Comparison of the protective effects of type III phosphodiesterase (PDE3) inhibitor (cilostazol) and acetylsalicylic acid on intestinal microcirculation after ischemia reperfusion injury in mice.

Antiplatelet therapy has been proposed as the treatment of choice for ischemia/reperfusion injury. The aim of this study is to elucidate the difference in effect between cilostazol (CZ) and acetylsalicylic acid (ASA) on microcirculatory disturbance in ischemia/reperfusion injury. Either 10 mg/kg of CZ (n = 14) or 100 mg/kg of ASA (n = 14) was administered orally to mice. Thereafter, 20 min of intestinal ischemia, followed by 60-min reperfusion, was applied; then, the status of submucosal microcirculation was observed under intravital microscopy. The blood cell counts and organ damage markers were examined in the portal blood. Next, 5 mm of the ileum was excised and was then histologically examined. Platelet-leukocyte aggregates were often observed in the postcapillary venules, and this formation was significantly reduced by both CZ and ASA. The number of adherent leukocytes was significantly lesser in the CZ-treated mice than in the ASA-treated mice (P < 0.01). The leukocyte number, lactate dehydrogenase, and lactate levels were best maintained in the CZ-treated mice (P < 0.05). The villus height was best preserved in the CZ-treated mice. Cilostazol inhibited not only the platelet aggregation but also the leukocyte adhesion to the endothelium, thereby inducing organ protection.

Pretreatment of sivelestat sodium hydrate improves the lung microcirculation and alveolar damage in lipopolysaccharide-induced acute lung inflammation in hamsters.

Damage to the lung microcirculation and alveoli caused by activated leukocytes is known to play an important role in the development of acute lung injury (ALI). The aim of this study is to evaluate the difference in the effect of pretreatment and posttreatment of a synthetic neutrophil elastase inhibitor sivelestat on ALI. Hamsters were instilled with 10.0 mg/kg of lipopolysaccharide (LPS) intratracheally for 1 h to simulate ALI. Two milligrams per kilogram of sivelestat was injected intraperitoneally either previously or after LPS infusion. One and 24 hours after the infusion of LPS, pulmonary microcirculation was observed under the intravital microscopy. In another series, the blood cell counts were evaluated. The adhesive leukocyte count on the endothelium was significantly lower in pretreatment group compared with control group (P < 0.01), whereas the difference was not significant in the posttreatment group. Similarly, the number of obstructed capillary was significantly lower in the pretreatment group (P < 0.01). The width of interstitium was significantly lower in the pretreatment and posttreatment group (P < 0.01 and 0.05, respectively). A comparison of white blood cell counts showed a better maintenance in pretreatment group (P < 0.05). Pretreatment of sivelestat demonstrated a protective effect on both intravascular and extravascular damage in the lung, whereas posttreatment only suppressed the latter damage.

Analysis of antimicrobial drug resistance of Staphylococcus aureus strains by WHONET 5: microbiology laboratory database software.

OBJECTIVES: To analyze our hospital laboratory microbiological data by using WHONET 5-Microbiology laboratory database software-, and to acquire information about antimicrobial resistance of Staphylococcus aureus strains among every ward. MATERIALS AND METHODS: The database of Staphylococcus aureus strains had been brought to our hospital microbiology laboratory from every ward in our hospital from September 2001 till December 2002. Analysis was performed under the condition as one isolate per one patient. Starting of "resistance profile" analysis in WHONET 5 and analyzing the microbiological laboratory testing reports for every ward. We chose Oxacillin, Levofloxacin, Erythromycin and Gentamicin as the antimicrobials that need to be investigated for resistance. We evaluated the monthly transition of resistance ratios with regard to the specific wards that have the moving lines of inpatients in order to verify the hypothesis that resistant strains may be carried from ward to ward along the moving lines of inpatients. RESULTS: The data of 2,113 Staphylococcus aureus strains were accumulated and analyzed. Overall Oxacillin resistance ratio in our hospital was 65.7%. The ward of the smallest Oxacillin resistance ratio was Pediatrics/Ophthalmology ward. The ratios of Oxacillin resistant were varied as from 67.9% to 96.7% regardless the categories of wards such as internal medicine or surgery. Multi-resistant MRSA strains were overwhelmingly dominant in the wards of surgery. The ratios of the Gentamicin sensitive strains that were resistant to Oxacillin were high over the every ward. The moving lines of inpatients existed between ICU/CCU ward and three rear wards. Two rear wards whose Oxacillin resistance changes were reflected to those of ICU/CCU, but one rear ward was not. CONCLUSION: Variation of resistant degree among wards were very obvious and large. We could survey the wards where patient-to-patient transmission of resistant organisms might occur along the moving lines of inpatients. WHONET 5 will be recognized as an analysis and surveillance tool for every infection control team to survey the suspicious wards.

Early access to patients with life-threatening cardiovascular disease by an air ambulance service.

The purpose of this study was to determine whether use of an air ambulance service using a helicopter with a critical care physician and nurse on board (doctor helicopter service; DHS) could shorten the prehospital delay. We evaluated the initial treatment time and the transport time in 30 patients transported by DHS and 30 patients transported by ground ambulance service (GAS). The initial treatment time was significantly shorter in the DHS group (11.3+/-5.4 min) than in the GAS group (29.5+/-15.3 min). But the transport time in the DHS group (26.1+/-8.6 min) was not different from that in the GAS group. The difference in the initial treatment time was remarkable for patients transported from distant areas (12.7+/-5.6 min for DHS, and 42.1+/-13.8 min for GAS) and DHS shortened the initial treatment time by 30 min compared with GAS. The transport time was shorter for DHS (30.5+/-9.9 min) than for GAS (42.1+/-13.8 min) for patients transported from distant areas, but it was not significantly different for patients transported from nearby areas (22.3+/-5.0 min for DHS, and 18.4+/-2.4 min for GAS). In conclusion, DHS is important in the management of life-threatening cardiovascular diseases, and has a significant impact when GAS cannot transport a patient to the hospital within 20 min.

[Damage control for thoracic injuries].

A critically injured chest trauma patient showing profound shock or cardiac arrest en route to the trauma center or in the emergency room sometimes requires emergency room thoracotomy and definitive repair. In some patients damage control must be performed because of the appearance of the deadly triad of hypothermia, acidosis, and coagulopathy. Indications for damage control are believed to be body temperature < 34 degrees C, pH < 7.2, and clinically uncontrollable bleeding. The strategy for damage control consists of three steps: step 1, rapid control of hemorrhaging and abbreviated surgery in the ER or OR; step 2, correction of hypothermia, acidosis, and coagulopathy and reevaluation of the injuries in the intensive care unit; and step 3, definitive surgery in the OR. Damage control procedures for chest injuries include aortic cross-clamping, hilar clamping, major vessel ligation, pulmonary tractotomy, simultaneously stapled pneumonectomy or lobectomy, cardiac stapling, balloon catheter tamponade, temporary intraluminal shunt, towel packing, towel clip closure, single en masse closure of the chest wall, etc. Every surgeon responsible for treating critical chest trauma patients should have knowledge of damage control and also be familiar with the techniques.