Search

Objective: We compare the cardioprotective effects of anesthetic preconditioning by propofol and/or isoflurane in rats with ischemia-reperfusion injury. Methods: Male adult Wistar rats were subjected to 60 min of anterior descending coronary artery occlusion followed by 120 min of reperfusion. Before the long ischemia, anesthetics were administered twice for 10 min followed by 5 min washout. Isoflurane was inhaled at 1 MAC (0.016) in I group, whereas propofol was inhaled intravenously at 37.5 mg/(kg·h) in P group. A combination of isoflurane and propofol was administered simultaneously in I+P group. Results: In control (without anesthetic preconditioning, C group), remarkable myocardial infarction and apoptosis accompanied by an increased level of cardiac troponin T were noted 120 min after ischemia-reperfusion. As compared to those of control group, I and P groups had comparable cardioprotection. In addition, I+P group shares with I and P groups the comparable cardioprotective effects in terms of myocardial infarction and cardiac troponin T elevation. Conclusion: A combination of isoflurane and propofol produced no additional cardioprotection.

To investigate the efficacy and safety of the corpus cavernosum-corpus spongiosum shunt (Al-Ghorab Shunt) plus intracavernous tunneling (CC-CSS+ICT) for prolonged ischemic priapism (PIP). Twelve patients with PIP were enrolled in this study. The mean age of patients was 38.3 ± 9.2 years old and the mean duration of PIP was 2.8 ± 1.0 days (range, 1.5-4 days). All patients received CC-CSS+ICT for treating PIP. The penile hardness score (PHS) and pain visual analogue score (PVAS) were used to assess the efficacy of the surgery 1, 3, and 5 days after surgery. Color duplex Doppler ultrasonography, International Index of Erectile Function, and quality of life (QOL) were used for evaluating penile morphology, erectile function, QOL, and response to sildenafil treatment. The mean duration of follow up was 21.6 ± 10.1 months. Penile detumescence was successfully restored for all 12 patients postsurgery, with the mean PHS and PVAS significantly decreased compared with that presurgery at different time points (1, 3, 5 days postsurgery; P < .001). The cavernosal arterial blood flow observed with the mean PSV at 1, 3, and 5 days postoperation were 17.79 ± 2.04, 19.14 ± 1.58, and 7.73 ± 2.02 cm/s respectively. All patients suffered from corpus cavernosum fibrosis and erectile dysfunction postoperation; only 2 cases (16.7%) with a short duration of PIP (1.5 days) showed response to sildenafil treatment, and 3 cases (25.0%) with severe fibrosis were satisfied with sexual life after excision of penile corpus cavernosum scar and penile prosthesis implantation. The CC-CSS+ICT could quickly reduce penile rigidity and pain for improving the symptoms of PIP and suggests a safe and effective therapeutic method for PIP.

We have studied the forms of cell death following ischemia/reperfusion, and the influence of diabetes mellitus (DM) as an additional factor. Based on the models of diabetes and middle cerebral artery occlusion (MCAO), characteristics of cell death after ischemia/reperfusion were evaluated synthetically by different methods: pathology, FCM, TUNEL and DNA agarose electrophoresis. The results showed that the occurrence of cerebral injury after ischemia/reperfusion was accompanied by cell necrosis and cell apoptosis. Cell apoptosis was mainly located in the ischemic penumbral (IP) zone around the densely ischemic focus. The ischemic core was characterized by cell necrosis. At the same time, the results showed that the process of ischemic cerebral injury worsened by DM was related to inducing cell apoptosis in IP and mid zone. In conclusion, there existed not only cell apoptosis but cell necrosis in brain damage following focal cerebral ischemia/reperfusion and showed a close, internal relationship between them. Brain damage following cerebral ischemia/reperfusion was worsened distinctly under diabetic conditions.

Objectives To examine whether Pitavastatin Preconditioning could effectively reduce ischaemia/reperfusion injury (IRI) and the underlying mechanisms involved. Methods Ligated the anterior descending coronary artery for 30 minutes and then loosen the ligation for 1 hour to establish ischaemia/reperfusion model in mice. A potent 3-hydroxy-3-methylglutaryl-coenzyme A reductase, pitavastatin was given to the mice as a single dose (5 mg/kg or 10 mg/kg) by gavage 1 hour before reperfusion. Animals were divided into 5 groups (control group, ischaemia group, ischaemia/reperfusion group, pitavastatin 5mg groups and pitavastain 10 mg group). Extravasated Evans blue dye measured by spectrophotometry 30 minutes after reperfusion to assess ischaemia/reperfusion injury (IRI)-induced vascular leakage. We introduced in vivo cryotechnique (IVCT), which immediately cryofixes beating heart tissue of living mice in situ , to measure the heart microvascular reperfusion situation. Results Pitavastatin Preconditioning prevented IRI-induced vascular leakage and improve microvascular blood reflow, decreased the LDH, CK-MB, CRP and immflammatory factors expression (P Conclusions Our results demonstrated that Pitavastatin Preconditioning reduces Myocardium ischaemia/reperfusion injury through Microvascular protection: preventing microvascular endothelial cells dysfunction and improving Cx43 expression.

We report the first determination of lung endothelial barrier properties in ischemic, nonreperfused microvessels. We quantified the endothelial barrier in terms of hydraulic conductivity (Lp) in single pulmonary venules (diameter 20–50 microns) of isolated blood perfused lungs (dog, rat), held at constant inflation pressure (5 cmH2O) with a gas mixture containing 21% oxygen. Lp were determined by our split-drop technique in which an oil drop is first microinjected into a venule and then split by microinjection of a protein solution. Lp was interpreted from measurements of the rate of oil drop movement. Baseline Lp recorded in the first 30 min of perfusion averaged 3.4 +/- 0.9 x 10(-7) ml/(cm2.s.cmH2O). Then, in two separate groups of venules in which we established 1.3 +/- 0.1 h and 3.4 +/- 0.8 h of ischemia, we determined Lp which were, respectively, 145 +/- 6.5 and 308 +/- 13% above baseline (P < 0.05). We conclude that ischemia alone, in the absence of reperfusion, significantly deteriorates the lung endothelial barrier.

In order to find an objective criteria to determine ischemic intestinal necrosis and present the proof for intestinectomy by surgeons, the fluorescence spectrum on the normal and ischemic intestine, which were stimulated by N2-laser, was obtained. The intestine ischemic model was established in dogs by ligaturing the blood vessel of mesentery. The fluorescence spectrum was painted by enlarging its signals and inputing them into a computer control system. There is significant difference between normal and pathological tissue: the longer the ischemic duration of the intestine, the more severe its pathological changes and the lower its fluorescence peak. After 6 - 8 hours of ischemic duration going on and complete intestinal necrosis occurred, its fluorescence peak decreased from normal 1.96 - 2.41 to pathological 1. It seems that the laser fluorescence is a simple, quick, accurate, and non-invasive method which can be used in determinations of the ischemic intestinal necrosis.© (1993) COPYRIGHT SPIE--The International Society for Optical Engineering. Downloading of the abstract is permitted for personal use only.