[Acute geriatric treatment of older trauma patients : Influence on mobility, autonomy and postdischarge destination]. / Geriatrische Komplexbehandlung bei alterstraumatologischen Patienten : Einfluss auf Mobilität, Selbsthilfefähigkeit und Austrittsdestination.

BACKGROUND: Acute geriatric treatment is a type of early rehabilitation for hospitalized seniors to maintain personal autonomy and to avoid nursing home placement. OBJECTIVE: The aim of the study was to describe the changes of mobility and functional independence of older trauma patients during acute geriatric treatment. MATERIAL AND METHODS: This study analyzed admission and discharge assessment data from 164 patients in the geriatric department with fall-related injuries. Mobility and performance in activities of daily living were assessed using the short physical performance battery (SPPB), gait speed and Barthel index. We analyzed changes in mobility from admission to discharge (t-test) and examined differences in mobility between patients returning home and those admitted to long-term care (age-adjusted and gender-adjusted linear regression model). RESULTS: Patients improved their mobility measured by the SPPB by 1.8 points ±â€¯2.1 points, gait speed by 0.10 ±â€¯0.14 m/s and the Barthel index by 13 ±â€¯16 points, all p < 0.001). The number of patients not able to walk decreased from 43% to 14% (p = 0.003). Of the community-dwelling patients 73% were discharged either directly back home or after rehabilitation outside the hospital as a transitional solution. CONCLUSION: In the context of acute geriatric treatment older trauma patients significantly improved their mobility and performance. The majority of patients could return home.

[Evolution and principles of intramedullary locked nailing]. / Entwicklung und Prinzipien der Verriegelungsmarknagelung.

Key factors for successful osteosynthetic fracture stabilization are anatomical fracture reduction, restoration of axis and torsion alignment as well as tissue-preserving operative techniques. In long bone fractures, the use of intramedullary long bridging nailing offers ideal conditions for bone healing, as axial and rotational stability is provided by canal-filling nails and locking screws. In addition, the tissue in the fracture region is protected as the intramedullary nail insertion is distant from the fracture. The indication spectrum for modern intramedullary locked nailing includes diaphyseal fractures of long bones, metaphyseal fractures and reconstructions, as well as treatment of nonunion, osteotomy and arthrodesis of the lower extremities. Continuous improvements in nail design and instrumentation as well as the introduction of anatomical reconstruction nails will optimize the spectrum and effectiveness of intramedullary osteosynthesis even further.

[The Postero-Lateral Approach--An Alternative to Closed Anterior-Posterior Screw Fixation of a Dislocated Postero-Lateral Fragment of the Distal Tibia in Complex Ankle Fractures]. / Der posterolaterale Zugang--eine Alternative zur geschlossenen anterior-posterioren Schraubenosteosynthese bei komplexen Sprunggelenkfrakturen.

BACKGROUND: The dislocated posterolateral fragment of the distal tibia is considered as a key fragment for the successful reduction of comminuted ankle fractures. The reduction of this fragment can either be achieved indirectly by joint reduction using the technique of closed anterior-posterior screw fixation, or directly using the open posterolateral approach followed by plate fixation. The aim of this study was to compare the outcome after stabilization of the dislocated posterolateral tibia fragment using either closed reduction and screw fixation, or open reduction and plate fixation via the posterolateral approach in complex ankle fractures. PATIENTS/MATERIAL AND METHODS: In a prospective study between 01/2010 and 12/2012, all mono-injured patients with closed ankle fractures and dislocated posterolateral tibia fragments were assessed 12 months after osteosynthesis. Parameters included: size of the posterolateral tibia fragment relative to the tibial joint surface (CT scan, in %) as an indicator of injury severity, unreduced area of tibial joint surface postoperatively, treatment outcome assessed by using the "Ankle Fracture Scoring System" (AFSS), as well as epidemiological data and duration of the initial hospital treatment. RESULTS: In 11 patients (10 female, 1 male; age 51.6 ± 2.6 years [mean ± SEM], size of tibia fragment 42.1 ± 2.5 %) the fragment fixation was performed using a posterolateral approach. Impaired postoperative wound healing occurred in 2 patients of this group. In the comparison group, 12 patients were treated using the technique of closed anterior-posterior screw fixation (10 female, 2 male; age 59.5 ± 6.7 years, size of tibia fragment 45.9 ± 1.5 %). One patient of this group suffered an incomplete lesion of the superficial peroneal nerve. Radiological evaluation of the joint surface using CT scan imaging demonstrated significantly less dislocation of the tibial joint surface following the open posterolateral approach (0.60 ± 0.20 mm) compared to the closed anterior-posterior screw fixation (1.03 ± 0.08 mm; p < 0.05). Assessment of the treatment outcome using the AFSS demonstrated a significantly higher score of 97.4 ± 6.4 in the group with a posterolateral approach compared to a score of 74.4 ± 12.1 (p < 0.05) in the group with an anterior-posterior screw fixation. CONCLUSION: In comparison to the anterior-posterior screw fixation, open reduction and fixation of the dislocated, posterolateral key fragment of the distal tibia using a posterolateral approach resulted in a more accurate fracture reduction and significantly better functional outcome 12 months after surgery. In addition, no increased rate of postoperative complications, or extended hospital stay was observed but there was less severe post-traumatic joint arthritis. The results of this study suggest that in complex ankle factures the open fixation of the dislocated posterolateral fragment is recommended as an alternative surgical procedure and may be beneficial for both clinical and radiological long-term outcomes.

[Antegrade femoral intramedullary nailing in a lateral position]. / Technik der antegraden Femurmarknagelung in Seitenlage.

BACKGROUND: Intramedullary nailing is the gold standard for the treatment of femoral shaft fractures; however, rotational malalignment remains a common complication. The patient can be positioned on the fracture table in a supine position or alternatively in the lateral decubitus position without any traction. OBJECTIVE: The aim of this article is to describe an effective method to control intraoperative torsion of the femur. METHOD: The surgical technique described in this article is the standard procedure for femoral shaft fractures and subtrochanteric fractures in this level 1 trauma center. The patient is positioned in a lateral position on a radiolucent table with free draping of the injured leg. Using the C-arm, reduction can be performed with this technique with precise placing of the nails and torsion can be exactly adjusted and controlled with the aid of the femoral neck axis, the distal locking holes and both parallel femoral condyles. RESULTS: The described technique represents an effective method for the intraoperative control of femoral torsion. With an acceptable and most probably clinically irrelevant bias, this technique is able to avoid significant rotational malalignment. It does not prolong the operative procedure and does not require additional navigation settings. It has also been shown to be helpful in the treatment of subtrochanteric fractures. CONCLUSION: The surgical technique of anterograde intramedullary nailing using the lateral decubitus position without any traction device and free draping of the injured leg represents a safe and reliable treatment concept and offers logistical advantages compared to the supine position of the patient on a fracture table. Together with other described methods of intraoperative torsional control of femoral fractures, the radiological technique described in this study is an easily applicable and safe method, which needs to be confirmed in clinical studies.

[Intramedullary nailing vs. locking plate osteosynthesis in proximal humeral fractures: Long-term outcome]. / Marknagel- vs. winkelstabile Plattenosteosynthese bei proximalen Humerusfrakturen: Langzeitergebnisse.

BACKGROUND: For the treatment of proximal humeral fractures two major therapeutic principles can be employed: intramedullary nailing (PHN) or locking plate osteosynthesis. The aim of this study was to evaluate and compare clinical and radiological long-term outcome of proximal humeral fracture stabilization using PHN or angular stable plating. MATERIALS AND METHODS: In a retrospective study between March 2009 and March 2010, we analyzed 72 out of 118 patients with unified proximal humeral fracture who had been treated at least 3 years previously using PHN (44 patients) or angular stable plating (28 patients) in a level 1 trauma center. Functional and radiological outcomes were assessed at least 3 years after trauma using the Constant and Murley score and SF-36 score. RESULTS: According to the Neer classification, there were 31 3-part fractures (PHN: 23; plate: 8) and 41 4-part fractures (PHN: 21; plate: 20), respectively. No clinical symptoms after 3 years were observed in 42 patients, whereas in 30 patients clinical symptoms were evaluated related to pain and/or loss of function. Functional outcome using the Constant and Murley score demonstrated a total score of 73 points (ipsilateral side) vs. 88 points (contralateral side) in all evaluated patients, on average. CONCLUSION: Both PHN and angular stable plating are adequate treatment options for proximal humeral fractures. Both systems require precise preoperative planning and advanced surgical experience. No significant differences in long-term clinical and radiological outcome between implants regarding fracture classification, age of patient, and choice of implant were found.

[Auxiliary cerclage-wiring in internal fixation of displaced acetabular fractures]. / Auxiliäre Cerclage zur Reposition und Retention dislozierter Acetabulumfrakturen.

BACKGROUND: Displaced fractures of the acetabulum involving the quadrilateral plate continue to be a surgical challenge. In this study, we describe our operation technique of auxiliary acetabular cerclage-wiring combined with plate osteosynthesis and present our results as well as short-term outcome. PATIENTS AND METHODS: All patients aged 18 years and older treated with auxiliary cerclage-wiring between 2007 and 2012 were included in this study. Fractures were classified according to Letournel. Cerclage wiring was used when reposition and retention of the fracture was insufficient with plates and screws alone. Short-term outcome was evaluated by the German Short Musculoskeletal Functional Assessment (SMFA-D) questionnaire. RESULTS: Data from 23 patients were collected. The follow-up period was 7 months (range 2-23 months). Of the 23 patients, 22 showed excellent fracture reduction and retention. One patient had to undergo revision surgery due to loss of reposition. Patients showed good functional outcome. CONCLUSION: Auxiliary acetabular cerclage-wiring is a safe and effective method for fracture reduction and retention especially in displaced acetabular fractures involving the quadrilateral plate.

Factors influencing survival after resection of pulmonary metastases from colorectal cancer.

BACKGROUND: Selection of patients for resection of lung metastases from colorectal cancer is problematic. The aim of this study was to evaluate clinically relevant prognostic factors and to define a subgroup of patients who would most benefit from such surgery. PATIENTS: Seventy-five patients (median age 58 (range 33-82) years) with pulmonary metastases from colorectal cancer underwent 104 R0 lung resections. Median follow-up was 33 (range 4-116) months. Patients who had no evidence of recurrent extrathoracic disease, no more than three metastases on either side, lobectomy as the maximal surgical procedure, and adequate cardiorespiratory function were eligible for surgery. Univariate and multivariate Cox regression, and classification and regression tree subgroup analyses were performed. RESULTS: Overall median survival was 33 months, with 3- and 5-year survival rates of 47 and 27 per cent respectively. Size of metastases (relative risk (RR) 2.6) and extent of resection (RR 0.4) were identified as independent prognostic factors. Primary tumour stage was significant in univariate analysis. Subgroup analysis defined two statistically relevant prognostic groups: patients with a maximum metastasis size of 3.75 cm or less with a disease-free interval of more than 10 months and patients with larger metastases and a shorter disease-free interval. Median survival and 5-year survival were 45 months and 39 per cent in the former group, and 24 months and less than 11 per cent in the latter. CONCLUSION: Subgroup analysis provided criteria for the selection of patients for R0 resection of lung metastases from colorectal cancer and differentiated between those at high or low risk of early tumour progression; the latter patients would benefit most from surgery.

Reduced hepatic transcription factor activation and expression of IL-6 and ICAM-1 after hemorrhage by NO scavenging.

BACKGROUND: Hemorrhagic shock (HS) elicits an inflammatory response characterized by increased cytokine production and recruitment of polymorphonucleated neutrophilic granulocytes (PMN) that we reported to be inducible nitric oxide synthase (iNOS) dependent. In a previous study, we demonstrated that removing excess induced nitric oxide (NO) by administration of the NO scavenger NOX resulted in reduced PMN infiltration, attenuated liver injury, and improved survival. In this study, we examined the role of NOX treatment in down-modulating the inflammatory response in the liver following HS. METHODS: Rats ( n=5) were subjected to severe HS with mean arterial blood pressure (MAP) of 40 mmHg for 100 min followed by resuscitation and killing at 24 h. RESULTS: Shock animals demonstrated increased mRNA levels of interleukin (IL)-6 and intercellular adhesion molecule (ICAM)-1 and increased activation of the transcription factors nuclear factor kappa B (NF-kappa B) and signal transducers and activators of transcription 3 (Stat3). Treatment with NOX (30 mg/kg/h) infused 60 min following the onset of shock over 4 h resulted in significant reduction in cytokine mRNA expression and transcriptional factor activation. These results suggest that excessive NO contributes to hemorrhage-induced tissue inflammation and that reducing the bioavailability of NO using NOX may be beneficial in HS. CONCLUSION: These data indicate that NOX prevents liver injury in this HS model, possibly through down-modulation of proinflammatory signaling and the shock-induced inflammatory response.

[Psoas abscess after anterior spinal fusion]. / Psoasabszess nach ventraler Spondylodese.

We present 3 cases of secondary psoas abscess after anterior spinal fusion. Psoas abscess is still a rare clinical entity. It is often associated with unspecific symptomatology and may present as late infection. A high index of suspicion is required for early diagnosis and treatment. Computed tomography is the imaging technology of choice. Treatment includes open abscess drainage and antibiotic therapy. In secondary psoas abscess causative treatment of the primary infection focus is essential. For psoas abscess after anterior spondylodesis this includes treatment of a deep wound infection. Predisposing factors for postoperative infection are large implants, bone grafting, long operating times, previous spinal surgery, immunodeficiency and metabolic disorders. Usually several operations are necessary to eradicate infection. As long as stability is guaranteed, implant materials should be removed. Continuing antibiotic therapy for 2-3 weeks after normalization of infectious parameters is suggested. Delayed therapy results in an increase of the morbidity and mortality of psoas abscess.

Stent placement in short unilateral iliac occlusion. Technique and 24-month results.

PURPOSE: To determine the success rate and 24-month follow-up results of primary stent implantation for reconstruction of unilateral short iliac occlusion involving the aortic bifurcation. MATERIAL AND METHODS: In 90 patients attempts of percutaneous transluminal recanalization of a short unilateral occlusion of the iliac arteries were performed. In 72/90 patients, the treatment was successful. Stent implantation was performed after recanalization in all 72 patients. Pre-interventional angiography of successfully treated patients showed unilateral occlusions and contralateral stenosis in 34/72 patients. In 38/72 patients unilateral occlusion without contralateral stenosis was diagnosed. The recanalization of the common iliac artery obstructions were performed with a guidewire and excimer laser angioplasty. Totally 152 stents were used for the treatment of iliac occlusion. Standardized treadmill testing and color-coded Doppler ultrasound were performed before treatment and during the follow-up. RESULTS: In all patients, stents were placed successfully; 5 major and 7 minor complications were observed. A clinical improvement of +2 to +3 according to the American Heart Association criteria was observed in 62 and 10 patients, respectively. Angiographic control was performed after 1-30 months. The primary angiographic patency rate was 83.1%. Angiography revealed significant restenoses in 4 patients successfully treated with transluminal angioplasty, and re-occlusion in 6 patients which were referred to surgery. The patency rate after 24 months was 90.0%. CONCLUSION: Primary stent implantation is an effective treatment for short iliac obstructions and represents a true endovascular alternative to surgery.

Molecular mechanisms in the early phase of hemorrhagic shock.

Hemorrhagic shock (HS) results in the initiation of an inflammatory cascade that is critical for survival following successful resuscitation. We identified a complex sequence of molecular events including shock-dependent and reperfusion-dependent responses that offer a new comprehensive approach for consequences of HS. Shock-dependent initializing mechanisms include the induction of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, and CD14 and play a catalyzing role for subsequent phenotypic changes following resuscitation. The early immediate response genes iNOS and COX-2 promote the inflammatory response by the rapid and excessive production of nitric oxide (NO) and prostaglandins. The transcription factor hypoxia-inducible factor-1 (HIF-1) may regulate the induction of iNOS during the ischemic phase of shock. NO is an important signaling molecule which is involved in redox-sensitive mechanisms including the downstream activation of nuclear factor (NF)-kappaB. NO-dependent NF-kappaB activation promotes the induction of inflammatory cytokine expression during the reperfusion phase. Peroxynitrite-mediated direct toxicity and NO-mediated inflammatory toxicity contribute to organ injury. Patients suffering consequences of severe HS are susceptible to systemic inflammation, organ injury, and mortality if physiologic and therapeutic mechanisms are ineffective in limiting the activation of the inflammatory cascade.

Hypoxia-inducible factor-1 activation and cyclo-oxygenase-2 induction are early reperfusion-independent inflammatory events in hemorrhagic shock.

Hemorrhagic shock (HS) initiates an inflammatory response that includes increased expression of inducible nitric oxide synthase (iNOS) and production of prostaglandins. Induction of iNOS during the ischemic phase of HS may involve the activation of the hypoxia-inducible factor-1 (HIF-1). Increased expression of cyclooxygenase-2 (COX-2) during HS contributes to prostaglandin production. The aim of this study was to determine whether the ischemic phase of HS results in the activation of HIF-1 and the induction of COX-2. The lungs of rats subjected to HS demonstrated a twofold increase in HIF-1 activation (P < 0.01) and a 7.4-fold increase in expression of COX-2 mRNA (P < 0.01) compared with sham controls. The upregulation of iNOS and COX-2 during ischemia are two important early response genes that promote the inflammatory response and may contribute to organ damage through the rapid and exaggerated production of nitric oxide and prostaglandins.

Impaired gut contractility following hemorrhagic shock is accompaied by IL-6 and G-CSF production and neutrophil infiltration.

Recovery from hemorrhagic shock (HS) is frequently accompanied by bowel stasis. The aim of this study was to examine whether or not HS initiates an inflammatory response that includes production of cytokines, specifically G-CSF and interleukin-6 (IL-6), and recruitment of leukocytes within the intestinal muscularis which contribute to impaired muscle contractility. Sprague-Dawley rats were subjected to HS (MAP 40 mm Hg for 156 min) followed by resuscitation, and then they were killed at 4 hr. Shock animals demonstrated accumulation of PMNs in the jejunal muscularis and decreased spontaneous and bethanechol-stimulated muscle contractility. Semiquantitative RT-PCR demonstrated elevated levels of IL-6 and G-CSF mRNA in shock animals in full-thickness jejunum and in mucosa and muscularis layers compared to sham controls. Immunostaining demonstrated increased IL-6 protein production within the muscularis externa and submucosa. In situ hybridization studies localized G-CSF mRNA production to the submucosa. Gel shift assays revealed increased NF-kappaB and Stat3 activity in full-thickness jejunum and jejunal layers of shock animals. Activation of Stat3 also was demonstrated in normal muscularis tissue exposed to IL-6 and G-CSF in vitro. IL-6 and G-CSF are produced in the muscularis and mucosa layers of the gut in HS where they may contribute to PMN recruitment and smooth muscle dysfunction.

Molecular and functional contractile sequelae of rat intestinal ischemia/reperfusion injury.

BACKGROUND: Pathophysiological states that produce intestinal ischemia/reperfusion injury (I/R) initiate an inflammatory cascade and cause ileus. The aims of this study were to investigate the local cellular responses and molecular mechanisms, which contribute to intestinal dysmotility after selective intestinal I/R injury. METHODS: ACI rats were subjected to 75 min SMA clamp-induced ischemia followed by reperfusion and were killed at 0 min, 30 min, and 24 hr. Whole mounts of the jejunum were used to immunohistochemically quantify alterations in leukocytes, and circular muscle strips were used to assess organ bath muscle function. Muscularis and mucosa extracts were isolated from the intestine and used for reverse transcription assisted polymerase chain reaction mRNA measurements of granulocyte-colony stimulating factor and interleukin-6, and for determination of nuclear factor kappa B and Stat3 activation. RESULTS: Intestinal I/R injury resulted in the significant recruitment of neutrophils and monocytes into the intestinal muscularis and a functional suppression in jejunal circular muscle contractions. These I/R injury induced cellular responses were preceded by the molecular activation of nuclear factor kappa B, up-regulation of granulocyte colony-stimulating factor and interleukin-6 mRNA and phosphorylation of the downstream signaling and transcription factor Stat3. CONCLUSIONS: I/R injury evokes a molecular and cellular inflammatory response within the intestinal muscularis that is associated with a subsequent decrease in intestinal motility.

Biphasic response to gut manipulation and temporal correlation of cellular infiltrates and muscle dysfunction in rat.

BACKGROUND: Surgical manipulation of the intestine results in the massive movement of leukocytes into the intestinal muscularis at 24 hours. This is associated with muscle inhibition. The aim of this study was to temporally associate leukocyte extravasation with ileus after surgical manipulation. METHODS: Rats underwent a simple manipulation of the small bowel and were killed at various times (0, 0.25, 0.5, 1, 3, 6, 12, and 24 hours) postoperatively. Jejunal circular-muscle contractile activity was assessed in a standard organ bath. Both extravasating and resident leukocytes were immunohistochemically stained in muscularis whole mounts. RESULTS: Contractile activity was significantly reduced immediately after surgery, but rapidly returned to control levels at 3 hours. After recovery, muscle function decreased at 12 and 24 hours (41% and 81%, respectively). The resident muscularis macrophage network demonstrated cellular activation 1 hour postoperatively. The number of leukocytes increased over time (neutrophils, 67.5-fold; monocytes, 98.2-fold; and mast cells, 47-fold at 24 hours). CONCLUSIONS: The functional results demonstrate a biphasic response in the suppression of muscle activity after surgical manipulation. Regression analysis (r2 = 0.998) of the temporal development of leukocyte infiltration and the protracted phase of muscle inhibition provides evidence for a correlation between cellular inflammation and postoperative dysmotility.

Rapid and simultaneous activation of Stat3 and production of interleukin 6 in resuscitated hemorrhagic shock.

The inflammatory response of the liver to hemorrhagic shock includes the production of acute phase proteins and a variety of mediators, such as the cytokine interleukin (IL)-6. The transcription of acute phase protein genes in hepatocytes has been shown to be activated by Stat3, one of six distinct signal transducers and activators of transcription (STAT) proteins. IL-6 signals through activation of Stat3. In this study, we examined whether or not Stat3 was activated and IL-6 mRNA produced in the liver of rats subjected to hemorrhagic shock and whether or not both phases of shock, the ischemic and the resuscitation phases, were required. We report here that Stat3 activation and increased IL-6 expression required resuscitation and displayed identical kinetics following resuscitation, suggesting that liver production of IL-6 was responsible for liver Stat3 activation in hemorrhagic shock.

A novel nitric oxide scavenger decreases liver injury and improves survival after hemorrhagic shock.

We tested the ability of a nitric oxide (NO) scavenger to reduce tissue injury in a rodent model of hemorrhagic shock. Rats were hemorrhaged to a mean arterial blood pressure (MAP) of 40 mmHg and then resuscitated when either 30% of their shed blood had been returned (group 1) or after 100 min of continuous shock (group 2). Selected animals were treated with the NO scavenger NOX (30 mg. kg(-1). h(-1)) infused over 4 h. Hemorrhaged rats had a lower MAP after resuscitation compared with sham-shock control rats. NOX treatment significantly increased MAP after resuscitation from hemorrhage. Hemorrhagic shock also increased liver injury as reflected by elevated ornithine carbamoyltransferase (OCT) plasma levels, and NOX treatment significantly reduced OCT release. In addition, NOX was associated with significantly decreased hepatic neutrophil infiltration and improved 24-h survival (n = 8 of 9) compared with saline-treated shock animals (n = 3 of 9). These data suggest that excess NO mediates shock-induced tissue injury and that suppression of NO availability with NO scavengers may reduce the pathophysiological sequelae of severe hemorrhage.

Neutrophil accumulation and damage to the gastric mucosa in resuscitated hemorrhagic shock is independent of inducible nitric oxide synthase.

Polymorphonuclear leukocytes (PMN) and inducible nitric oxide synthase (iNOS) appear to play important roles in the liver and in lung injury induced by hemorrhagic shock. Their precise roles in hemorrhagic shock-induced acute gastric mucosal lesions (AGML), however, are still poorly understood. In this study, we investigated the effect of neutropenia on hemorrhagic shock-induced AGML. We also examined the roles of iNOS in PMN infiltration into the mucosa and AGML during hemorrhagic shock by using L-N6-(1-iminoethyl)-lysine, a potent inhibitor of iNOS, and by reverse transcriptase polymerase chain reaction. Remarkable gastric mucosal damage occurs after hemorrhagic shock. PMN depletion caused by Vinblastine pretreatment significantly attenuates this AGML. Although low-dose L-N6-(1-iminoethyl)-lysine (50 microg/kg, iNOS inhibition) has no effect on AGML, high-dose L-N6-(1-iminoethyl)-lysine (250 microg/kg, iNOS + endothelial NOS inhibition) significantly exacerbates AGML without increasing PMN infiltration into the mucosa. The mRNA expression of iNOS in the stomach during hemorrhagic shock cannot be detected by reverse transcriptase polymerase chain reaction. We conclude that PMN play a pivotal role in hemorrhagic shock-induced AGML, iNOS does not regulate PMN infiltration into the mucosa, and endothelial NOS provides important protection against AGML during hemorrhagic shock.

Hemorrhagic shock results in intestinal muscularis intercellular adhesion molecule (ICAM-1) expression, neutrophil infiltration, and smooth muscle dysfunction.

Intestinal stasis followed by mucosal barrier breakdown and the generation of locally produced cytokines has been proposed as the cause of systemic infection and multiple organ failure following hemorrhagic shock. The aim of this study was to investigate the underlying mechanisms of impaired intestinal muscle function leading to ileus following hemorrhagic shock. Rats were subjected to severe hemorrhagic shock (mean arterial pressure 40 mm Hg) followed by resuscitation and were killed early at 4 h or late at 24 h. Other groups consisted of control and sham animals. Intercellular adhesion molecule (ICAM-1) mRNA levels were significantly elevated in the muscularis but not in the mucosa using the semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR). There was a marked infiltration of neutrophils into the muscularis early and late after shock. Furthermore, smooth muscle contractility in response to bethanechol was significantly decreased, being more pronounced in the early group. Immunohistochemistry revealed signal for ICAM-1 in the muscularis microvasculature and on infiltrating cells. These results suggest that the expression of ICAM-1 within the muscularis vasculature after hemorrhagic shock promotes the local recruitment of leukocytes and that this inflammatory response is accompanied by a subsequent impairment of intestinal contractility.