[Effects of naoxintong capsule on the inflammation and prognosis in borderline lesion coronary heart disease patients].

OBJECTIVE: To study the effects of Naoxintong Capsule (NC) on the inflammation and long-term prognosis in the borderline lesion coronary heart disease patients. METHODS: A total of 240 coronary heart disease patients with angina symptoms and accompanied with borderline lesion coronary heart disease (with the diameter stenosis in critical 50% -70%) by means of coronary angiography or multislice computed tomography coronary angiography were recruited. These patients were randomly assigned to the conventional treatment group (including nitrate, beta blockers, anti-platelet, anticoagulation, angiotensin converting enzyme inhibitors, and so on) and the NC treatment group (treated the same way as those for the conventional treatment group and NC). All patients were treated for 12 months. The occurrence of cardiovascular events was observed after treatment. The inflammatory factors in serum [interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and high sensitive C reaction protein (hs-CRP)], matrix metalloproteinases-9 (MMP-9), blood lipids and blood sugar, liver and kidney functions were measured before and after treatment. RESULTS: After 12 months of treatment, the incidence of angina pectoris patients (6.67% vs 15.83%, P < 0.05) and hospitalization due to acute coronary syndrome (ACS) attacks (4.17% vs 10.83%) was significantly lower in the NC treatment group than in the conventional treatment group. There was no statistical difference in the serum levels of IL-6, TNF-alpha, hs-CRP, and MMP-9 between the two groups before treatment (P > 0.05). After 12 months of treatment, serum levels of IL-6, TNF-alpha, hs-CRP, and MMP-9 were significantly lower when compared with before treatment in the same group (P < 0.05). Besides, the serum levels of IL-6, TNF-alpha, hs-CRP, and MMP-9 were significantly lower in the NC group than in the conventional treatment group (P < 0.05). By means of Logistic regression analysis we found that the post-treatment MMP-9 level and IL-6 level were independent risk factors influencing the recurrence of angina pectoris. CONCLUSIONS: NC could alleviate the inflammation. Long-term administration of NC could reduce the recurrence of angina pectoris and decrease the incidence of ACS attack in borderline lesion coronary heart disease patients. The post-treatment MMP-9 level and IL-6 level were independent risk factors influencing the recurrence of angina pectoris.

Norepinephrine can act via alpha(2)-adrenoceptors to reduce the hyper-excitability of spinal dorsal horn neurons following chronic nerve injury.

BACKGROUND/PURPOSE: Rats display behavioral signs of neuropathic pain lasting for months in the chronic constriction injury (CCI) model. During intrathecal anesthesia, the administered drugs mainly diffuse directly into the superficial neurons in the spinal dorsal horn. This study aimed to investigate the effect of bath application of norepinephrine on whole cell patch clamp recordings from spinal cord slices of CCI rats with allodynia. METHODS: An assessment of paw withdrawal threshold in response to mechanical stimulation was performed on the operated side on the day before surgery and was repeated after recovery from anesthesia and on the 7(th) and 14(th) days after surgery. Spinal cord slice preparations containing dorsal horn neurons were obtained from both sham-operated rats and CCI rats (after the 14(th) postoperative day behavior test). RESULTS: Compared with normal controls, CCI rats had significantly lower levels of both hyperpolarization and spike threshold in single action potentials recorded from lamina I and II neurons of the spinal dorsal horn. In contrast, a series of action potential recordings showed that the percentage of spiking neurons of the spinal dorsal horn of CCI rats were significantly higher than those of normal controls. The CCI-induced reduction in hyperpolarization, as well as the increased numbers of spinal dorsal horn spiking neurons could be significantly reduced by norepinephrine application. The norepinephrine-induced increased hyperpolarization and input resistance could be abolished by the application of an alpha(2)-adrenoceptor antagonist (idazoxan; 200 nM). CONCLUSION: The results suggest that chronic nerve injury may induce neuropathic pain by increasing the excitability of spinal dorsal horn neurons. This excitability can be reduced by norepinephrine.

[Effect of bone mesenchymal stem cells transplantation on malignant ventricular arrhythmia induced byelectrophysiological stimulation in a mini-swine model of acute myocardial infarction].

OBJECTIVE: To investigate the effects of autologous bone mesenchymal stem cells (MSC) transplantation on malignant arrhythmia induced by electrophysiological (EP) stimulation and cardiomyocyte ion channels remodeling in a mini-swine model of acute myocardial infarction (AMI). METHODS: Immediately after AMI (LAD occluded for 120 min), MSC (10 x 10(7), labeled by colloidal gold and co-cultivated with 5-azacytidine, 5-aza, n = 12) or equal volume saline (n = 10) were injected through over-the-wire (OTW) balloon in LAD at distal over D(1). EP stimulation is performed after 2 hours and 4 weeks in both groups to induce arrhythmia. The variance of heterogeneity of sodium currents (I(Na)) and I(Na) steady-state inactivation curves in different zones of infracted wall were investigated by patch clamp technology and the relationship between ionic channel and ventricular arrhythmia is analyzed. RESULTS: EP induced malignant ventricular arrhythmia (VT) rate was similar (MSC 75% vs. saline 90%, P = 0.455) at 2 hours post AMI and was significantly lower in MSC group (25% vs. 80%, P = 0.012) at 4 weeks post AMI. The Peak I(Na) current densities of the Endo, Media and Epi were significantly lower in MSC group [(-14.04 +/- 3.82) pA/pF, (-29.26 +/- 5.70) pA/pF, (-12.43 +/- 3.04) pA/pF] compared those in saline group [(-9.71 +/- 3.38) pA/pF, (-18.98 +/- 4.05) pA/pF, (-8.47 +/- 3.34) pA/pF, all P < 0.05]. The I(Na) steady-state inactivation curves of the Epi, Endo and Media in mini-swine with VT in MSC group [(-126.2 +/- 10.9) mV, (-106.7 +/- 11.9) mV, (-105.4 +/- 11.0) mV] were similar as those in saline group with VT [(-129.1 +/- 10.9) mV, (-112.2 +/- 9.9) mV, (-109.7 +/- 9.2) mV, all P > 0.05] while significantly lower compared to MSC group without VT [(-93.1 +/- 13.8) mV, (-95.2 +/- 15.5) mV, (-103.4 +/- 8.7) mV, all P < 0.05]. The multiple logistic regression analysis showed that I(Na) current density (RR = 1.449, 95% CI 1.276 - 2.079, P = 0.029) and I(Na) steady-state inactivation curves (RR = 1.092, 95% CI 1.008 - 1.917, P = 0.012) were the independent factors for reduced VT. CONCLUSIONS: Autologous MSC attenuated malignant ventricular arrhythmia induced by EP at 4 weeks in mini-swine with AMI which might due to altered cardiomyocyte ion channels remodeling induced by MSC.

Mechanisms of improvement of left ventricle remodeling by trans-planting two kinds of autologous bone marrow stem cells in pigs.

BACKGROUND: The necrosis of a large number of myocardial cells after acute myocardial infarction (AMI) results in a decrease of cardiac function and ventricle remodeling. Stem cell transplantation could improve cardiac function after AMI, but the involving mechanisms have not been completely understood. The present study aimed to investigate the effects of transplantation of autologous bone marrow mononuclear cells (BM-MNC) and mesenchymal stem cells (MSCs) via the coronary artery on the ventricle remodeling after AMI as well as the mechanisms of the effects of transplantation of different stem cells on ventricle remodeling. METHODS: A total of 36 male pigs were enrolled in this study, which were divided into 4 groups: control group, simple infarct model group, BM-MNC transplantation group, and MSCs transplantation group. At 90 minutes when a miniature porcine model with AMI was established, transplantation of autologous BM-MNC ((4.7 +/- 1.7) x 10(7)) and MSCs ((6.2 +/- 1.6) x 10(5)) was performed in the coronary artery via a catheter. Ultrasound, electron microscope, immunohistochemical examination and real time reverse transcriptase-polymerase chain reaction were used respectively to observe cardiac functions, counts of blood vessels of cardiac muscle, cardiac muscle nuclear factor (NF)-kappaB, myocardial cell apoptosis, and the expression of the mRNA of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in cardiac muscles. Multivariate Logistic regression was used to analyze the correlation factors of left ventricular end-diastolic diameter (EDD). RESULTS: The number of blood vessels in the infarct zone and around its border in the BM-MNC transplantation group was more than those in the infarct model group and MSCs group (P = 0.0001) and there was less myocardial cell apoptosis in the stem cell transplantation group than that in the infarct model group (all P < 0.01). The positive rate of NF-kappaB in the stem cell transplantation group was lower than that in the infarct model group (P = 0.001). The gene expression of VEGF in the infarct border zone of the BM-MNC group was higher than that in the MSCs group (P = 0.0001). The gene expression of bFGF in the infarct border zone in the MSCs transplantation group was higher than that in the infarct model group and the BM-MNC group (P = 0.0001). Left ventricular ejection fraction was inversely proportional to the apoptotic rate of myocardial cells and cardiac muscle NF-kappaB but positively correlated with the number of blood vessels and the expression of VEGF and bFGF in the infarct zone and infarct border zone. The Multivariate Logistic regression analysis on the factors influencing the left ventricular end-diastolic diameter after stem cell transplantation showed that the expression of VEGF mRNA in the cardiac muscles in the infarct zone, the number of apoptotic myocardial cells and the expression of NF-kappaB in the infarct border zone were independent factors for predicting the inhibitory effect on the dilation of left ventricular EDD after stem cell transplantation. CONCLUSIONS: Transplantation of autologous BM-MNC and MSCs in pigs can improve the condition of left ventricular remodeling and recover the cardiac functions after AMI. The improvement of cardiac functions is related to the increase of blood vessels, the increased expression of VEGF and bFGF, the reduction of myocardial cell apoptosis, and the decrease of NF-kappaB level in cardiac muscle tissues after stem cell transplantation.

[Impact of propofol on the optimal sedative depth in patients undergoing gastroscopy].

OBJECTIVE: To explore the optimal sedative depth and adequate bispectral index (BIS) value in patients undergoing gastroscopy treated with propofol and to explore the maneuverability and practicability of using BIS value as a variable to control the infusion of propofol. METHODS: 160 patients, 76 males and 84 females, aged 44 +/- 15 voluntarily undergoing painless gastroscopy were randomly divided into 4 equal sex and age-matched groups. Propofol was given intravenously at the speed of 60 ml/min. Encephalographic monitoring was conducted to observe the BIS value. The first administration of propofol was stopped when the BIS value decreased to 80 ~ 75 (Group A), 65 ~ 74 (Group B), 55 ~ 64 (Group C), or < 55 (Group D). The amount of drug administered was recorded. Thirty seconds after the first administration the gastroscope was inserted. If the patients felt uncomforted an additional dose of 30 approximately 50 mg was used. The blood pressure, heart rate, respiratory rate, SpO(2), and BIS value before and during the gastroscopy, times needed for awakening and recovery of orientation were recorded. The patients were asked about if they were conscious during the operation. RESULTS: The doses of propofol in group A, B, C, and D were (1.15 +/- 0.34) mg/kg, (1.43 +/- 0.27) mg/kg, (1.78 +/- 0.31) mg/kg, and (2.15 +/- 0.27) mg/kg respectively, with a significant difference between each 2 groups (all P < 0.05). The successful rate of gastroscope insertion were 17.5%, 47.5%, 92.5%, and 97.5% in group A, B, C, and D respectively, with a. significant difference between each 2 groups (P < 0.05) except between Groups C and D. The heart rate and mean arterial pressure decreased significantly compared with those before the examination in Group D (both P < 0.05). 17 patients of Group A and 4 cases in Group B remembered that they felt unwell during the operation, and 11 patients in Group B said they heard voices but failed to remember the concrete contents. CONCLUSION: It is safe, reliable and feasible to regulate the sedative depth and the dosage of propofol infusion with the BIS monitor. The optimal BIS value in patients undergoing gastroscopy is from 55 to 64.

[The effect of isoflurane induced hypotension on intraoperative cerebral vasospasm in intracranial aneurysm surgery].

OBJECTIVE: To evaluate whether isoflurane induced hypotension increases the incidence of cerebral vasospasm in intracranial aneurysm surgery. METHODS: Thirty consecutive patients undergoing intracranial aneurysmal surgery without preexisting cerebral ischemia were prospectively randomized into 2 groups: isoflurane induced hypotension group (group A, n = 15) and isoflurane maintained anesthesia group (group B, n = 15). The patients in the group A were performed isoflurane induced hypotension after dura opening by increasing the inhaled concentration of isoflurane to decrease the mean arterial pressure (MAP) by 30 - 40 percent of that of baseline value. After the aneurysm was clipped, the concentration of inhaled isoflurane was decreased so as to stop blood pressure reduction. The patient in group B was given 1 minimum alveolar concentration (MAC) of isoflurane during the whole procedure. The indicators of blood circulation were measured before blood pressure reduction, 30 minutes after blood pressure reduction, just after the clipping of the aneurysm, and 30 minutes after stopping blood pressure reduction. The S100B protein level in cerebrospinal fluid was observed before the controlled hypotension and 0, 2, and 4 h after the aneurysm was clipped. Assessment of the mean blood flow velocity of parent artery and its main branches was performed by microvascular ultrasonics before and after the aneurysm was clipped. The patients were followed-up for one week after the operation to observe the neurological complication. RESULTS: The MAP was decreased from 95 mm Hg +/- 12 mm Hg to 59 mm Hg +/- 5 mm Hg 30 minutes after the induced hypotension, and resumed to 75 mm Hg +/- 8 mm Hg 30 minutes after the aneurysm was clipped. Compared with those in the group B, both the total systemic vascular resistance and myocardial contract acceleration were decreased in group A, whereas the cardiac output and heart rate remained stable. (2) 4 hours after the aneurysm was clipped the S100B protein level in CSF was increased significantly in both groups, and that in the group A being significantly higher than that in the group B (t = 2.854, P < 0.01). (3) In the group A, the mean arterial flow velocity of distal parent vessels increased by more than 30 percent in 8 out of the 15 patients and 3 of these 8 patients suffered from neurological deficits postoperatively. However, the mean arterial flow velocity of distal parent vessels in the group B increased by more than 30 percent in only 3 of the 15 patients and 2 of these 3 patients suffered from neurological deficits postoperatively. CONCLUSION: Isoflurane controlled hypotension may increase the incidence of cerebral vasospasm. Isoflurane induced hypotension for intracranial aneurysm surgery should be cautioned.

[The effect of intraoperative continuous nimodipine infusion on cerebral vasospasm during intracranial aneurysm surgery].

OBJECTIVE: To evaluate the effect of intraoperative continuous nimodipine infusion on cerebral vasospasm during intracranial aneurysm surgery. METHODS: Thirty consecutive patients under-going intracranial aneurysmal surgery were prospectively randomized into two groups: Isoflurane (group A, n = 15) and nimodipine (group B, n = 15). The patients in group A were maintained with 1 minimum alveolar concentration (MAC) isoflurane anesthesia during the whole procedure. The patients in group B were given nimodipine infusion continuously (20 microg.kg(-1).h(-1)) after induction of anesthesia and anesthetized with 1 MAC isoflurane. S100B levels in cerebrospinal fluid were determined before aneurysm clipping and 0, 2, 4 h after aneurysm clipping by enzyme linked immunosorbent assay. Assessment of mean blood flow velocity of parent arterial and arterial branches were performed before and after aneurysm clipping. RESULTS: (1) S100B in cerebrospinal fluid was increased significantly at 4 h after aneurysm was clipped in group A (F = 4.11, P < 0.05). However, S100B in cerebrospinal fluid was stable in group B in the whole procedure. (2) Mean arterial flow velocity of parent vessels in group B was lower significantly than that in group A (t = 2.08, P < 0.05). However, mean arterial flow velocity of distal vessels in both groups has no significant difference. CONCLUSION: Intraoperative nimodipine infusion may prevent cerebral vasospasm during intracranial aneurysm surgery.