File Download
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.3760/cma.j.issn.2095-4352.2014.08.014
- Scopus: eid_2-s2.0-84927173008
- PMID: 25124911
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: Effects of hypertonic sodium chloride hydroxyethyl starch solution on cerebral vasospasm following subarachnoid hemorrhage and its mechanism
Title | Effects of hypertonic sodium chloride hydroxyethyl starch solution on cerebral vasospasm following subarachnoid hemorrhage and its mechanism 高渗氯化钠羟乙基淀粉溶液对蛛网膜下腔出血后脑血管痉挛的影响及机制研究 |
---|---|
Authors | |
Keywords | Apoptosis Cerebral vasospasm Hypertonic sodium chloride hydroxyethyl starch solution Subarachnoid hemorrhage |
Issue Date | 2014 |
Publisher | Zhonghua Yixuehui. The Journal's web site is located at http://www.cccm-em120.com/guokanliulan.htm |
Citation | Chinese Critical Care Medicine, 2014, v. 26 n. 8, p. 589-593 How to Cite? 中华危重病急救医学, 2014, v. 26 n. 8, p. 589-593 How to Cite? |
Abstract | OBJECTIVE:
To investigate the protective effect and potential mechanisms of hypertonic sodium chloride hydroxyethyl starch solution (HSH) against the cerebral vasospasm (CVS) following subarachnoid hemorrhage (SAH).
METHODS:
Twenty-four male Sprague-Dawley (SD) rats were randomly assigned to four groups according to the random number table, with 6 rats in each group. The SAH-CVS model was reproduced by injection of the blood twice through the cisterna magna. Rats in both model and HSH treatment groups received 8 mL/kg normal saline (NS) or HSH treatment everyday via caudal vein. Rats in sham group were injected with 1.5 mL/kg NS into cisterna magna followed by 8 mL/kg NS treatment. Rats in normal group received no treatment. Rats were sacrificed to harvest basilar artery after 7 days. The thickness of vessel wall and lumen area were measured using hematoxylin-eosin (HE) staining. The rate of apoptosis of vascular smooth muscle cell (VSMC) was assessed using flow cytometry. Caspase-3 activity was measured by a fluorometric assay. The expressions of Bax and Bcl-2 were determined by Western Blot. Intracellular reactive oxygen species (ROS) was detected by H2DCFDA.
RESULTS:
Compared with normal group, increased thickness of vessel wall (27.72 ± 1.94 μm vs. 18.30 ± 1.10 μm, P<0.05), decreased lumen area (26 115 ± 1 991 μm² vs. 55 080 ± 2 091 μm², P<0.05), and elevation of rate of apoptosis of VSMCs [(35.05 ± 5.54) % vs. (5.93 ± 1.53) %, P<0.05] were found in model group. Compared with model group, decreased thickness of vessel wall (22.55 ± 1.50 μm vs. 27.72 ± 1.94 μm, P<0.05), increase of lumen area (48 115 ± 2 460 μm² vs. 26 115 ± 1 991 μm², P<0.05), and depressed rate of apoptosis of VSMCs [(16.54 ± 5.94) % vs. (35.05 ± 5.54) %, P<0.05] were found in HSH treatment group. Caspase-3 activity, intracellular ROS level, Bax and Bcl-2 expressions in model group were (188.40 ± 19.35)%, (163.50 ± 17.02)%, (208.71 ± 26.04)% and (44.52 ± 9.61) % of those of normal group, and the differences of these parameters between model and normal groups were statistically significant (all P<0.05). Caspase-3 activity, intracellular ROS level, Bax and Bcl-2 expressions in HSH treatment group were (135.05 ± 19.52)%, (119.44 ± 11.50)%, (139.20 ± 18.04)% and (85.35 ± 13.12)% of those of normal group, respectively, and the differences of these parameters between HSH treatment and model groups were statistically significant (all P<0.05). The differences of all measurements between sham and normal groups were not statistically significant.
CONCLUSIONS:
The current results demonstrate that HSH attenuates the SAH-induced CVS, alleviates thickness of vessel wall, and increases lumen area via inhibition of VSMCs apoptosis. |
Persistent Identifier | http://hdl.handle.net/10722/202480 |
ISSN |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Li, T | - |
dc.contributor.author | Li, J | - |
dc.contributor.author | Li, H | - |
dc.contributor.author | Xia, Z | - |
dc.contributor.author | Shi, X | - |
dc.contributor.author | Li, X | - |
dc.contributor.author | Liu, Y | - |
dc.date.accessioned | 2014-09-19T07:59:39Z | - |
dc.date.available | 2014-09-19T07:59:39Z | - |
dc.date.issued | 2014 | - |
dc.identifier.citation | Chinese Critical Care Medicine, 2014, v. 26 n. 8, p. 589-593 | - |
dc.identifier.citation | 中华危重病急救医学, 2014, v. 26 n. 8, p. 589-593 | - |
dc.identifier.issn | 1003-0603 | - |
dc.identifier.uri | http://hdl.handle.net/10722/202480 | - |
dc.description.abstract | OBJECTIVE: To investigate the protective effect and potential mechanisms of hypertonic sodium chloride hydroxyethyl starch solution (HSH) against the cerebral vasospasm (CVS) following subarachnoid hemorrhage (SAH). METHODS: Twenty-four male Sprague-Dawley (SD) rats were randomly assigned to four groups according to the random number table, with 6 rats in each group. The SAH-CVS model was reproduced by injection of the blood twice through the cisterna magna. Rats in both model and HSH treatment groups received 8 mL/kg normal saline (NS) or HSH treatment everyday via caudal vein. Rats in sham group were injected with 1.5 mL/kg NS into cisterna magna followed by 8 mL/kg NS treatment. Rats in normal group received no treatment. Rats were sacrificed to harvest basilar artery after 7 days. The thickness of vessel wall and lumen area were measured using hematoxylin-eosin (HE) staining. The rate of apoptosis of vascular smooth muscle cell (VSMC) was assessed using flow cytometry. Caspase-3 activity was measured by a fluorometric assay. The expressions of Bax and Bcl-2 were determined by Western Blot. Intracellular reactive oxygen species (ROS) was detected by H2DCFDA. RESULTS: Compared with normal group, increased thickness of vessel wall (27.72 ± 1.94 μm vs. 18.30 ± 1.10 μm, P<0.05), decreased lumen area (26 115 ± 1 991 μm² vs. 55 080 ± 2 091 μm², P<0.05), and elevation of rate of apoptosis of VSMCs [(35.05 ± 5.54) % vs. (5.93 ± 1.53) %, P<0.05] were found in model group. Compared with model group, decreased thickness of vessel wall (22.55 ± 1.50 μm vs. 27.72 ± 1.94 μm, P<0.05), increase of lumen area (48 115 ± 2 460 μm² vs. 26 115 ± 1 991 μm², P<0.05), and depressed rate of apoptosis of VSMCs [(16.54 ± 5.94) % vs. (35.05 ± 5.54) %, P<0.05] were found in HSH treatment group. Caspase-3 activity, intracellular ROS level, Bax and Bcl-2 expressions in model group were (188.40 ± 19.35)%, (163.50 ± 17.02)%, (208.71 ± 26.04)% and (44.52 ± 9.61) % of those of normal group, and the differences of these parameters between model and normal groups were statistically significant (all P<0.05). Caspase-3 activity, intracellular ROS level, Bax and Bcl-2 expressions in HSH treatment group were (135.05 ± 19.52)%, (119.44 ± 11.50)%, (139.20 ± 18.04)% and (85.35 ± 13.12)% of those of normal group, respectively, and the differences of these parameters between HSH treatment and model groups were statistically significant (all P<0.05). The differences of all measurements between sham and normal groups were not statistically significant. CONCLUSIONS: The current results demonstrate that HSH attenuates the SAH-induced CVS, alleviates thickness of vessel wall, and increases lumen area via inhibition of VSMCs apoptosis. | - |
dc.language | chi | - |
dc.publisher | Zhonghua Yixuehui. The Journal's web site is located at http://www.cccm-em120.com/guokanliulan.htm | - |
dc.relation.ispartof | Chinese Critical Care Medicine | - |
dc.relation.ispartof | 中华危重病急救医学 | - |
dc.subject | Apoptosis | - |
dc.subject | Cerebral vasospasm | - |
dc.subject | Hypertonic sodium chloride hydroxyethyl starch solution | - |
dc.subject | Subarachnoid hemorrhage | - |
dc.title | Effects of hypertonic sodium chloride hydroxyethyl starch solution on cerebral vasospasm following subarachnoid hemorrhage and its mechanism | - |
dc.title | 高渗氯化钠羟乙基淀粉溶液对蛛网膜下腔出血后脑血管痉挛的影响及机制研究 | - |
dc.type | Article | - |
dc.identifier.email | Xia, Z: zyxia@hkucc.hku.hk | - |
dc.identifier.email | Liu, Y: liuyt@hku-szh.org | - |
dc.identifier.authority | Xia, Z=rp00532 | en_US |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.3760/cma.j.issn.2095-4352.2014.08.014 | - |
dc.identifier.pmid | 25124911 | - |
dc.identifier.scopus | eid_2-s2.0-84927173008 | - |
dc.identifier.hkuros | 235553 | - |
dc.identifier.volume | 26 | - |
dc.identifier.issue | 8 | - |
dc.identifier.spage | 589 | - |
dc.identifier.epage | 593 | - |
dc.publisher.place | China | - |
dc.identifier.issnl | 1003-0603 | - |