Vanaie Mahdi, Valiyan Boroujeni Majid, Motavallipour Abarghuie Hamed, Pourshanazari Ali Asghar, Rezazadeh Hossein
School of Medicine, Medical Student Research Committee, Isfahan University of Medical Sciences, Isfahan, Iran.
Physiology - Pharmacology Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Adv Biomed Res. 2018 Nov 27;7:142. doi: 10.4103/abr.abr_119_18. eCollection 2018.
Sneezing transiently elevates cerebral blood flow. We speculated that induced sneezing, following embolism would restore arterial flow, thereby diminishing infarct volume and improving neurological deficits.
Male rats were subjected to middle cerebral artery occlusion (MCAO) using prepared clots (embolization) and randomized into four equal groups as follows: (1) pre-MCAO-induced sneezing (PRMIS), (2) post-MCAO-induced sneezing (POMIS), and (3) pre- and POMIS (PRPOMIS) and the control group (eight rats per group). In the treatment groups, rats' sneezing episodes were induced before MCAO in PRMIS group or before regaining consciousness from surgical anesthesia in other treatment groups by cutting their whiskers during their anesthesia and subsequently inserted them into the rats' nostrils. Infarct volume was evaluated by 2, 3, 5-triphenyl tetrazolium chloride staining, and neurological deficits and brain edema were assessed by Bederson scale deficit scores 24-h post-MCAO.
The infarct volume and brain edema reduced and neurological deficits improved in the induced sneezing groups as compared with the MCAO control group. Compared to the control group, the highest improvements in the infarct volume and neurological deficits were seen in the PRPOMIS group, and POMIS group showed the most significant differences concerning the results of both ischemic and nonischemic brain edema. The highest protective effect was observed in the central region of the MCA territory.
The reduction in ischemia-induced brain injury, brain edema, and neurological deficits by sneezing suggest that brief episodes of acute hypertension after stroke can increase blood flow to the ischemic area and improve recovery.
打喷嚏会使脑血流量短暂升高。我们推测，栓塞后诱发打喷嚏可恢复动脉血流，从而减少梗死体积并改善神经功能缺损。
雄性大鼠通过使用制备好的血凝块（栓塞）进行大脑中动脉闭塞（MCAO），并随机分为四组，每组数量相等：（1）MCAO前诱发打喷嚏组（PRMIS），（2）MCAO后诱发打喷嚏组（POMIS），（3）MCAO前后均诱发打喷嚏组（PRPOMIS）以及对照组（每组8只大鼠）。在治疗组中，PRMIS组在MCAO前诱发大鼠打喷嚏，其他治疗组在手术麻醉苏醒前通过在麻醉期间剪去大鼠胡须并随后将其插入大鼠鼻孔来诱发打喷嚏。通过2,3,5-三苯基氯化四氮唑染色评估梗死体积，在MCAO后24小时通过贝德森量表缺损评分评估神经功能缺损和脑水肿。
与MCAO对照组相比，诱发打喷嚏组的梗死体积和脑水肿减小，神经功能缺损得到改善。与对照组相比，PRPOMIS组在梗死体积和神经功能缺损方面改善最为明显，POMIS组在缺血性和非缺血性脑水肿结果方面差异最为显著。在MCA区域的中央部分观察到最高的保护作用。
打喷嚏可减轻缺血性脑损伤、脑水肿和神经功能缺损，这表明中风后短暂的急性高血压发作可增加缺血区域的血流量并改善恢复情况。
