AIM： To investigate the role of gastric oxidative stress and nitric oxide （NO） in the formation of gastric hemorrhagic erosion and their protection by drugs in rats with ischemic brain. METHODS： Male Wistar rats w...AIM： To investigate the role of gastric oxidative stress and nitric oxide （NO） in the formation of gastric hemorrhagic erosion and their protection by drugs in rats with ischemic brain. METHODS： Male Wistar rats were deprived of food for 24 h. Under chloral hydrate （300 mg/kg） anesthesia, bilateral carotid artery ligation was performed. The pylorus and carotid esophagus of the rats were also ligated. The stomachs were then irrigated for 3 h with either normal saline or simulated gastric juice containing 100 mmol/L HCI plus 17.4 mmol/L pepsin and 54 mmol/L NaCI. Rats were killed and stomachs were dissected. Gastric mucosa and gastric contents were harvested. The rat brain was dissected for the examination of ischemia by triphenyltetrazolium chloride staining method. Changes in gastric ulcerogenic parameters, such as decreased mucosal glutathione level as well as enhanced gastric acid back-diffusion, mucosal lipid peroxide generation, histamine concentration, luminal hemoglobin content and mucosal erosion in gastric samples, were measured. RESULTS： Bilateral carotid artery ligation produced severe brain ischemia （BI） in rats. An exacerbation of various ulcerogenic parameters and mucosal hemorrhagic erosions were observed in these rats. The exacerbated ulcerogenic parameters were significantly （P〈 0.05） attenuated by antioxidants, such as exogenous glutathione and allopurinol. These gastric parameters were also improved by intraperitoneal aminoguanidine （100 mg/kg） but were aggravated by N^G-nitro-L-argininemethyl ester （L-NAME： 25 mg/kg）. Intraperitoneal L-arginine （0-500 mg/kg） dose-dependently attenuated BI-induced aggravation of ulcerogenic parameters and hemorrhagic erosions that were reversed by L-NAME. CONCLUSION： BI could produce hemorrhagic erosions through gastric oxidative stress and activation of arginine-nitric oxide pathway.展开更多
Objective: To comparatively study the different effects of open heart surgery on brain tissues of patients with congenital and rheumatic heart disease. Methods: Forty patients with congenital heart disease (CHD, CHD g...Objective: To comparatively study the different effects of open heart surgery on brain tissues of patients with congenital and rheumatic heart disease. Methods: Forty patients with congenital heart disease (CHD, CHD group, n=20) or rheumatic heart disease (RHD, RHD group, n=20) underwent on-pump (cardiopulmonary bypass, CPB) heart-beating open heart surgery. Blood samples before CPB, and 20 minutes, 1 hour, 24 hours and 7 days after CPB were collected, and the levels of neuron-specific enolase (NSE) and protein S-100b in the plasma were determined with enzyme-linked immunoadsorbent assay (ELISA), respectively. All the patients were examined with electroencephalogram (EEG) before and 1 week after operation. The changes of NSE, S-100b and EEG compared to verify the difference of postoperative cerebral injury between CHD cases and RHD cases. Results: The plasma level of S-100b increased significantly 20 minutes after CPB and was still higher than the preoperative level at 24 hours after operation in both groups (P< 0.01). The plasma level of NSE increased more significantly in the CHD group than in the RHD group 20 minutes after CPB and it returned to the normal level 24 hours after CPB in the CHD group but remained at a high level in the RHD group (P< 0.01). The levels of NSE and S-100b returned to the normal levels on the 7th day after CPB. Abnormal EEG was found in 75% of the patients in the CHD group and 60% in the RHD group. Conclusions: On-pump heart-beating open heart surgery can cause certain cerebral injury in the patients with CHD or RHD. The injury was more severe and recovered more quickly in the CHD group than in the RHD group.展开更多
Vascular injury,remodeling,as well as angiogenesis,are the leading causes of coronary or cerebrovascular disease.The blood vessel functional imbalance trends to induce atherosclerosis,hypertension,and pulmonary arteri...Vascular injury,remodeling,as well as angiogenesis,are the leading causes of coronary or cerebrovascular disease.The blood vessel functional imbalance trends to induce atherosclerosis,hypertension,and pulmonary arterial hypertension.As several genes have been identified to be dynamically regulated during vascular injury and remodeling,it is becoming widely accepted that several types of non-coding RNA,such as microRNAs(miRNAs)and long non-coding RNAs(lncRNAs),are involved in regulating the endothelial cell and vascular smooth muscle cell(VSMC)behaviors.Here,we review the progress of the extant studies on mechanistic,clinical and diagnostic implications of miRNAs and lncRNAs in vascular injury and remodeling,as well as angiogenesis,emphasizing the important roles of miRNAs and lncRNAs in vascular diseases.Furthermore,we introduce the interaction between miRNAs and lncRNAs,and highlight the mechanism through which lncRNAs are regulating the miRNA function.We envisage that continuous in-depth research of non-coding RNAs in vascular disease will have significant implications for the treatment of coronary or cerebrovascular diseases.展开更多
基金Supported by a grant from National Sciences Council of Taiwan,NSC 88-2314-B006-028
文摘AIM： To investigate the role of gastric oxidative stress and nitric oxide （NO） in the formation of gastric hemorrhagic erosion and their protection by drugs in rats with ischemic brain. METHODS： Male Wistar rats were deprived of food for 24 h. Under chloral hydrate （300 mg/kg） anesthesia, bilateral carotid artery ligation was performed. The pylorus and carotid esophagus of the rats were also ligated. The stomachs were then irrigated for 3 h with either normal saline or simulated gastric juice containing 100 mmol/L HCI plus 17.4 mmol/L pepsin and 54 mmol/L NaCI. Rats were killed and stomachs were dissected. Gastric mucosa and gastric contents were harvested. The rat brain was dissected for the examination of ischemia by triphenyltetrazolium chloride staining method. Changes in gastric ulcerogenic parameters, such as decreased mucosal glutathione level as well as enhanced gastric acid back-diffusion, mucosal lipid peroxide generation, histamine concentration, luminal hemoglobin content and mucosal erosion in gastric samples, were measured. RESULTS： Bilateral carotid artery ligation produced severe brain ischemia （BI） in rats. An exacerbation of various ulcerogenic parameters and mucosal hemorrhagic erosions were observed in these rats. The exacerbated ulcerogenic parameters were significantly （P〈 0.05） attenuated by antioxidants, such as exogenous glutathione and allopurinol. These gastric parameters were also improved by intraperitoneal aminoguanidine （100 mg/kg） but were aggravated by N^G-nitro-L-argininemethyl ester （L-NAME： 25 mg/kg）. Intraperitoneal L-arginine （0-500 mg/kg） dose-dependently attenuated BI-induced aggravation of ulcerogenic parameters and hemorrhagic erosions that were reversed by L-NAME. CONCLUSION： BI could produce hemorrhagic erosions through gastric oxidative stress and activation of arginine-nitric oxide pathway.
文摘Objective: To comparatively study the different effects of open heart surgery on brain tissues of patients with congenital and rheumatic heart disease. Methods: Forty patients with congenital heart disease (CHD, CHD group, n=20) or rheumatic heart disease (RHD, RHD group, n=20) underwent on-pump (cardiopulmonary bypass, CPB) heart-beating open heart surgery. Blood samples before CPB, and 20 minutes, 1 hour, 24 hours and 7 days after CPB were collected, and the levels of neuron-specific enolase (NSE) and protein S-100b in the plasma were determined with enzyme-linked immunoadsorbent assay (ELISA), respectively. All the patients were examined with electroencephalogram (EEG) before and 1 week after operation. The changes of NSE, S-100b and EEG compared to verify the difference of postoperative cerebral injury between CHD cases and RHD cases. Results: The plasma level of S-100b increased significantly 20 minutes after CPB and was still higher than the preoperative level at 24 hours after operation in both groups (P< 0.01). The plasma level of NSE increased more significantly in the CHD group than in the RHD group 20 minutes after CPB and it returned to the normal level 24 hours after CPB in the CHD group but remained at a high level in the RHD group (P< 0.01). The levels of NSE and S-100b returned to the normal levels on the 7th day after CPB. Abnormal EEG was found in 75% of the patients in the CHD group and 60% in the RHD group. Conclusions: On-pump heart-beating open heart surgery can cause certain cerebral injury in the patients with CHD or RHD. The injury was more severe and recovered more quickly in the CHD group than in the RHD group.
文摘Vascular injury,remodeling,as well as angiogenesis,are the leading causes of coronary or cerebrovascular disease.The blood vessel functional imbalance trends to induce atherosclerosis,hypertension,and pulmonary arterial hypertension.As several genes have been identified to be dynamically regulated during vascular injury and remodeling,it is becoming widely accepted that several types of non-coding RNA,such as microRNAs(miRNAs)and long non-coding RNAs(lncRNAs),are involved in regulating the endothelial cell and vascular smooth muscle cell(VSMC)behaviors.Here,we review the progress of the extant studies on mechanistic,clinical and diagnostic implications of miRNAs and lncRNAs in vascular injury and remodeling,as well as angiogenesis,emphasizing the important roles of miRNAs and lncRNAs in vascular diseases.Furthermore,we introduce the interaction between miRNAs and lncRNAs,and highlight the mechanism through which lncRNAs are regulating the miRNA function.We envisage that continuous in-depth research of non-coding RNAs in vascular disease will have significant implications for the treatment of coronary or cerebrovascular diseases.
