Dizziness Result From Anomalous Origin of Left Common Carotid Artery.

BACKGROUND: The anomalous origin of the left common carotid artery from the pulmonary artery is extremely scarce. At present, there are few relevant research and medical treatment data. This case is intended to provide relevant information and share treatment experiences. Case information: A 6-year-old child was diagnosed with patent ductus arteriosus and underwent surgery five years ago with occasional dizziness. After examination, it was found that the abnormality of her left common carotid artery originated from the pulmonary artery, and the patient underwent arterial ligation with the monitoring of cerebral oxygen consumption by near-infrared spectroscopy after careful preoperative evaluation. At present, it has been two years after the operation, and the patient is in good condition and has received regular follow-up. CONCLUSION: For patients with an abnormal left common carotid artery from the pulmonary artery, after careful preoperative evaluation such as cerebral angiography, under the monitoring of cerebral oxygen consumption by near-infrared spectroscopy, ligation of the proximal end of the artery of abnormal origin is safe and feasible.

Cerebral infarction after cardiac surgery.

Cerebral infarction, a common central nervous system complication after adult cardiac surgery, is one of the main factors leading to the poor prognosis of cardiac surgery patients besides cardiac insufficiency. However, there is currently no effective treatment for cerebral infarction. Therefore, early prevention and diagnosis of postoperative cerebral infarction are particularly important. There are many factors and mechanisms during and after cardiac surgery that play an important role in the occurrence of postoperative cerebral infarction, such as intraoperative embolism, systemic inflammatory response syndrome, atrial fibrillation, temperature regulation, blood pressure control, use of postoperative blood products, and so forth. The mechanism by which most risk factors act on the human body, leading to postoperative cerebral infarction, is not well understood, and further research is needed. Therefore, this paper aims to summarize and explain the relevant risk factors, mechanisms, clinical signs, imaging characteristics, and early diagnosis methods of cerebral infarction complications after cardiac surgery, and provides useful data for the establishment of related diagnosis and treatment standards.

Role of Phosphorylated AMP-Activated Protein Kinase (AMPK) in Myocardial Insulin Resistance After Myocardial Ischemia-Reperfusion During Cardiopulmonary Bypass Surgery in Dogs.

BACKGROUND The aim of this study was to determine the role of AMP-activated protein kinase (AMPK) in myocardial insulin resistance after myocardial ischemia-reperfusion during cardiopulmonary bypass surgery in dogs. MATERIAL AND METHODS Twenty-four mongrel dogs were randomly assigned to 4 groups. The control group did not undergo aortic cross-clamping; the model group underwent 60 mins of aortic cross-clamping with 150 ml cardioplegic solution. The treatment group, the inhibition group respectively with 0.11mg/kg AICAR (AMPK agonist) in 150 ml cardioplegic solution and 0.11mg/kg Compound C (AMPK inhibitor) in 150 ml cardioplegic solution. The blood flow was determined and left ventricular myocardial tissue were taken at pre-bypass, 15, 60, and 90 min after aorta declamping, respectively. Expression of AMPK mRNA, p-AMPK and GLUT-4 proteins was determined by RT-PCR, IHC and WB. RESULTS Compared with the control group, receiving 60 min ischemia at 15 min after reperfusion, Myocardial Glucose Extraction Ratio were significantly decreased in the other 3 groups, it was significantly decreased from 20.0% to 1.2% at 60 min of reperfusion, and recovered to 6.1% after 90 min reperfusion in model group, while recovered to 4.1%, 12.0% after 90 min reperfusion respectively exposed to Compound C and AICAR. The expressions of p-AMPK, GLUT-4 protein and AMPK mRNA in myocardium were decreased in different experiment groups, but these changes occurred to a lesser extent in the treatment group. CONCLUSIONS The inability of GLUT-4 expression induced by the decreases in p-AMPK protein expression that may be one of the reasons for myocardial insulin resistance.

Effects of RNA silencing of matrix metalloproteinase-2 on the growth of esophageal carcinoma cells in vivo.

Esophageal carcinoma is one of the most common malignancies in China. Previous studies reported that matrix metalloproteinases (MMPs) have important roles in the progression and invasion of numerous types of solid tumors. Among the MMPs, MMP-2 has been closely associated with tumor growth and invasion. In the present study, a short hairpin RNA (shRNA) lentiviral expression vector targeting the MMP-2 gene was constructed in order to observe the inhibitory effect of MMP-2 gene silencing on the growth of the KYSE150 esophageal carcinoma cell line in vivo. Three small hairpin RNA sequences targeting MMP-2 were designed and cloned into lentiviral vectors. Following transfection of the lentiviral vectors into KTSE150 cells, MMP-2 mRNA and protein expression levels were examined by reverse transcription-quantitative polymerase chain reaction and western blotting, and the growth rate of cells was analyzed by MTT assays. Subsequently, tumor growth was assessed in nude mice. Lentivirus-mediated RNA interference effectively inhibited the expression of MMP-2 mRNA and protein in KYSE150 esophageal carcinoma cells, and suppressed the growth of esophageal carcinoma cells in vivo. The results of the present study suggested that lentivirus-mediated gene therapy targeting MMP-2 may be an attractive strategy for the treatment of esophageal carcinoma and justifies the performance of further studies on the application of lentivirus vectors to cancer gene therapy.

Effect of Si-RNA-silenced HIF-1α gene on myocardial ischemia-reperfusion-induced insulin resistance.

OBJECTIVE: To explore the effect (expression and implication) of hypoxia-inducible factor-1α (HIF-1α) silence induced by siRNA on the myocardial ischemia-reperfusion-induced insulin resistance in adult rats. METHODS: One-step enzymolysis method was used to isolate adult rat cardiomyocytes; adult rat cardiomyocytes were cultured; HIF-1α gene-specific Si-RNA was constructed and transfected into rat cardiomyocytes using liposome method. Myocardial IRI model was prepared. HIF-1α and glucose transporter 4 (GLUT-4) mRNA expression was detected by RT-PCR; distribution of GLUT-4 protein expression in adult rat cardiomyocytes was detected by immunofluorescence; Western blot was used for the detection of HIF-1α protein expression; isotope tracer assay was used to detect the changes in cell glucose (Glu) uptake rate. RESULTS: This method can stably get 85% to 90% active calcium tolerant adult rat cardiac myocytes, and the cultured cells were proved to be cardiomyocytes. After experiencing ischemia-reperfusion injury, HIF-1α mRNA expression levels in adult rat hypoxia cardiomyocytes had different degrees of increase compared with the control group (compared with the control group, P < 0.05). Compared with the model group, HIF-1α mRNA expression levels after ischemia and reperfusion in HIF-1αsi-RNA group and empty-vector group were lower than that in the control group and the model group; the expression reached the peak after 60 min of reperfusion, which did not change significantly in the control group. Expression of HIF-1α protein in myocardial cells was quite low in the control group; in the model group and intervention group, only after hypoxia-ischemia for 60 min, expression bands could be detected; especially in the model group, the expression had been increased until 60 min after reperfusion and began to decline from the time point of 180 min after reperfusion, but was still higher than that in the control group; in the intervention and empty-vector groups, it also increased rapidly at 60 min, but the expression was significantly lower than that in the model group; at 180 min after reperfusion, its protein expression peaked; while at 8 h after reperfusion, all the expression was extremely low. Compared with the control group, Glut4 mRNA expression in model group, transfected group and empty-vector group was reduced at the time points of T1-T4 (P < 0.05); the decline was the most significant at the time points of T1 and T2, followed by slightly increase at T3 and gradual recovery at T4; Compared with model group, Glut4 mRNA expression in transfection group was significantly reduced (P < 0.05); the decline was the most obvious at T1-T2, and then there was an increasing trend and it was recovered at T5 point. After experiencing ischemia, GLUT-4 protein expression changing trend was as follows: it was significantly reduced on the cell membrane, which was the most obvious from T1 to T3 and began to improve at T3, but still had not reached the level in the control group; it had been reached the levels of the control group at T5. After HIF-1αsi-RNA transfection and ischemia, GLUT-4 protein expression was increased in plasma and reduced on cell membrane; the decline was slightly improved at T3 and recovered to control distribution level at T5. After cardiac ischemia-reperfusion, glucose uptake rate decreased to varying degrees in myocardial cells and reached the lowest value after 60 min of ischemia, then gradually increased. After 8 h of reperfusion, the level in model group returned to the control level; compared with the model group, glucose concentration increased more serious in transfection group and empty-vector group after reperfusion. CONCLUSION: HIF-1α played a central regulatory role in this mechanism; HIF-1α may be one of the molecular mechanisms triggering myocardial IR.

[The effect of SenQi FuZheng injection on lung cell apoptosis following cardiopulmonary bypass in dogs].

OBJECTIVE: To study the effect and possible mechanism of SenQi FuZheng injection on lung cell apoptosis in dogs with ischemia reperfusion (I/R) following cardiopulmonary bypass (CPB). METHODS: CPB dog models were established. The 12 mongrel dogs were randomly divided into two groups: CPB I/R group (control) and SenQi FuZheng injection group (therapy). The lung tissue samples of 1.0 cm3 from the same lobes of lung were obtained at 10 min before CPB (T1) and 60 (T2), 120 min (T3) after reperfusion. These samples were fixed and then embedded in paraffin imbedding, and cut into thin slices (5 microm). Streptavidin/peroxidase (SP) immunohistochemical method was employed to detect Caspase -3, Bcl-2, and Bax protein expressions. RESULTS: The expressions of Caspase-3 and Bax protein in the tissues with SenQi FuZheng therapy were significantly lower at 60 and 120 min after reperfusion than the controls (P < 0.05). The expression of Bcl-2 protein and the Bcl-2/Bax ratio in the tissues with SenQi FuZheng therapy were significantly higher at 60 and 120 min after reperfusion than the controls (P < 0.05). CONCLUSION: Administration of SenQi FuZheng injection in CPB dogs can inhibit apoptosis of alveolar cells by reducing the expressions of Caspase-3 and Bax protein and increasing the expression of Bcl-2 protein.

Cardiac glucose uptake and suppressed expression/translocation of myocardium glucose transport-4 in dogs undergoing ischemia-reperfusion.

Impaired glucose metabolism is implicated in cardiac failure during ischemia-reperfusion. This study examined cardiac glucose uptake and expression of glucose transport-4 (GLUT-4) in dogs undergoing ischemia-reperfusion. Cardiac ischemia was induced by cardiopulmonary bypass for 30 min or 120 min in dogs. Plasma insulin and glucose concentrations were measured at pre-bypass (control), and aortic cross-clamp off (ischemia-reperfusion) at 15, 45, and 75 min. At the same time, the left ventricle biopsies were taken for GLUT-4 immunohistochemistry and glycogen content analysis. In dogs receiving 120-min ischemia, coronary arterial and venous glucose concentrations were increased, but the net glucose uptake in ischemia-reperfusion heart were significantly decreased from 25% (control) to zero at 15 and 45 min of reperfusion, and recovered to only 7% after 75 min reperfusion. Myocardium glycogen contents were decreased by 65%. Plasma insulin levels and Insulin Resistant Index were markedly increased in dogs undergoing 120-min ischemia and reperfusion. These changes were relatively mild and reversible in dogs receiving only 30-min ischemia followed by reperfusion. Expression of total GLUT-4 in myocardium was decreased 40% and translocation of GLUT-4 from cytoplasm to surface membrane was decreased 90% in dogs receiving 120-min ischemia followed by 15-min reperfusion. Suppressed translocation of GLUT-4 was also evident in dogs receiving 30-min ischemia, but to a lesser extent. Reduced myocardium glucose uptake, utilization, and glycogen content are clearly associated with ischemia-reperfusion heart injury. This appears to be due, at least in part, to suppressed expression and translocation of myocardium GLUT-4.

[The protective efficacy of rabbit endogenous nitric oxide against acute rabbit lung ischemia-reperfusion injury and its mechanism].

OBJECTIVE: To investigate the protective efficacy of rabbit endogenous nitric oxide (NO) against acute rabbit lung injury associated with ischemia-reperfusion and explore the possible mechanism. METHODS: The rabbit lung ischemia-reperfusion (LIR) model was established; thirty-two adult New Zealand white rabbits were randomly divided into four groups. The rabbits of control group underwent sham operation. In group LIR, the rabbits' left lung hili were clamped for 60 minutes and then released. In group LIR+L-Arg (L-arginine), the rabbits were operated upon as those in group LIR, but L-Arg (200 mg/kg) was infused into blood circulation as substrate for NO generation before removal of the clip. In group LIR+L-NNA (L-ng-nitro-Arginine), the rabbits passed through the same operation as in group LIR, but L-NNA (10 mg/kg) was infused into circulation as an inhibitor against NO generation before reperfusion. After reperfusion for 60 minutes, the lung tissues were harvested for histological examination, and the wet to dry ratio of lung tissue weight (W/D), myeloperoxidase (MPO) activity, malondialdehyde (MDA) content as well as the ratio of nitrate/nitrite (N/N) were measured respectively. RESULTS: The group LIR had greater lung tissue W/D, higher MPO activity and MDA content, lower ratio of N/N, and serious pulmonary edema as compared with group ShO (P<0.01). But in group LIR+L-Arg, the degree of pulmonary edema was alleviated, the MPO activity and MDA content were decreased, and the ratio of N/N increased; there was statistically significant difference between group LIR and group LIR+Arg in respect to the above indices (P<0.01). However, in group LIR+L-NNA, the pulmonary edema was even more severe, the MPO activity and MDA content were significantly higher those that in group LIR or group LIR+L-Arg (P<0.01). CONCLUSION: The endogenous release of pulmonary NO can attenuate the acute lung injury associated with LIR, and the mechanisms may involve the protective efficacy conferred by endogenous NO against accumulation of neutrophil in lung, against pulmonary microvascular permeability, and against the oxygen free radical injury to lung.