ObjectiveTo study the changes of levels of α subunits of stimulatory (Gsα) and inhibitory guanine nucleotide binding protein (Giα) in newborn guinea pig (0 2 days old) myocardium undergoing global ischemic reperfusion, and influences on the changes by St.Thomas Ⅱ and cold blood cardioplegic solution.MethodsThirty newborn guinea pigs were randomly assigned to three groups. GroupⅠ ( n = 10): the newborn hearts suffered by hypothermic global ischemia; group Ⅱ( n =10): the newborn hearts arrested by St. Thomas Ⅱ , and group Ⅲ ( n = 10): the newborn hearts arrested by cold blood cardioplegic solution. Levels of Gsα and Giα were investigated with Western blot analysis.ResultsNo differences of levels of Gsα and Giα were found in three groups before ischemia ( P gt;0.05). The level of Gsα after ischemia was significantly decreased than before ischemia in groupⅠand group Ⅱ ( P lt; 0 01), whereas no pronounced changes in group Ⅲ ( P gt;0.05) were noted after ischemia. The level of Gsα in group Ⅲ was not significantly changed after reperfusion compared with before ischemia( P gt;0 05), and it was much higher than those in groupⅠand group Ⅱ ( P lt; 0 01). Level of Giα was found not markedly changed in group Ⅲ after reperfusion compared with that before ischemia, but was notable higher in groupⅠand group Ⅱ( P lt;0.01). ConclusionsSignificant decrease of level of Gsα, whereas marked increase of level of Giα are found in myocardium of newborn guinea pig undergoing hypothermic (20℃) ischemic reperfusion. No impact of St. Thomas Ⅱ on these changes is verified, but recovery to the level of Gsα and Giα before ischemia is achieved by cold blood cardioplegic solution after ischemia and reperfusion. Unbalance between Gsα and Giα is the one of the mechanisms of ischemic reperfusion injury for immature myocardium.
摘要:目的:探討卡配因抑制劑3（MDL28170）對新生大鼠缺氧缺血性腦損傷(HIBD)神經細胞凋亡的影響。方法:建立新生SD大鼠HIBD模型,治療組于缺養缺血后即刻、2 h、4 h腹腔內注射MDL28170,對照組及手術組同時予生理鹽水。缺氧缺血后24 h用免疫組化方法觀察大腦皮質及海馬CA1區Caspase3 蛋白表達、TUNEL法檢測細胞凋亡,觀察組織病理改變并計算海馬神經元死亡數,透射電鏡觀察細胞超微結構。結果:缺氧缺血后24 h缺血側大腦皮質及海馬CA1區Caspase3和TUNEL陽性細胞數較對照組明顯增加,透射電鏡證實有凋亡細胞;MDL28170可減少陽性細胞數量,抑制神經元死亡,差異有顯著性(Plt;0.05)。結論:MDL28170可通過抑制神經凋亡而對新生大鼠HIBD具有一定保護作用。Abstract: Objective: To investigate the effect of (Calpain inhibitor3) MDL28170 on neural apoptosis in a neonatal model of hypoxicischemic brain damage (HIBD). Methods: A neonatal model of HIBD was established, 7dayold SD rats were divided into three groups. The treatment group received MDL28170(ip) at 0 h,2 h,4 h after HI, whereas the other two groups were administered normal saline simultaneously. The expression of caspase3 (by immunohistochemistry), neural apoptosis (by TUNEL) in cortex and hippocampus ipsilateral to the insult were observed 24 h after HI; hippocampal CA1 neural loss and electromicroscopic changes were assessed at the same time. Results: Apoptotic body was observed by electromicroscopy. Caspase3 positive cells and apoptotic cells increased significantly in the ipsilateral cortex and hippocampal CA1 region compared to the control, and MDL28170 reduced the number of positive cells, attenuated CA1 neural loss with significance (Plt;0.05). Conclusion: It is suggested that MDL28170 may protect the brain of neonatal rats after HIBD by suppressing neural apoptosis.
Objective To evaluate the clinical efficacy of t ransplantation of autologous peripheral blood stemcells ( PBSC) for the t reatment of lower limb arterial ischemic disease. Methods From March 2004 to February2007 , 16 patient s with severe lower limb arterial ischemic disease were t reated with autologous PBSC t ransplantation. Recombinated granulocytecolony stimulating factor ( G2CSF) was used to mobilize the proliferation of bonemarrow stem cells and then the stem cells were released into peripheral blood. Af ter 5 - 6 days , PBSC were collected by CS23000 PLUS blood2cells separator. Such concent rated stem cells fluid was int ramuscularly injected into theischemic areas of the lower limbs. Results The result s of 3 to 242month following2up after the t ransplantation ofstem cells showed that the resting pains of the affected limb were greatly relieved , and ulcers were healed. The distance and duration of intermittent limping became farther and longer. Conclusion Transplantation of autologousPBSC would be a novel and effective method for the t reatment of arterial ischemic disease. However , this method isstill at the stage of initial clinical application , so it still need to be further studied.
Objective To study the effect of dexamethasone to protect flaps from an ischemia-reperfusion injury and elucidate its mechanism of regulating the death course of the neutrophils.Methods The rats were randomly divided into 3 groups.The vein of the rat was clamped for 8 h after the flap had formed. Group A: the normal flap; Group B: the saline control flap; Group C: the treatment flap with dexamethasone. The survival area of the flaps was measured at 7 days; the apoptotic and necrotic neutrophils,tumor necrosis factor α （TNF-α）, and interleukin 10 （IL-10） concentrations were measured. Results The flap survival areas in Groups A and C were larger than those in Group B. The apoptotic neutrophils in Group B were fewer than those in Groups A and C on the 1st and 3rd days after operation; however, they were more in number in Group B than in groups A andC on the 6th day. The necrotic cells in Group B were more in number than those in Groups A and C. In Group B, the plasma TNF-α concentration reached the maximum level at 1 h,while the IL-10 level reached the lowest 3 h after the reperfusion. In Group C, the TNF-α concentration was lower than that in Group B and decreased dramatically at 6 h. The IL-10 concentration was the lowest at 1 h, and increased rapidly at 3 h. Thus, ischemia reperfusion could injure the flaps, probably through the abnormal action of the neutrophils, such as the disordered secretion of the cytokines and abnormal death course of the neutrophils. Conclusion Dexamethasone can protect the flap from an ischemia-reperfusion injury by its regulation for the neutrophil function.
In order to explore a new method to treat the ischemic necrosis of the head of 2nd metatarsal bone in adult, transposition of reversed vascularized metatarsal bone graft was adopted in the treatment of 4 cases, 2 of which were followed up for one and a half years. The postoperative X-ray showed the round head of the 2nd metatarsal bone became round and even density. The clinical observation showed that there was excellent function of metatarsophalangeal joint. It was concluded that the reversed vascularized metatarsal bone graft could provide a reliable blood supply and various osteogenic factors to the avascularized head of the metatarsal bone, and the operation could also debride the joint cavity and carry out decompression.
Abstract： Objective To evaluate the effect of a surgical method for treating mild- to moderate-ischemic mitral regurgitation（IMR） using a self-designed device during off-pump coronary artery bypass grafting（OPCAB）. Methods From September 2009 to August 2011, six patients（4 males, 2 females； age was 52-73 years） with mild- to moderate-IMR underwent OPCAB and concomitant mitral valvuloplasty using a self-designed device in Beijing An Zhen Hospital. Their degree of IMR, anteroposterior diameter of mitral annulus, left ventricular long-axis diameter, left ventricular short-axis diameter and left ventricular spherical index（left ventricular short-axis diameter/left ventricular long -axis diameter）were measured using transesophageal Doppler echocardiography before and after mitral valvuloplasty. Their mean aorta pressure, mean pulmonary artery pressure and central venous pressure were also measured via Swan-Ganz catheter before and after mitral valvuloplasty. Perioperative cardiac function indexes were compared. Results There was no in-hospital death. IMR of all patients disappeared postoperatively. After mitral valvuloplasty their anteroposterior diameter of mitral annulus（3.43±0.08 cm vs.3.68±0.08 cm；t=5.430, P=0.001）, left ventricular short-axis diameter（4.80±0.21 cm vs.5.53±0.11 cm；t=7.530, P=0.001）and left ventricular spherical index（0.64±0.02 vs.0.74±0.01；t=11.110, P=0.002）significantly decreased than those before mitral valvuloplasty . But their left ventricular long-axis diameter and hemodynamic indexes did not change significantly after mitral valvuloplasty. All the six patients were followed up at the out-patient department 3 months postoperatively without autonomous symptoms. Their heart function improved to I class（New York Heart Association）. Echocardiography showed 4 patients without IMR and 2 patients with trace of minimalIMR. Conclusion Off-pump surgical therapy for mild- to moderate- IMR during OPCAB can help the patients reverseremodeling of the left ventricle, avoid the risks of cardiopulmonary bypass and improve cardiac function with good short-term effects. This method may be a good choice for treating patients with IMR.
