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The origin of fatigue failure that occurs on the air ventilation holes of a newly designed heavy commercial vehicle steel wheel in dynamic radial fatigue tests is studied. In these tests, all of the test samples failed in the same regions. The cause of this damage was studied via finite element analysis. In order to determine the reason of the fatigue failure, stress analysis was performed via the finite element method. In this way, stress concentrated regions, where fatigue failure is expected, were determined. Mechanical properties of the wheel material were determined by tensile tests and hardness measurements. The fatigue life of the damaged wheel was estimated using the stress-life (S-N) approach, utilising the ultimate tensile strength of the processed wheel material and the Mann factors determined for the critical regions. To extend the life of the wheel disc and delay the onset of fatigue, design enhancement solutions were applied. (C) 2011 Elsevier Ltd. All rights reserved.

Background: Although inflammation is a normal part of wound healing, if the inflammatory response is excessive the repair process might be prolonged. Nitric oxide (NO) has been implicated in healing inflammation and wounds. Objective: Endotoxins and cytokines associated with sepsis induce NO synthesis in the tissues. This study used tensile strength and tissue hydroxyproline levels as proxies for wound healing to determine whether wound healing in the presence of endotoxemia is improved when NO synthase is inhibited by N-nitro-l-arginine methyl ester (L-NAME) or N5-(1-Imino-methyl)-l-ornithine (L-NIO). Methods: In this investigator-blinded, controlled, experimental study, male Wistar albino rats (275-300 g) were divided into 4 groups. The first group received an intraperitoneal (IP) injection of Escherichia coli endotoxin 10 mg/kg and an SC injection of 0.9% sodium cloride (NaCl). The second group received IP E coli 10 mg/kg and SC L-NAME 2 mg/kg. The third group received IP E coli 10 mg/kg and L-NIO 10 mg/kg. The control group was administered an IP and an SC injection of 0.9% NaCl. Each group received both injections at 24 and 16 hours before surgery. All rats underwent a 3-cm dorsal midline incision, which was subsequently closed. Five days after surgery, all rats were euthanized and skin from the healing wound was excised. Hydroxyproline levels and tensile strength were then measured. Results: Forty-four male rats (mean age, 16 weeks; mean [SD] weight, 284 [16] g) were included in the study. Each of the groups receiving endotoxin (endotoxin, L-NAME, and L-NIO groups) had 12 rats; the control group consisted of 8 rats. All the groups that received endotoxin showed significant declines in hydroxyproline levels versus controls (P < 0.001, P = 0.001, and P = 0.002, respectively). Compared with the control group, the endotoxin-only group had a significant reduction in both mean (SD) hydroxyproline levels and mean (SD) wound tensile strength (298.27 [17.66] vs 175.82 [18.73] g/cm2 and 7.16 [0.51] vs 4.01 [0.29] μg/mg wet tissue; both, P < 0.001). Compared with the endotoxin- only group, rats that received L-NIO had significantly greater mean (SD) hydroxyproline levels and mean (SD) wound tensile strength (6.44 [0.34] vs 4.01 [0.29] μg/mg wet tissue and 280.12 [14.38] vs 175.82 [18.73] g/cm2; both, P < 0.001). Wound tensile strength in the L-NIO group was not significantly different from that in the control group. A significant difference was observed between the L-NIO and L-NAME groups in wound tensile strength (280.12 [14.38] vs 241.38 [20.69] g/cm2; P = 0.001), but not in tissue hydroxyproline levels. Conclusion: Inhibition of NO synthesis might improve wound tensile strength, which suggests a possible role for NO inhibitors in improved wound healing in the presence of endotoxemia. © 2006 Excerpta Medica, Inc.

In this study, the effects of BQ123 (an ET A receptor antagonist), bosentan (a nonselective ET A -ET B antagonist), and phosphoramidon (an endothelin converting enzyme inhibitor) were investigated on intestinal mucosal lesion formation and changes in tissue PGE 2 and LTC 4 levels due to intestinal ischemia-reperfusion (I/R) injury in rats. Following 30 min of ischemia, the substances were given via the inferior caval vein, and 10 min later the intestine was subjected to reperfusion for 30 min. The intestinal specimens were evaluated both microscopically and the tissue PGE 2 and LTC 4 levels were obtained for each group. The histopathologic examination revealed a significant reduction in tissue injury in both BQ123 and phosphoramidon pretreated groups compared with the control group. Bosentan, on the contrary, did not decrease the injury. The pharmacologic examination revealed a significant reduction of PGE 2 -like activity in both BQ123 and phosphoramidon pretreated groups, compared with the control group, while LTC 4 -like activity remained unchanged except for an increase in the bosentan pretreated group.

The effects of ZK 36374, a prostacyclin analogue and UK 38485, a thromboxane synthetase inhibitor were studied in guinea pigs after performing mesenteric arterial occlusion. In this study, while ZK 36374 significantly lowered the alkaline phosphatase and creatine phosphokinase values two hours after mesenteric arterial occlusion when compared with the control group (p less than 0.005), UK 38485 did not induce any change. In guinea pigs, when given together, ZK 36374 and UK 38485 lowered the enzyme levels to preligation values and the difference was nonsignificant (p greater than 0.1). The histopathologic investigation of the small intestine after giving ZK 36374 and UK 38345 together revealed minimal changes. These findings stress the importance of preserving the PGI2 levels in the PGI2/TXA2 ratio in preventing the increase of lysosomal enzyme levels and histopathologic changes after mesenteric arterial occlusion in guinea pigs.

To assess the effects of microvascular temporary clip application on vessel relaxing capability and endothelial substance release, the carotid rings of rats clipped for various durations were studied via bioassay. Noradrenaline and phenylephrine produced an immediate contraction and subsequent relaxation that failed to be suppressed by lysine acetylsalicylate or nicotine in the controls and in the arteries clipped for 0.5, 1, and 5 minutes; however, this relaxation was greatly reduced when the duration was 10 minutes. The results suggest the possible role of inadequate endothelium-derived relaxing factor release following prolonged application of the clips.