Pericardial tamponade after removal of an epicardial pacemaker wire

Pericardial tamponade may arise from multiple traumatic and nontraumatic etiologies, resulting in unrecognized rapid deterioration and often death. A previously unreported case of pericardial tamponade after removal of an epicardial pacemaker wire is presented, demonstrating the everpresent potential for serious complications from seemingly innocuous invasive procedures.     

Oxygen free radicals in ischemic acute renal failure in the rat.

During renal ischemia, ATP is degraded to hypoxanthine. When xanthine oxidase converts hypoxanthine to xanthine in the presence of molecular oxygen, superoxide radical (O-2) is generated. We studied the role of O-2 and its reduction product OH X in mediating renal injury after ischemia. Male Sprague-Dawley rats underwent right nephrectomy followed by 60 min of occlusion of the left renal artery. The O-2 scavenger superoxide dismutase (SOD) was given 8 min before clamping and before release of the renal artery clamp. Control rats received 5% dextrose instead. Plasma creatinine was lower in SOD treated rats: 1.5, 1.0, and 0.8 mg/dl vs. 2.5, 2.5, and 2.1 mg/dl at 24, 48, and 72 h postischemia. 24 h after ischemia inulin clearance was higher in SOD treated rats than in controls (399 vs. 185 microliter/min). Renal blood flow, measured after ischemia plus 15 min of reflow, was also greater in SOD treated than in control rats. Furthermore, tubular injury, judged histologically in perfusion fixed specimens, was less in SOD treated rats. Rats given SOD inactivated by prior incubation with diethyldithiocarbamate had plasma creatinine values no different from those of control rats. The OH X scavenger dimethylthiourea (DMTU) was given before renal artery occlusion. DMTU treated rats had lower plasma creatinine than did controls: 1.7, 1.7, and 1.3 mg/dl vs. 3.2, 2.2, and 2.4 mg/dl at 24, 48, and 72 h postischemia. Neither SOD nor DMTU caused an increase in renal blood flow, urine flow rate, or solute excretion in normal rats. The xanthine oxidase inhibitor allopurinol was given before ischemia to prevent the generation of oxygen free radicals. Plasma creatinine was lower in allopurinol treated rats: 2.7, 2.2, and 1.4 mg/dl vs. 3.6, 3.5, and 2.3 mg/dl at 24, 48, and 72 h postischemia. Catalase treatment did not protect against renal ischemia, perhaps because its large size limits glomerular filtration and access to the tubular lumen. Superoxide-mediated lipid peroxidation was studied after renal ischemia. 60 min of ischemia did not increase the renal content of the lipid peroxide malondialdehyde, whereas ischemia plus 15 min reflow resulted in a large increase in kidney lipid peroxides. Treatment with SOD before renal ischemia prevented the reflow-induced increase in lipid peroxidation in renal cortical mitochondria but not in crude cortical homogenates. In summary, the oxygen free radical scavengers SOD and DMTU, and allopurinol, which inhibits free radical generation, protected renal function after ischemia. Reperfusion after ischemia resulted in lipid peroxidation; SOD decreased lipid peroxidation in cortical mitochondria after renal ischemia and reflow. We concluded that restoration of oxygen supply to ischemic kidney results in the production of oxygen free radicals, which causes renal injury by lipid peroxidation.     

Extensor tendon repair in the emergency department

Extensor tendon lacerations of the hand are commonly seen in the emergency department. These injuries can often be definitively managed by the emergency physician who has a working knowledge of the complex extensor mechanism anatomy plus basic surgical skills. A thorough initial assessment including a tourniquet examination for adequate exposure is the key to making the complete diagnosis. Surgical indications, materials, techniques, complications, and postoperative management involved in extensor tendon repair are reviewed. The emergency physician's decision to treat or refer these injuries will depend greatly on the clinical setting, familiarity with the procedure, and the availability of and relationship with appropriate consultants.     

Elastolytic activity in the lungs of rats exposed to cadmium aerosolization

Rats were exposed for 1 hr per day for up to 35 days to an aerosol of 0.1% cadmium chloride. At periodic intervals, animals were sacrificed and their lungs lavaged. The lung lavage fluid was examined for polymorphonuclear leukocytes (PMN) and alveolar macrophages (AM). A portion of the cells of the lavage fluid was lysed, and the remainder of the cells were cultured. The lavage fluids, cell lysates, and conditioned media were assayed for elastolytic activity in the presence and absence of a peptide chloromethyl ketone and EDTA. Exposure to cadmium evoked a biphasic cellular response characterized by an initial influx (1–3 days) of PMN followed by a gradual increase in AM. This biphasic cellular response was accompanied by a shift in the type of elastolytic activity which was present in the lung lavage and its cellular components. The initial PMN phase was accompanied by the enhanced production of an elastase inhibited only by the peptide chloromethyl ketone, while the subsequent AM phase was associated with an elastase activity which was inhibited only by EDTA. The possible implication of these results with respect to the pathogenesis of emphysema is considered.     

Granulomatous pneumonitis following bone marrow transplantation

We describe the rare occurrence of a granulomatous pneumonitis seen in a patient following allogeneic bone marrow transplantation. Interestingly sarcoidosis was diagnosed in the marrow donor less than a year after donating his bone marrow.     

Role of a novel KCa opener in regulating K+ channels of hypoxic human pulmonary vascular cells

Hypoxic pulmonary vasoconstriction (HPVC) is mediated, in part, via membrane depolarization and inhibition of K+ channels. We recently observed that the naturally occurring steroid dehydroepiandrosterone (DHEA) reversed and prevented HPVC in isolated perfused and ventilated ferret lungs. In the current study, we investigated the effects of DHEA on the major K+ channels of chronically hypoxic human pulmonary smooth-muscle cells (HPSMC). K+ channels were recorded by using the patch-clamp technique in whole-cell and single-channel configurations. Single-channel recordings were performed in inside-out and outside-out excised patches, and in intact HPSMC in cell-attached configuration. Using whole-cell current recording, chronic hypoxia decreased the high-amplitude, high-noise, and charybdotoxin-sensitive Ca2+-dependent K+ channels (KCa). DHEA reversed the effect of chronic hypoxia on KCa, but had no effect on the low-amplitude, low-noise, and 4-aminopyridine-sensitive delayed rectifying K+ channels. In the cell-attached configuration, chronic hypoxia caused a decrease in KCa sensitivity to membrane potential (Em). DHEA reversed the effect of hypoxia on KCa sensitivity to Em and caused a mean of 40-mV left shift in voltage-dependent activation of KCa. DHEA increased KCa activation from both sides of membrane patches of hypoxic HPSMC via a cyclic adenosine monophosphate- and cyclic guanosine monophosphate-independent pathway. We concluded that DHEA is a novel KCa opener of the human pulmonary vasculature.     

Differences in phagocytosis and killing by alveolar macrophages from humans, rabbits, rats, and hamsters.

Phagocytosis and killing by alveolar macrophages from humans, rabbits, rats, and hamsters, were compared in vitro. In the absence of serum opsonins, human alveolar macrophages could phagocytize Staphylococcus aureus Cowan I (protein A positive), but not S. aureus EMS (protein A negative) or Pseudomonas aeruginosa MN. In contrast, rabbit, rat, and hamster alveolar macrophages did not phagocytize S. aureus Cowan I or other nonopsonized bacteria. Human alveolar macrophages, but not other species, stained positively with fluorescein isothiocyanate-conjugated protein A. When opsonized bacterial were studied, phagocytosis by human, rabbit, and hamster alveolar macrophages was found to be mediated by both Fc and C3 receptors. However, only Fc receptor-mediated phagocytosis of bacteria was demonstrated for rat alveolar macrophages. Differences were also found in the kinetics of bacterial killing by alveolar macrophages from different species. Human and rabbit alveolar macrophages rapidly killed opsonized S. aureus Cowan I. However, bacterial killing by hamster alveolar macrophages proceeded at a slower rate, and rat alveolar macrophages completely failed to kill S. aureus. These significant differences in the function of alveolar macrophages from four different species emphasize the need to document the appropriateness of animal models before using them to predict the biological activities of human alveolar macrophages.     

单核细胞向巨噬细胞分化过程中CD44 mRNA表达和黏附功能的变化

目的 探讨单核细胞向巨噬细胞分化过程中CD44 mRNA表达和黏附功能的变化.方法 应用豆蔻佛波醇乙酯(PMA)诱导单核细胞系U937向巨噬细胞分化;应用RT-PCR分析U937细胞CD44 mRNA表达变化,并以β-actin作为内参进行半定量评价,并对主要条带进行测序;应用荧光染料BCECF/AM作为探针,测定黏附于激活的内皮细胞上的U937细胞数目.结果 与对照组比较,PMA诱导的U937细胞CD44 mRNA总体表达显著增加(P=0.01037),异构体/标准CD44比例显著上升(P=0.0005551),测序结果显示PMA刺激后显著增加的是947 bp(V8+V9+V10)和1 208 bp(V7+V8+V9+V10)CD44异构体.同时.PMA刺激后U937细胞黏附功能显著增加(P=0.0029).结论 单核细胞向巨噬细胞分化过程中CD44 mRNA,特别是947bp(V8+V9+V10)和1 208 bp(V7+V8+V9+V10)CD44异构体的表达显著增加,可能与细胞黏附功能的增强相关.     

Alterations in leukocyte oxidative metabolism in cigarette smokers

The polymorphonuclear leukocyte (PMN) may play an important role in the pathogenesis of lung disease associated with cigarette smoking. To investigate its potential for oxidant-mediated lung injury in cigarette smokers, we studied PMN oxidative metabolism in asymptomatic cigarette smokers and nonsmoking control subjects. We found a marked increase in oxidant release in a group of cigarette smokers. After stimulation by phorbol myristate acetate, release of superoxide anion (O-2) by PMN in smokers with white blood counts (WBC) greater than 9,000 was 50% greater than in nonsmokers with similar WBC or smokers and nonsmokers with WBC less than 9,000. Abstinence from smoking did not affect the alterations in O-2 release nor did a serum factor appear responsible. The changes appeared to be part of a generalized increase in oxidative metabolism, as there was greater oxidation of glucose (1-14C) and chemiluminescence by PMN from smokers with WBC greater than 9,000. A further estimate of lung oxidant load was determined by evaluating the marginated pool of PMN. Smokers with WBC greater than 9,000 showed a 70% increase in WBC after epinephrine, and PMN oxidative metabolism remained increased in this group. This study demonstrates that cigarette smokers with elevated WBC have increased release of potentially toxic oxygen metabolites. These cigarette smokers also demonstrated increased oxidant release from the marginated PMN pool. Because leukocyte-generated oxygen metabolites are highly reactive and can cause tissue injury, these findings may have important implications in the pathogenesis of smoking-related lung disease.     

Cellularity of the alveolar walls in smokers and its relation to alveolar destruction. Functional implications

Inflammatory cells are believed to play an important role in the pathogenesis of emphysema; however, a relationship between presence of cells in the lung parenchyma and its destruction has never been shown. The aim of this study was to quantitate alveolar septal cellularity in smokers' lungs and to investigate its relationship with parenchymal destruction and lung function. The lungs of 23 smokers (SS) undergoing thoracotomy for localized pulmonary lesions were compared with those of eight nonsmokers (NS) and five smokers (AS) who died suddenly of nonrespiratory causes. Pulmonary function tests were performed within 1 wk of surgery in SS. For each subject, we quantitated alveolar wall cells (CELLS), an index of alveolar wall destruction (DI), and the mean linear intercept (Lm). As no significant differences were found between S and AS with regard to these indices, we combined them (Group S) for comparison with NS. Although Lm was not significantly different between S and NS, (0.331 +/- 0.072 versus 0.288 +/- 0.038), CELLS and DI were higher in S than in NS (48 +/- 8 versus 25 +/- 2 cells/mm, p less than 0.001; 47 +/- 20 versus 17 +/- 5, p less than 0.001, respectively). Further, CELLS and DI were significantly correlated (r = 0.799, p less than 0.001). The number of polymorphonuclear cells (PMN) in S can exceed that in NS by as much as 5-fold; however, PMN were inversely correlated with parenchymal destruction (DI) (r = 0.598, p less than 0.01). Thus, smokers' lungs have alveolar septal hypercellularity, possibly inflammatory, and closely related to destruction involving cells other than the PMN.