Effects of hypoxia on the formation of traumatic brain swelling in rats with acute subdural hematoma
10.3760/cma.j.cn501098-20240401-00254
- VernacularTitle:缺氧对急性硬膜下血肿大鼠发生外伤性脑肿胀的影响
- Author:
Liang XIAN
1
;
Li CHEN
;
Long LIN
;
Dan YE
;
Liangfeng WEI
;
Shousen WANG
Author Information
1. 福建医科大学福总临床医学院（第九〇〇医院）神经外科，福州 350025
- Keywords:
Brain injuries;
Rats;
Hypoxia;
Pericytes;
Microcirculation
- From:
Chinese Journal of Trauma
2024;40(9):826-836
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the effects of hypoxia on traumatic brain swelling (TBS) in rats with acute subdural hematoma (ASDH).Methods:Forty-five SD rats were divided into 5 groups according to the random number table method, with 9 rats in each group: sham surgery normal oxygen group which underwent sham surgical procedures and were placed in a closed container with ventilation, sham surgery hypoxia group which underwent sham surgical procedures and were placed in a closed container with oxygen volume fraction of 8% for hypoxia induction, ASDH normal oxygen group which made into the ASDH model and placed in a closed container with ventilation, ASDH hypoxia group were made into the ASDH models and placed in a closed container with oxygen volume fraction of 8% for hypoxia induction, and ASDH hypoxia+oxygen inhalation group which inhaled oxygen continuously with oxygen volume fraction of 40% after being made into the ASDH models and induced for hypoxia. Six rats were selected from each group immediately after the modeling and craniotomy was performed to observe the brain swelling during the surgery and evaluate the degree of TBS. Microvascular blood flow was observed by laser speckle imaging system before modeling, before craniotomy, and immediately after craniotomy. The remaining 3 rats in each group were killed directly after modeling and brain tissue specimens were collected. The expression levels of pericellular protein α-smooth muscle actin (α-SMA) and platelet-derived growth factor receptor-β (PDGFR-β) at 0, 30 and 60 minutes after modeling were detected through Western blot analysis. The expression levels of α-SMA, PDGFR-β and microvascular marker platelet-endothelial cell adhesion molecule 31 (CD31) at 0 minute after modeling were tested through immunofluorescent staining.Results:No brain bulge was observed in the sham surgery normal oxygen group. The height of brain bulge in sham surgery hypoxia group was 0.5(0.0, 1.0)mm, with no significant difference from that in the sham surgery normal oxygen group ( P>0.05); it was 2.2(2, 2.5)mm in the ASDH normal oxygen group, significantly higher than that in the sham surgery normal oxygen group and sham surgery hypoxia group ( P<0.01), it was 3.1(2.9, 3.2)mm in the ASDH hypoxia group, significantly higher than that in the sham surgery normal oxygen group, sham surgery hypoxia group and ASDH normal oxygen group ( P<0.01); it was 2.8(2.7, 2.9)mm in the ASDH hypoxia+oxygen inhalation group, not statistically different from that in the ASDH hypoxia group ( P>0.05), but significantly increased compared with that in the sham surgery normal oxygen group, sham surgery hypoxia group and ASDH normal oxygen group ( P<0.01). Before modeling, before craniotomy and after craniotomy, the microvascular blood flow was 224.2±49.7, 224.8±50.3, 225.1±50.3 respectively in the sham surgery normal oxygen group and 224.7±43.7, 220.9±45.9, 221.8±45.5 respectively in the sham surgery hypoxia group, with no significant difference between the two groups ( P>0.05); it was 226.5±52.7, 173.4±40.7, 172.0±40.7 respectively in the ASDH normal oxygen group, significantly decreased compared with that in the sham surgery normal oxygen group and sham surgery hypoxia group ( P<0.05); it was 225.7±46.4, 131.4±23.6 and 131.0±23.5 respectively in the ASDH hypoxia group, significantly decreased compared with that in the sham surgery normal oxygen group, sham surgery hypoxia group and ASDH normal oxygen group ( P<0.05); it was 226.2±56.1, 132.6±21.7 and 131.7±21.9 respectively in ASDH hypoxia+oxygen inhalation group, significantly decreased compared with that in the sham surgery normal oxygen group, sham surgery hypoxia group and ASDH normal oxygen group ( P<0.05), with no significant difference from that in the ASDH hypoxia group ( P>0.05). At 0, 30 and 60 minutes after modeling, the expression levels of α-SMA and PDGFR-β were 0.70±0.02, 0.67±0.01, 0.55±0.05 and 0.65±0.03, 0.56±0.03 and 0.59±0.02 respectively in the sham surgery normal oxygen group and were 0.63±0.04, 0.60±0.01 0.55±0.05 and 0.62±0.01, 0.51±0.01 and 0.60±0.02 respectively in the sham surgery hypoxia group, with no significant difference between the two groups ( P>0.05); they were 0.88±0.06, 0.87±0.05, 0.82±0.03 and 0.85±0.03, 0.85±0.03, 0.88±0.04 respectively in the ASDH normal oxygen group, significantly higher than those in the sham surgery normal oxygen group and sham surgery hypoxia group ( P<0.01); they were 1.19±0.08, 1.10±0.10, 0.97±0.04 and 1.04±0.06, 1.19±0.07, 1.27±0.08 respectively in the ASDH hypoxia group, significantly higher than those in sham surgery normal oxygen group, sham surgery hypoxia group and ASDH normal oxygen group ( P<0.05 or 0.01); they were 1.20±0.07, 1.10±0.04, 0.96±0.04 and 1.04±0.05, 1.15±0.11, 1.20±0.07 respectively in ASDH hypoxia+oxygen inhalation group, significantly higher than those in sham surgery normal oxygen group, sham surgery normal group and ASDH normal oxygen group ( P<0.01), but with no significant difference from those in ASDH hypoxia group ( P>0.05). At 0 minute after modeling, the fluorescence expression of α-SMA and PDGFR-β was weaker in the sham surgery normal oxygen group and the fluorescence expression of CD31 was stronger. There was no significant difference in the fluorescence expressions of α-SMA, PDGFR-β and CD31 between the sham surgery hypoxia group and sham surgery normal oxygen group. The fluorescence expressions of α-SMA and PDGFR-β in the ASDH normal oxygen group were stronger than those in the sham surgery normal oxygen group and sham surgery hypoxia group, while the fluorescence expression of CD31 was weaker. The fluorescence expressions of α-SMA and PDGFR-β in ASDH hypoxia group were stronger than those in the sham surgery normal oxygen group, sham surgery hypoxia group and ASDH normal oxygen group, while the fluorescence expression of CD31 was weaker. The fluorescence expressions of α-SMA and PDGFR-β in the ASDH hypoxia+oxygen inhalation group were stronger than those in the sham surgery normal oxygen group, sham surgery hypoxia group and ASDH normal oxygen group, while the fluorescence expression of CD31 was weaker, with no significant difference from the fluorescence expressions of α-SMA, PDGFR-β and CD31 in ASDH hypoxia group. Conclusions:Hypoxia in ASDH rats will stimulate pericytes contraction, which causes cerebral microcirculatory disturbance, thus leading to TBS. Short-term inhalation of oxygen of medium concentration cannot dilate pericytes or microcirculation vessels, with no obvious effect on improving the conditions of TBS.
