Pulmonary contusion induces alveolar type 2 epithelial cell apoptosis: role of alveolar macrophages and neutrophils

Alveolar type 2 (AT-2) cell apoptosis is an important mechanism during lung inflammation, lung injury, and regeneration. Blunt chest trauma has been shown to activate inflammatory cells such as alveolar macrophages (AMs) or neutrophils (polymorphonuclear granulocytes [PMNs]), resulting in an inflammatory response. The present study was performed to determine the capacity of different components/cells of the alveolar compartment (AMs, PMNs, or bronchoalveolar lavage [BAL] fluids) to induce apoptosis in AT-2 cells following blunt chest trauma. To study this, male Sprague-Dawley rats were subjected to either sham procedure or blunt chest trauma induced by a single blast wave. Various time points after injury (6 h to 7 d), the lungs were analyzed by immunohistochemistry, for AT-2 cells, or with antibodies directed against caspase 3, caspase 8, Fas, Fas ligand (FasL), BAX, and BCL-2. Bronchoalveolar lavage concentrations of TNF-alpha, IL-1beta, and soluble FasL were determined by enzyme-linked immunosorbent assay. Furthermore, cultures of AT-2 cells isolated from healthy rats were incubated with supernatants of AMs, PMNs, or BAL fluids obtained from either trauma or sham-operated animals in the presence or absence of oxidative stress. Annexin V staining or TUNEL (terminal deoxynucleotidyl transferase) assay was used to detect apoptotic AT-2 cells. Histological evaluation revealed that the total number of AT-2 cells was significantly reduced at 48 h following trauma. Fas, FasL, active caspase 8, and active caspase 3 were markedly up-regulated in AT-2 cells after chest trauma. BAX and BCL-2 did not show any significant changes between sham and trauma. IL-1beta, but not TNF-alpha, levels were markedly increased at 24 h after the injury, and soluble FasL concentrations were significantly enhanced at 6, 12, 24, and 48 h after the insult. Apoptosis of AT-2 cells incubated with supernatants from cultured AMs, isolated at 48 h following chest trauma was markedly increased when compared with shams. In contrast, no apoptosis was induced in AT-2 cells incubated with supernatants of activated PMNs or BAL fluids of traumatized animals. In summary, blunt chest trauma induced apoptosis in AT-2 cells, possibly involving the extrinsic death receptor pathway. Furthermore, mediators released by AMs appeared to be involved in the induction of AT-2 cell apoptosis.     

川芎嗪干预钝性肺挫伤急性期大鼠肺组织细胞的凋亡

背景：急性胸部撞击后所致的肺挫伤（钝性肺挫伤）常引起呼吸功能异常和继发性炎性反应,并参与全身炎性反应综合征和多器官功能障碍综合征,其发病原因及致病机制亟待明确。目的：观察胸部撞击所致钝性肺挫伤急性期细胞凋亡的变化及其川芎嗪对其的影响。方法：健康雄性SD大鼠随机分为正常对照组、模型组、川芎嗪治疗组,后两组制备胸部撞击伤模型,川芎嗪治疗组建模后立即腹腔注射川芎嗪80mg／kg1次。在创伤发生后1,2,3h观察肺组织病理形态学及细胞凋亡的改变、检测肺水肿程度和肺血管通透性改变,免疫组织化学检测肺组织Bcl-2、Bax和Caspase-3的表达及血液中肿瘤坏死因子α水平变化。结果与结论：模型组肿瘤坏死因子α水平在创伤后1h即显著增加,创伤后2h及3h间急剧增加（P〈0．05）;创伤后2h及3h肺组织细胞凋亡指数及肺组织损伤程度显著增高（均P〈0．05）;肺血管通透性及肺水肿程度增加（P〈0．05）;Caspase-3表达显著增高（P〈0．05）,Bcl-2／Bax比值显著降低（P〈0．05）。川芎嗪治疗组在相应时间点相对于模型组肿瘤坏死因子α水平显著降低（P〈0．05）,肺组织内细胞凋亡指数及肺组织损伤程度降低（P〈0．05）,肺血管通透性及肺水肿程度减轻（P〈0．05）;Caspase-3表达下降（P〈0．05）,Bcl-2／Bax比值增加（P〈0．01）。结果提示,川芎嗪可通过抑制肿瘤坏死因子CI表达,下调Caspase-3的表达并提高Bcl-2／Bax的比值,以降低胸部撞击所致肺组织急性期的异常凋亡并减轻胸部撞击所致急性期肺挫伤。     

Role of phagocytosis in the activation of macrophages

Macrophages were obtained by peritoneal lavage from untreated mice or from mice which had received either Brewer's thioglycollate broth or a suspension of streptococcus A cell walls intraperitoneally 4 days before. 3 h after harvesting, adherent cells from untreated mice were allowed to phagocytose zymosan, formaldehyde-treated sheep erythrocytes, or latex beads. Phagocytosis was stopped after 1 h and culture was continued for up to 10 days. Phagocytosis of zymosan or sheep erythrocytes triggered the immediate release of lysosomal glycosidases, stimulated the synthesis of cellular lactate dehydrogenase, and induced the delayed production and secretion of plasminogen activator . No such changes were observed upon phagocytosis of latex. Although all three particles used were phagocytosed, only zymosan and sheep erythrocytes stimulated glucose oxidation via the hexose monophosphate shunt. Similar findings were obtained in macrophages elicited with streptococcus A cell walls after zymosan phagocytosis. Thioglycollate-elicited macrophages, however, which were already secreting lysosomal hydrolases and plasminogen activator, could not be activated further by zymosan. The results of this study show that macrophages become activated after phagocytosis of particles that stimulate the activity of their hexose monophosphate shunt. The triggering event appears to be the burst of shunt activity itself or shunt-related biochemical reactions rather than phagocytic uptake per se or particle-dependent complement activation by the alternative pathway. Once initiated, macrophage activation proceeds independently of the intracellular fate of the ingested material .     

Blunt chest trauma induces delayed splenic immunosuppression

Severe blunt chest trauma is frequently associated with multiple organ failure and sepsis. Posttraumatic immunosuppression seems to play a major role in their development. However, the immunologic alterations following pulmonary contusion are insufficiently elucidated. Specifically, it remains unknown whether immunocompetent cells located distant from the site of the impact are affected. We therefore aimed to characterize the influence of pulmonary contusion on lymphocytes and splenic macrophages. Male C3H/HeN mice (n = 8-10/group) were anesthetized and subjected to trauma or sham procedure. Blunt chest trauma was induced by a blast wave focused on the thorax. Two or 24 h later, splenocytes and splenic macrophages were isolated and stimulated for 48 h. The cytokine release (IFN-gamma, IL-2, IL-3, IL-10, IL-12, IL-18) from splenocytes as well as from splenic macrophages (TNF-alpha, IL-10, IL-12, IL-18) and plasma levels of TNF-alpha and IL-6 were quantified by ELISA. The results indicate that at 2 h after blunt chest trauma, plasma TNF-alpha and IL-6 were markedly increased. At the same time, no differences in splenocyte cytokine production were detectable. However, at 24 h a significantly depressed cytokine release was observed in trauma animals. Furthermore, splenic macrophages showed a significantly decreased production of TNF-alpha, IL-10, and IL-12 at 24 h and markedly increased release of IL-18 at 2 h after trauma. These results indicate that blunt chest trauma causes severe immunodysfunction of lymphocytes and splenic macrophages. Thus, lung contusion as a localized type of trauma causes dysfunction of immunocompetent cell populations, which are located distant from the site of injury.     

Pulmonary contusion causes impairment of macrophage and lymphocyte immune functions and increases mortality associated with a subsequent septic challenge

OBJECTIVE AND DESIGN: Pulmonary contusion is frequently followed by acute respiratory distress syndrome, pneumonia, and sepsis. However, immunologic alterations of circulating and resident immune cell populations contributing to the posttraumatic immunosuppression are poorly understood. We therefore characterized the influence of pulmonary contusion on peripheral blood mononuclear cells, peritoneal macrophages, splenocytes, and splenic macrophages. To address the significance of the immunosuppression associated with lung contusion, we investigated how the consecutive addition of moderate or severe sepsis affected survival after blunt chest trauma. SUBJECTS: Male C3H/HeN mice (n = 10 per group) were anesthetized and subjected to chest trauma or sham procedure. MEASUREMENTS: The cytokine release of cultured peripheral blood mononuclear cells, peritoneal macrophages, splenocytes, and splenic macrophages and plasma levels of tumor necrosis factor-alpha and interleukin-6 from those animals were quantified. Sepsis was induced via cecal ligation and puncture 24 hrs after lung contusion. MAIN RESULTS: Two hours after blunt chest trauma, plasma tumor necrosis factor-alpha and interleukin-6 were markedly increased, as was peripheral blood mononuclear cell cytokine production, lung myeloperoxidase activity, and lung chemokine concentrations. At 24 hrs and, in part, already at 2 hrs, cytokine release from peritoneal macrophages, splenic macrophages, and splenocytes was significantly suppressed. Furthermore, pulmonary contusion when followed by moderate sepsis significantly diminished survival rate when compared with chest trauma or moderate sepsis alone. CONCLUSIONS: These results indicate that pulmonary contusion causes severe immunodysfunction of splenocytes, macrophages, and monocytes in different local compartments and systemically. Moreover, this immunosuppression is associated with an increased susceptibility to infectious complications, which results in a decreased survival rate if blunt chest trauma is followed by a septic insult.     

Induction of apoptosis following blunt chest trauma

The cause for the high morbidity of blunt chest trauma is not fully understood. It is still unclear if and to what extent a second insult, e.g., apoptotic tissue damage initiated by the primary insult itself, may contribute to the development of serious complications. This study was done to elucidate whether a pulmonary contusion may induce programmed cell death. Sixty-four Wistar rats were evenly randomized to eight experimental groups: four sets were subjected to a standardized blast wave injury and sacrificed 6, 24, 48, and 72 h after the trauma; four groups served as controls for the same time points. Lung and liver samples were stained (H & E; TUNEL), and PMN infiltration was determined by myeloperoxidase (MPO) activity. Caspase 8 was analyzed by Western blot, and TNF-alpha plasma levels by ELISA. Postmortem examination revealed bilateral pulmonary contusion in trauma animals with higher (P < 0.05) numbers of apoptotic cells in lung but not in liver tissue as early as 6 h after the injury. This amount gradually increased and reached a maximum after 48 h: 6.8 +/- 1.1 apoptotic cells/hpf vs. 0.6 +/- 0.06 in controls. Chest trauma caused an increased expression of active caspase 8 in lung but not in liver tissue at 48 and 72 h. TNF-alpha plasma levels were not different. MPO activity in lung tissue of trauma animals increased (P < 0.05) after 6 h and peaked at 72 h. This study has provided the first evidence that apoptotic cell death in lung tissue is initiated following (experimental) pulmonary contusion. The exact mechanism remains, however, unclear and has to be elucidated further.     

Phagocytic capacity and apoptosis of peripheral blood cells from patients with iron deficiency anemia.

Following clinical observations that patients with iron deficiency anemia (IDA) are more susceptible to infections than non-anemic individuals, the phagocytic capacity and number of apoptotic peripheral white blood cells (PWBC) from patients with IDA were examined. PWBC from 15 patients with IDA and from 18 healthy donors were incubated with various doses of iron. Phagocytosis was examined using latex particles and apoptosis was evaluated by a flow cytometric assay using propidium iodide staining. The percentage of phagocyting polymorphonuclear cells was lower in IDA patients compared to that of the controls. However, there was no difference in the percentage of phagocyting monocytes from individuals of both groups. The number of latex beads engulfed by each polymorphonuclear or monocyte was lower in IDA patients. Incubation with 100 microg% of iron did not affect the phagocytic ability of both cell types in IDA patients, but increased that of control cells. Incubation with 300 microg% of iron caused an increase in the phagocytic capacity of patients' cells and a decrease in that function in cells from controls. Higher dose (500 microg%) induced suppression of phagocytosis in cells from both groups. There was no difference in the number of apoptotic cells from individuals of both groups. Apoptosis of polymorphonuclears, but not mononuclear cells from both controls and IDA patients showed a linear dependency on the iron concentration in the medium. It is possible that the impaired phagocytic capacity of the PBWC found in patients with IDA contribute to the increased susceptibility to infections observed in these individuals.     

Complete Atrioventricular Block Associated with Non-penetrating Cardiac Trauma in a 40-year-old Man

Background

Myocardial contusion is a rare complication of blunt chest trauma. Transient conduction and rhythm problems, right ventricular dysfunction, or pulmonary embolism may occur after chest trauma, but these complications almost always occur early in the post-operative period.

Objectives

The objective is to describe a case illustrating that trauma may induce high-grade atrioventricular block.

Case Report

We report the case of a patient who developed delayed onset of complete atrioventricular block after transient complete atrioventricular block and alternating bundle branch block secondary to blunt chest trauma.

Conclusion

Even with an injury that does not seem to be caused by direct penetrating trauma to the heart, maybe every trauma patient needs an electrocardiographic evaluation. It is important to note that myocardial healing is a continuous process after trauma, and additional pathology may be revealed later in the course of healing from myocardial contusion.     

Inhaled hydrogen sulfide induces suspended animation, but does not alter the inflammatory response after blunt chest trauma

The treatment of acute lung injury and septic complications after blunt chest trauma remains a challenge. Inhaled hydrogen sulfide (H?S) may cause a hibernation-like metabolic state, which refers to an attenuated systemic inflammatory response. Therefore, we tested the hypothesis that inhaled H?S-induced suspended animation may attenuate the inflammation after pulmonary contusion. Male Sprague-Dawley rats were subjected to blunt chest trauma (blast wave) or sham procedure and subsequently exposed to a continuous flow of H?S (100 ppm) or control gas for 6 h. Body temperature and activity were measured by an implanted transmitter. At 6, 24, or 48 h after trauma, animals were killed, and the cellular contents of bronchoalveolar lavage (BAL) as well as cytokine concentrations in BAL, plasma, and culture supernatants of blood mononuclear cells, Kupffer cells, splenic macrophages, and splenocytes were determined. Hydrogen sulfide inhalation caused a significant reduction in body temperature and activity. The trauma-induced increase in alveolar macrophage counts was abrogated 48 h after trauma when animals received H?S, whereas the trauma-induced increase in neutrophil counts was unaltered. Furthermore, H?S inhalation partially attenuated the mediator release in BAL and culture supernatants of Kupffer cells as well as splenic cells; it altered plasma cytokine concentrations but did not affect the trauma-induced changes in mononuclear cell culture supernatants. These findings indicate that inhaled H?S induced a reduced metabolic expenditure and partially attenuated inflammation after trauma. Nevertheless, in contrast to hypoxic- or pathogen-induced lung injury, H?S treatment appears to have no protective effect after blunt chest trauma.     

Value of a conventional approach to the diagnosis of traumatic cardiac contusion after chest injury

We wanted to evaluate whether current screening techniques effectively determine a patient's need for hospital admission and intensive care monitoring after blunt chest trauma. Consequently, we reviewed 104 consecutive admissions for "blunt chest trauma; rule out cardiac contusion." Neither clinical findings, cardiac enzyme levels, chest x-rays, nor ECGs predicted the high-risk patients who would subsequently develop complications related to myocardial contusion. Since only 23% of the study patients developed such complications, the plurality of study patients did not require admission and monitoring. There is, therefore, a definite need to develop new, accurate screening tests for patients at risk for myocardial contusion complications.     

Effect of human polymorphonuclear and mononuclear leukocytes on chromosomal and plasmid DNA of Escherichia coli. Role of acid DNase

Phagocytosis and killing by polymorphonuclear and mononuclear leukocytes are important host resistance factors against invading microorganisms. Evidence showing that killing is rapidly followed by degradation of bacterial components is limited. Therefore, we studied the fate of Escherichia coli DNA following phagocytosis of E. coli by polymorphonuclear and mononuclear leukocytes. [3H]thymidine-labeled, unencapsulated E. coli PC2166 and E. coli 048K1 were incubated in serum, washed, and added to leukocytes. Uptake and killing of the bacteria and degradation of DNA were measured. Although phagocytosis and killing by mononuclear leukocytes was less efficient than that by polymorphonuclear leukocytes, only mononuclear leukocytes were able to degrade E. coli PC2166 DNA. Within 2 h, 60% of the radioactivity added to mononuclear leukocytes was released into the supernate, of which 40% was acid soluble. DNA of E. coli 048K1 was not degraded. To further analyze the capacity of mononuclear leukocytes to degrade E. coli DNA, chromosomal and plasmid DNA was isolated from ingested bacteria and subjected to agarose gel-electrophoresis. Only chromosomal DNA was degraded after phagocytosis. Plasmid DNA of E. coli carrying a gene coding for ampicillin resistance remained intact for a 2-h period after ingestion, and was still able to transform recipient E. coli cells after this period. Although we observed no DNA degradation during phagocytosis by polymorphonuclear leukocytes, lysates of both polymorphonuclear and mononuclear leukocytes contained acid-DNase activity with a pH optimum of 4.9. However, the DNase activity of mononuclear leukocytes was 20 times higher than that of polymorphonuclear leukocytes. No difference was observed between DNase activity from polymorphonuclear and mononuclear leukocytes from a chronic granulomatous disease patient with DNase activity from control polymorphonuclear and mononuclear leukocytes.     

Electrocardiographic ST-segment elevation in the trauma patient: acute myocardial infarction vs myocardial contusion

The diagnosis of myocardial contusion in the setting of blunt trauma engenders much discussion and controversy-partly because of the lack of a gold standard for its identification other than histologic findings at autopsy. Furthermore, blunt cardiac trauma represents a spectrum of disorders ranging from transient electrocardiographic change to sudden death from myocardial rupture; hence, no single terminology exists to define such a wide range of scenarios. Here, we present 2 cases of electrocardiographic ST-segment elevation after high-speed motor vehicle crashes resulting in numerous injuries, including blunt chest trauma. Both patients demonstrated electrocardiographic ST-segment elevation, resulting from myocardial contusion and acute myocardial infarction.     

Mononuclear cells phagocytic activity affects the crosstalk between immune and cancer cells

The “professional phagocytes”, i.e. monocytes and macrophages, play an important role as eliminators of pathogens and as essential components of the immune system. It is well established that monocytes induced for phagocytosis by various stimulators, produce cytokines that are closely related to inflammation. Considering the role of inflammation in carcinogenesis and the existence of an immune dialog between mononuclear and cancer cells, the aim of the present work was to examine cytokine production by immune cells stimulated for phagocytosis by latex particles and incubated with cells from HT-29 and RKO human cancer lines. Human peripheral blood mononuclear cells (PBMC) were incubated with various numbers of polysterene latex beads, 0.8 μm in diameter and the secretion of the following cytokines: TNF-α, IL-1β and IL-6, IL-10 and IL-1ra was examined before and after further incubation with cells of the both cancer lines. Phagocytosis of latex beads by PBMC caused an increased production of TNF-α, IL-1β and IL-10, whereas that of IL-6 declined. PBMC activated by latex beads and co-cultured with cancer cells generated lesser amount of the three pro-inflammatory cytokines TNF-α, IL-1β and IL-6, while that of the anti-inflammatory IL-10 and IL-1ra remained unchanged. The results indicate that phagocytosis of polystyrene latex beads by human PBMC alters the dialogue between immune and cells of human colon carcinoma lines, an observation that may clarify the role of the immune cells in attenuating inflammation and restraining carcinogenesis.     

Late cardiac arrhythmias after blunt chest trauma

Objective: Case reports of two patients who developed fatal cardiac arrhythmias several days after blunt chest trauma.¶Design: Case reports.¶Setting: Surgical intensive care unit of a university hospital.¶Patients: A 23-year-old man and a 9-year-old girl with blunt chest trauma and multiple further injuries following car crashes were transferred to our institution. Although ECG on admission was normal, both patients developed fatal cardiac arrhythmias after 6 and 4 days, respectively. In both patients, post-mortem analysis confirmed myocardial contusion without coronary artery lesions. Histological findings included severe interstitial oedema, haemorrhages and infiltration of lymphocytes and neutrophils, fresh myocardial necrosis and fatty degeneration.¶Conclusion: Blunt chest trauma with myocardial contusion may lead to fatal cardiac arrhythmias even after several days, particularly when other severe injuries are present. Thus, a normal ECG on admission and absence of cardiac arrhythmias during the first 24 h of intensive care treatment do not necessarily exclude the occurrence of life-threatening arrhythmias in the further course.     

Cardiac contusion following blunt chest trauma.

Cardiac contusion following blunt chest trauma is not rare, and the works in the literature report incidence rates between 5 and 50%. Traffic accidents are the most frequent cause of cardiac contusion followed by violent fall impacts, aggressions and the practice of risky sports. The spectrum of post-traumatic cardiac lesions varies greatly, ranging from no symptoms to decrease in cardiac function. Cardiogenic shock is a rarely encountered manifestation of blunt cardiac contusion. We review our experience of cardiac contusion after blunt chest trauma, and we describe two very severe cases that manifested as cardiogenic shock. We emphasize an early diagnosis by continuous electrocardiographic monitoring, serial electrocardiograms, echocardiography, serum determination of biochemical cardiac markers, radionuclide imaging and coronary angiography. The treatment includes continuous monitoring of cardiac rhythm, use of inotropic drugs, insertion of a catheter in the pulmonary artery for continuous assessment of cardiac output and, in extreme cases, the insertion of a contrapulsation balloon to maintain haemodynamics until improvement of cardiac function.     

Role of activated neutrophils in chest trauma-induced septic acute lung injury

More than 50% of severely injured patients have chest trauma. Second insults frequently result in acute lung injury (ALI), with sepsis being the main underlying condition. We aimed to develop a standardized, reproducible, and clinically relevant double-hit mouse model of ALI induced by chest trauma and polymicrobial sepsis and to investigate the pathophysiologic role of activated neutrophils. Lung contusion was applied to C57Bl/6 mice via a focused blast wave. Twenty-four hours later, sepsis was induced by cecal ligation and puncture. For polymorphonuclear leukocyte (PMN) depletion, animals received intravenous injections of PMN-depleting antibody. In response to blunt chest trauma followed by sepsis as well as after sepsis alone, a significant local and systemic inflammatory response with increased cytokine/chemokine levels in lung and plasma was observed. In contrast, lung apoptosis was markedly elevated only after a double hit. Intra-alveolar neutrophils and total bronchoalveolar lavage protein concentrations were markedly increased following isolated chest trauma or the combined insult, but not after sepsis alone. Lung myeloperoxidase activity was enhanced only in response to the double hit accompanied by histological disruption of the alveolar architecture, lung congestion, and marked cellular infiltrates. Neutrophil depletion significantly diminished lung interleukin 1β and interleukin 6 concentrations and reduced the degree of septic ALI. Here we have established a novel and highly reproducible mouse model of chest trauma-induced septic ALI characterizing a clinical relevant double-hit scenario. In particular, the depletion of neutrophils substantially mitigated the extent of lung injury, indicating a pathomechanistic role for neutrophils in chest trauma-induced septic ALI.     

Cardiopulmonary,histological, and inflammatory alterations after lung contusion in a novel mouse model of blunt chest trauma

Severe blunt chest trauma remains an important injury with high morbidity and mortality. However, the associated immunological alterations are poorly understood. Existing big animal models require large-scale settings, are often too expensive, and research products for immunological studies are limited. In this study we aimed to establish a new model of blunt, isolated and bilateral chest trauma in mice and to characterize its effects on physiological and inflammatory variables. Male C3H/HeN mice (n = 9-10/group) were anesthetized and a femoral artery was catheterized. The animals were subjected to trauma or sham procedure and monitored for 180 min. Blunt chest trauma was induced by a blast wave focused on the thorax. Trauma intensity was optimized by varying the exposure distance. Blood pressure, heart rate, respiratory rate, arterial blood gases and plasma cytokine levels were measured. Macroscopic and microscopic examinations were performed. In addition, outcome was evaluated in a 10-day survival study. Chest trauma caused a drop (P < 0.05) in blood pressure and heart rate, which partly recovered. Blood gases revealed hypoxemia and hypercarbia (P < 0.05) 180 min after trauma. There was marked damage to the lungs but none to abdominal organs. Histologically, the characteristic signs of a bilateral lung contusion with alveolar and intrabronchial hemorrhage were found. Plasma interleukin-6 and tumor necrosis factor alpha were considerably increased after 180 min. Blunt chest trauma resulted in an early mortality of 10% without subsequent death. On the basis of these findings, this novel mouse model of blunt chest trauma appears suitable for detailed studies on immunological effects of lung contusion.     

The evolution of isolated bilateral lung contusion from blunt chest trauma in rats: cellular and cytokine responses

Lung contusion is the leading cause of death from blunt thoracic trauma in adults, but its mechanistic pathophysiology remains unclear. This study uses a recently developed rat model to investigate the evolution of inflammation and injury in isolated lung contusion. Bilateral lung contusion with minimal cardiac trauma was induced in 54 anesthetized rats by dropping a 0.3-kg hollow cylindrical weight onto a precordial shield (impact energy, 2.45 Joules). Arterial oxygenation, pressure-volume (P-V) mechanics, histology, and levels of erythrocytes, leukocytes, albumin, and inflammatory mediators in bronchoalveolar lavage (BAL) were assessed at 8 min, at 4, 12, 24, and 48 h, and at 7 days after injury. The role of neutrophils in the evolution of inflammatory injury was also specifically studied by depleting these cells with intravenous vinblastine before lung contusion. Arterial oxygenation was severely reduced at 8 min to 24 h postcontusion, but became almost normal by 48 h. Levels of erythrocytes, leukocytes, and albumin in BAL were increased at 相似文献   

Unusual cardiac injury following blunt chest trauma.

Cardiac injury following blunt chest trauma is known to occur, but traumatic rupture of ventricular septum is a rare injury, especially following blunt chest trauma. A case of a 20-year-old male is presented who fell on his back from a 9th-floor window and was resuscitated for 3 hours to no avail. Post-mortem examination confirmed a fracture of the pelvis, pulmonary contusion and rupture of ventricular septum of the heart.