day 1. Exposure to HTa increased venom protein concentration on day 4 and diminished the decreased proportion effect of frequent venom collection on phospholipase A component.

CONCLUSION

Increased heart rate and fluid shift from the intravascular compartment appeared to be the underlying mechanism for heat dissipation during HTa exposure. Under the study condition, HTa caused heat stress, but the snake could adapt after continued exposure. Additionally, HTa increased venom protein concentration in , particularly phospholipase A component.

摘要

背景

温度调节对于蛇等变温动物的生存至关重要。蛇通过行为和生理反应来调节体温。全球变暖危机,加上需要在有限空间内饲养大量蛇,增加了蛇暴露于高环境温度(HTa)的可能性,这使得它们依赖生理反应。本研究旨在探讨HTa暴露对生理反应和毒液产生的影响,而这方面的研究很少。

方法

将11条成年眼镜王蛇(Lesson,1831)分为两组。同期对照组饲养在温度可控的房间内,热暴露组饲养在同一房间,温度连续四天逐渐升高(25°C - 35°C),持续4小时。在实验前3天收集数据作为基线,然后与HTa暴露后第1天和第4天的数据进行比较,分别代表即时和长期影响。测量体温、体重、饮水量、心率、血液学指标、血浆生化指标、体液成分、激素反应、热休克蛋白表达和毒液产生情况。

结果

HTa暴露后,体温和心率升高,血浆量显著减少,但饮水量增加。实验后期血细胞比容和血浆蛋白逐渐下降,但HTa减弱了这种影响。HTa仅在第1天增加了血浆皮质酮水平。暴露于HTa使第4天的毒液蛋白浓度增加,并减弱了频繁采集毒液对磷脂酶A成分比例下降的影响。

结论

心率增加和血管内液体转移似乎是HTa暴露期间散热的潜在机制。在本研究条件下,HTa引起了热应激,但蛇在持续暴露后能够适应。此外,HTa增加了毒液蛋白浓度,尤其是磷脂酶A成分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a808/11832193/da413c9225f6/1678-9199-jvatitd-31-e20240058-gf10.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a808/11832193/03c9e07d5f55/1678-9199-jvatitd-31-e20240058-gf4.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a808/11832193/4af0e7dd1ff1/1678-9199-jvatitd-31-e20240058-gf6.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a808/11832193/da413c9225f6/1678-9199-jvatitd-31-e20240058-gf10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a808/11832193/458e308fc8e8/1678-9199-jvatitd-31-e20240058-gf1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a808/11832193/88b1b1ec1b57/1678-9199-jvatitd-31-e20240058-gf2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a808/11832193/1989e1aa7b01/1678-9199-jvatitd-31-e20240058-gf3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a808/11832193/03c9e07d5f55/1678-9199-jvatitd-31-e20240058-gf4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a808/11832193/b8102bf8cf33/1678-9199-jvatitd-31-e20240058-gf5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a808/11832193/4af0e7dd1ff1/1678-9199-jvatitd-31-e20240058-gf6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a808/11832193/30ab173c328f/1678-9199-jvatitd-31-e20240058-gf7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a808/11832193/e5e58aa0fa53/1678-9199-jvatitd-31-e20240058-gf8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a808/11832193/919fd1ba855d/1678-9199-jvatitd-31-e20240058-gf9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a808/11832193/da413c9225f6/1678-9199-jvatitd-31-e20240058-gf10.jpg

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