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Copyright of Zeitschrift für Medizinische Physik is the property of Elsevier GmbH, Urban & Fischer Verlag and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Acute pancreatitis (AP) is characterized by disturbances of pancreatic microcirculation. It remains unclear whether platelets contribute to these perfusion disturbances. The aim of our study was to investigate platelet activation and function in experimental AP. Acute pancreatitis was induced in rats: (1) control (n=18; Ringer's solution), (2) mild AP (n=18; cerulein), and (3) severe AP (n=18; glycodeoxycholic acid (GDOC) + cerulein). After 12 h, intravital microscopy was performed. Rhodamine-stained platelets were used to investigate velocity and endothelial adhesion in capillaries and venules. In addition, erythrocyte velocity and leukocyte adhesion were evaluated. Serum amylase, thromboxane A2, and histology were evaluated after 24 h in additional animals of each group. Results showed that 24 h after cerulein application, histology exhibited a mild AP, whereas GDOC induced severe necrotizing AP. Intravital microscopy showed significantly more platelet-endothelium interaction, reduced erythrocyte velocity, and increased leukocyte adherence in animals with AP compared to control animals. Thromboxane levels were significantly elevated in all AP animals and correlated with the extent of platelet activation and severity of AP. In conclusion, platelet activation plays an important role in acute, especially necrotizing, pancreatitis. Mainly temporary platelet-endothelium interaction is observed during mild AP, whereas severe AP is characterized by firm adhesion with consecutive coagulatory activation and perfusion failure. [ABSTRACT FROM AUTHOR]

Background. The aim of this experimental study was to compare the protective efficacy of the cardioplegic solutions Celsior and Custodiol. Canine hearts were examined with regard to energy metabolism and early postischemic recovery after 8 or 12 hours of ischemia at 5°C.Methods. Canine hearts were preserved with Celsior or Custodiol (each n = 19). Five hearts of each group were used to determine myocardial content of energy-rich phosphates immediately after preservation and after 8 and 12 hours of ischemia at 5°C; the remainder were reperfused after 8 and 12 hours of ischemia. Control variables during reperfusion were myocardial content of energy-rich phosphates, myocardial K+ uptake, left ventricular dP/dtmax and dP/dtmin, and incidence of arrhythmias in percentage of heart rate.Results. Custodiol-preserved hearts contained more ATP than Celsior-preserved hearts after 8 and 12 hours of ischemia (8 hours p = ns, 12 hours, p < 0.05). During reperfusion after 8 hours of ischemia, dP/dtmax and dP/dtmin showed the same values for both solutions, after 12 hours values were significantly higher in Custodiol-preserved hearts (p < 0.005). The incidence of reperfusion arrhythmias was higher in hearts of the Celsior group (8 hours p < 0.01, 12 hours p = ns). Myocardial K+ uptake during reperfusion after 8 and 12 hours of ischemia was about twice as high in Celsior-preserved compared to Custodiol-preserved hearts (p < 0.005).Conclusions. In the Langendorff model of the canine heart, cardioplegia with Celsior showed no advantage over cardioplegia with Custodiol. Differences were observed, however, which may be clinically important, especially in the case of long cold-storage times. [Copyright &y& Elsevier]

Abstract: Advances in the treatment of ischemia–reperfusion injury have created an opportunity for plastic surgeons to apply these treatments to flaps and implanted tissues. Using an extended inferior epigastric artery skin flap as a flap ischemia–reperfusion injury (IRI) model, we examined the capability of extracorporeal shock wave treatment (ESWT) to protect tissue against IRI in a rat flap model. Twenty-four rats were used and randomly divided into three groups (n =8 for each group). Group I was the sham group and did not undergo ischemic insult; rather, the flap was raised and immediately sutured back (non-ischemic control group). Group II (ischemia control) and Group III (ESWT) underwent 3h of ischemic insult. During reperfusion Group III was treated with ESWT and Group II was left untreated. Histological evaluation was made to investigate treatment induced tissue alterations. Survival areas were assessed at 5d postoperatively. Skin flap survival and perfusion improved significantly in the ischemic animals following ESWT (p <0.001, respectively). The tissue protecting effect of ESWT resulted in flap survival areas and perfusion data equal to non-ischemic, sham operated flaps. In line with the observation of better flap perfusion, tissue from ESWT-treated animals (Group III) revealed a significantly increased frequency of CD31-positive vessels compared to both the ischemic (Group II; p =0.003) and the non-ischemic, sham operated control (Group I; p <0.005) and an enhanced expression of pro-angiogenic genes. This was accompanied by a mild suppression of pro-inflammatory genes. Our study suggests that ESWT improves flap survival in IRI by promoting angiogenesis and inhibiting tissue inflammation. The study identifies ESWT as a low-cost and easy to use technique for surgical techniques that aim at reducing ischemia–reperfusion-induced tissue injury [Copyright &y& Elsevier]

Abstract: Recent findings suggest that the presence of cancer stem cells could be linked with patients’ survival. We profiled suggested cancer stem cell markers in tissue specimens of hepatocellular carcinoma and colorectal carcinoma liver metastases. About 1% of cells co-expressed cancer stem cell antigens, but there was no correlation between the amount of CD133+, CD133+/CD44+ or CD133+/CD24− cells and the patients’ clinical–pathological status or with the cancer stem cell marker-positive cells localization. CD133+ and CD133− fractions of Huh7 cells did not differ in migratory properties. Therefore, presence of markers alone should be taken with caution as single prognostic parameters. [Copyright &y& Elsevier]