An immunohistochemical study of MAP2 and clathrin in gerbil hippocampus after cerebral ischemia

Changes in MAP2 and clathrin immunoreactivity were studied in gerbil hippocampus after transient cerebral ischemia. MAP2 immuno-reactivity decreased significantly by 1 h in the subiculum-CA1 and CA2 areas which correspond to reactive change, while no decrease was observed in CA1 until day 4. Before the initiation of delayed neuronal death, MAP2 immunoreactivity was not changed in CA1. On the other hand clathrin immunoreactivity increased in the pyramidal cell layer of CA1 by 3 h after ischemia and remained high for 2 days. Clathrin immunoreactivity in the pyramidal cell layer of CA1 diminished after delayed neuronal death. The transient change of clathrin was noted especially in CA1 in the period prior to delayed neuronal death. These results imply an abnormal change in clathrin turnover after ischemia, which may participate in the pathogenesis of delayed neuronal death.     

Effect of prostaglandin E1 on graft function of kidneys from living related donors

Prostaglandin E₁ (PGE₁) was used in renal transplant recipients with living related donors. The drug was given intravenously from day 1 to day 7 after transplantation at a dose of 40 µg/kg twice a day. A total of 45 patients were studied divided into two groups: 25 patients were treated with PGE₁ (group B) and the remaining 20 patients did not receive the drug (group A). In group B, 24-h creatinine clearance (Ccr) was 66 ± 12.8 ml/min compared with 40.3 ± 13.4 ml/min in group A on the fifth postoperative day (P < 0.05). Urinary levels of N-acetyl-β-d -glucosaminidase (NAG) and serum levels of platelet factor 4 (PF4) in group B were significantly lower than in group A. On the fourth postoperative day, the urinary excretion of thromboxan B₂ (TxB₂) in group A was higher than in group B, but not significantly (5.1 ± 3.0 ng/day and 2.8 ± 1.1 ng/day, respectively). Acute rejection occurred in four patients in group B and in 10 patients (40%) in group A. The percentage of Leu2a-positive lymphocytes in group B was higher than in group A. We conclude that postoperative administration of PGE₁ improves graft function in kidneys from living related donors.     

Protective effects of serotonin reuptake inhibitors, citalopram and clomipramine, against hippocampal CA1 neuronal damage following transient ischemia in the gerbil

To clarify the role of serotonin in cerebral ischemia, we examined the effects of selective serotonin reuptake inhibitors, citalopram and clomipramine, on ischemic neuronal damage in the gerbil. Pretreatment with citalopram (40 mg/kg i.p.) and clomipramine (20 mg/kg i.p.) protected against neuronal destruction of hippocampal CA1 pyramidal cells following 5 min of forebrain ischemia. Furthermore, microdialysis assays showed that a striking increase in extracellular excitatory amino acid levels during ischemia was significantly inhibited by pretreatment with citalopram and clomipramine. However, citalopram (40 mg/kg i.p.) did not alter the extracellular amino acid concentrations in normal gerbils. Thus, serotonin reuptake inhibitors have a protective effect against ischemic neuronal damage. Furthermore, the present result suggests that the protective effect is mediated through prevention of the accumulation of extracellular excitatory amino acids during and after ischemia.     

Local fibrinolysis for superior mesenteric artery thromboembolism

A 66-year-old man with atrial fibrillation was referred soon after developing left lower limb and abdominal pain with rectal bleeding. An immediate flush aortogram showed embolic occlusion of the left distal superficial femoral artery and superior mesenteric artery (SMA), 3 cm from its ostium. Recombinant tissue plasminogen activitor (rtPA) 40 mg was selectively in stilled in the SMA in two boluses. Abdominal symptoms resolved within 48 h, and complete recanalization of the SMA was shown on angiography. Exploratory laparotomy after 72 h showed a normal small bowel and right colon, and was completed by femoropopliteal embolectomy. Six months later, the patient remained asymptomatic.     

Initial cranial CT scan for the assessment of prognosis in head injury

Summary A total of 208 multiple trauma patients with head injury (HI) were investigated who had been treated in the period from 1990 to 1995. The average age was 35.2 ± 17.7 years; the injury severity according to ISS was 30.2 ± 8.6 points; 20.5 % died as a result of the HI; the mortality of all patients was 26.5 %. The Glasgow Coma Scale (GCS) was determined at an average of 22 min after trauma (8.0 ± 4.3 points) at the scene of accident. The patients were classified according to GCS into minor HI (group 1: 14–15 points), moderate HI (group 2: 9–13 points) and severe HI (group 3: 3–8 points). Patient outcome was assessed by the Glasgow Outcome Scale (GOS) and was classified as good (GOS 4 and 5) and poor (GOS 1, 2 and 3) outcome. At the latest, 2 h after trauma, a CT scan of the head (CCT) was done. The HI groups are compared regarding frequency of types of injury. In all HI groups the fractures of the bony face occurred at the same frequency (36.0–38.9 %). The frequency of calotte fractures (Kal-Fx) increased from group 1 (8.0 %) to 2 (19.2 %) and 3 (25.6 %); fractures of the skull base significantly differed between group 1 (16.0 %), 2 (7.8 %) and 3 (33.4 %). Epidural hemorrhage (EDB) appeared only in group 2 (7.8 %) and 3 (6.7); subdural hemorrhage was found in group 1 (2.7 %), 2 (7.8 %) and 3 (10.0 %). Subarachnoid hemorrhage (SAB) was significantly more frequently seen, dependent on HI severity, in group 3 (26.7 %) compared to group 2 (11.7 %) and 1 (8.0 %). Intracerebral contusion (ICK) significantly increased from group 1 (12.0 %) to 2 (27.3) and 3 (45.6 %). Brain swelling (BS) also significantly increased from group 1 (8.0 %) to 2 (19.5 %) and 3 (49.0 %) and lesions of ventricles (VL) from group 1 (2.7 %) to 2 (11.7 %) and 3 (20.0 %). Midline shift (13.4 %) and signs of herniation (4.5 %) only occurred in group 3. The analysis of correlation/regression and receiver operating characteristics was able to predict 79 % of patients' outcome accurately using GCS (r 0.54; P < 0.0001) alone, using CCT (r 0.65; P < 0.0001) 87 % were correctly predicted with significant variables Cal-Fx, EDB, SAB and BS. CCT with GCS (r 0.74; P < 0.0001) were able to predict 88 % accurately with significant variables Cal-Fx, EDB, BS and GCS. The combination of CCT with GCS, age and ISS (r 0.78; P < 0.0001) was able to predict only 87 % correctly, although the r value was the highest; significant variables were Kal-Fx, EDB, BS, VL, GCS, age and ISS.      

Ulnar distribution of reflex sympathetic dystrophy due to compression of the brachial plexus by a primary venous malformation

An atypical variant of reflex sympathetic dystrophy (RSD) is presented in a 45 year old female with a vascular malformation of the right arm and chest wall. The mechanism was thought to be compression of the brachial plexus by the malformation. The unique scintigraphic features of this presentation of RSD in the ulnar arterial distribution are illustrated.     

Role of group II and group III metabotropic glutamate receptors in spinal cord injury.

Spinal cord injury (SCI) produces an increase in extracellular excitatory amino acid (EAA) concentrations that results in glutamate receptor-mediated excitotoxic events. An important class of these receptors is the metabotropic glutamate receptors (mGluRs). mGluRs can activate a number of intracellular pathways that increase neuronal excitability and modulate neurotransmission. Group I mGluRs are known to modulate EAA release and the development of chronic central pain (CCP) following SCI; however, the role of group II and III mGluRs remains unclear. To begin evaluating group II and III mGluRs in SCI, we administered the specific agonists for group II, APDC, or group III, L-AP4, by interspinal injection immediately following SCI. Contusion injury was produced at spinal segment T10 with a New York University impactor (12.5-mm drop, 10-g rod 2 mm in diameter) in 30 adult male Sprague-Dawley rats (175-200 g). Evoked and spontaneous behavioral measures of CCP, locomotor recovery, changes in mGluR expression, and amount of spared tissue were examined. Neither APDC nor L-AP4 affected locomotor recovery or the development of thermal hyperalgesia; however, L-AP4 and APDC attenuated changes in mechanical thresholds and changes in exploratory behavior indicative of CCP. APDC- and L-AP4-treated groups had higher expression levels of mGluR2/3 at the epicenter of injury on post contusion day 28; however, there was no difference in the amount of spared tissue between treatment groups. These results demonstrate that treatment with agonists to group II and III mGluRs following SCI affects mechanical responses, exploratory behavior, and mGluR2/3 expression without affecting the amount of tissue spared, suggesting that the level of mGluR expression after SCI may modulate nociceptive responses.     

参附注射液对肠缺血-再灌注大鼠肿瘤坏死因子α的影响

目的观察肿瘤坏死因子α(TNF-α)在大鼠肠缺血-再灌注损伤过程中的作用及参附注射液对TNF-α的影响,探讨参附注射液防治肠缺血-再灌注损伤机制。方法 SD大鼠随机分为肠缺血-再灌注组(IR组)、参附注射液预处理组(SF组)和假手术组(C组)。采用阻断肠系膜上动脉(SMA)的方法制造肠缺血-再灌注模型。分别测定各组动物血浆、肠组织TNF-α含量及血液动力学变化;光镜观察肠粘膜损伤情况。结果IR组再灌注后MAP下降,与C组和SF组比有显著性差异(P<0.01);SF组肠粘膜损伤程度减轻,与IR组比有显著性差异(P<0.01);SF组血浆及肠组织TNF-α水平降低,与IR组比有显著性差异(P<0.01)。结论参附注射液可明显防治大鼠肠缺血-再灌注导致的肠粘膜损伤,这种作用可能是通过抑制TNF-α的释放实现的。