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烧伤后高血糖症

Hyperglycaemia after burn injury.

作者信息

Yü C C, Hua H A, Tong C

机构信息

Department of Physiology, First Military Medical College, Guangzhou, China.

出版信息

Burns. 1989 Jun;15(3):145-6. doi: 10.1016/0305-4179(89)90168-x.

DOI:10.1016/0305-4179(89)90168-x
PMID:2667559
Abstract

The effect of burn injury on blood sugar levels, serum insulin levels and glucose tolerance was studied in male rats. In the burned group (following 50 per cent surface burn injury), the blood sugar level was significantly increased after burn injury in comparison with control uninjured rats. Hyperglycaemia was blocked by injection of phentolamine (10 mg/kg) for 24 h or propranolol (50 micrograms/kg) 30 min before burn or if the animals were adrenalectomized 4 days before injury. Serum insulin levels were significantly decreased in the scalded rats and their glucose tolerance was impaired. Early hyperglycaemia probably arises as a result of adrenal medullary hyperactivity. The initial rise in blood glucose probably arises from glycogen breakdown, followed later by increased hepatic production of glucose. The 50 per cent body surface scald injury is followed, acutely, by a period of glucose intolerance. In part, this intolerance may be due to decreased serum levels of insulin. The inadequate response of insulin secretion in response to glucose loading may be due to inhibition of insulin secretion by pancreatic beta cells caused by elevated catecholamine levels, possibly in combination with the action of antagonists such as glucagon, which may be secreted in excess as a result of stimulation by catecholamines.

摘要

研究了烧伤对雄性大鼠血糖水平、血清胰岛素水平和葡萄糖耐量的影响。在烧伤组(50%体表烧伤后),与未受伤的对照大鼠相比,烧伤后血糖水平显著升高。在烧伤前24小时注射酚妥拉明(10毫克/千克)或普萘洛尔(50微克/千克)30分钟,或者在受伤前4天切除动物肾上腺,可阻止高血糖症的发生。烫伤大鼠的血清胰岛素水平显著降低,其葡萄糖耐量受损。早期高血糖症可能是由于肾上腺髓质功能亢进所致。血糖的最初升高可能源于糖原分解,随后是肝脏葡萄糖生成增加。50%体表烫伤后,紧接着会出现一段急性葡萄糖不耐受期。这种不耐受部分可能是由于血清胰岛素水平降低所致。胰岛素分泌对葡萄糖负荷反应不足可能是由于儿茶酚胺水平升高导致胰腺β细胞胰岛素分泌受抑制,可能还与胰高血糖素等拮抗剂的作用有关,胰高血糖素可能因儿茶酚胺刺激而分泌过多。

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Hyperglycaemia after burn injury.烧伤后高血糖症
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[Influences of exendin-4 on the secretion function of islet beta cells from rats in the early stage of severe scald].[艾塞那肽-4对严重烫伤早期大鼠胰岛β细胞分泌功能的影响]
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Acute pancreatic beta cell apoptosis by IL-1β is responsible for postburn hyperglycemia: Evidence from humans and mice.IL-1β 引起的急性胰腺β细胞凋亡是烧伤后高血糖的原因:来自人类和小鼠的证据。
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Attenuation of burn-induced changes in hemodynamics and glucose metabolism by the PAF antagonist SRI 63-675.血小板活化因子拮抗剂SRI 63 - 675对烧伤引起的血流动力学和葡萄糖代谢变化的抑制作用
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引用本文的文献

1
A rat model of concurrent combined injuries (polytrauma).并发复合伤(多发伤)大鼠模型
Int J Clin Exp Med. 2015 Nov 15;8(11):20097-110. eCollection 2015.
2
Physiologic and molecular changes in the tracheal epithelium of rats following burn injury.烧伤后大鼠气管上皮的生理和分子变化
Int J Burns Trauma. 2015 Mar 20;5(1):36-45. eCollection 2015.
3
XBP-1s is linked to suppressed gluconeogenesis in the Ebb phase of burn injury.XBP-1s 与烧伤损伤的 Ebb 相中受抑制的糖异生有关。
Mol Med. 2013 May 20;19(1):72-8. doi: 10.2119/molmed.2012.00348.
4
The role of hyperglycemia in burned patients: evidence-based studies.烧伤患者高血糖的作用:循证研究。
Shock. 2010 Jan;33(1):5-13. doi: 10.1097/SHK.0b013e3181af0494.