Orofacial skin inflammation increases the number of macrophages in the maxillary subregion of the rat trigeminal ganglion in a corticosteroid-reversible manner.

Inflammation of the cutaneous orofacial tissue can lead to a prolonged alteration of neuronal and nonneuronal cellular functions in trigeminal nociceptive pathways. In this study, we investigated the effects of experimentally induced skin inflammation by dithranol (anthralin) on macrophage activation in the rat trigeminal ganglion. Tissue localization and protein expression levels of ionized calcium-binding adaptor molecule 1 (Iba1), a macrophage/microglia-specific marker, and proliferation/mitotic marker antigen identified by the monoclonal antibody Ki67 (Ki67), were quantitatively analyzed using immunohistochemistry and western blots in control, dithranol-treated, dithranol- and corticosteroid-treated, and corticosteroid-treated trigeminal ganglia. Chronic orofacial dithranol treatment elicited a strong pro-inflammatory effect in the ipsilateral trigeminal ganglion. Indeed, daily dithranol treatment of the orofacial skin for 3-5 days increased the number of macrophages and Iba1 protein expression in the maxillary subregion of the ipsilateral ganglion. In the affected ganglia, none of the Iba1-positive cells expressed Ki67. This absence of mitotically active cells suggested that the accumulation of macrophages in the ganglion was not the result of resident microglia proliferation but rather the extravasation of hematogenous monocytes from the periphery. Subsequently, when a 5-day-long anti-inflammatory corticosteroid therapy was employed on the previously dithranol-treated orofacial skin, Iba1 immunoreactivity was substantially reduced in the ipsilateral ganglion. Collectively, our findings indicate that both peripheral inflammation and subsequent anti-inflammatory therapy affect macrophage activity and thus interfere with the functioning of the affected sensory ganglion neurons.

Determination of frail state and association of frailty with inflammatory markers among cardiac surgery patients in a Central European patient population.

INTRODUCTION: With the aging of the population, the screening of frail patients, especially before high-risk surgery, come to the fore. The background of the frail state is not totally clear, most likely inflammatory processes are involved in the development. METHODS: Our survey of patients over age of 65 who were on cardiac surgery were performed with Edmonton Frail Scale (EFS). Patients' demographic, perioperative data, incidence of complications and correlations of inflammatory laboratory parameters were studied with the severity of the frail state. RESULTS: On the basis of EFS, 313 patients were divided into non-frail (NF,163,52%), pre-frail (PF,89,28.5%) and frail (F,61,19.5%) groups. Number of complications in the three groups were different (NF:0.67/patient, PF:0.76/patient, F:1.08/patient). We showed significant difference between NF and F in both intensive care and hospital stay, but there was no statistical difference between the groups in hospital deaths (NF:5/163, PF:3/89, F:5/61). We also found a significant difference between NF and F patients in preoperative fibrinogen-, CRP- and white blood cell count levels. CONCLUSIONS: We first present the incidence of frailty in patients with heart surgery in a Central-European population. According to our results, inflammatory processes are likely to play a role in the development of the frail state.

Characterization of lymphocyte subpopulations and cardiovascular markers in pericardial fluid of cardiac surgery patients.

BACKGROUND: Composition of pericardial fluid (PF) may reveal immunological processes influencing oxidative stress and microcirculation of different tissues of the heart and may play a role in the course of myocardial infarction, atherosclerosis, and aortic stenosis. PATIENTS AND METHODS: We investigated lymphocyte populations, cardiovascular markers and immunoglobulin composition in PF and blood samples of patients undergoing CABG operation and compared them to those who had aortic valve surgery. RESULTS: The amount of CD8 + T, NK, memoT and activated T-cytotoxic cells were elevated in PF compared to blood, but naiveT and activated T-helper cell ratio were lower in PF. Amount of activated T-helper cells and regulatory T-lymphocytes were elevated in CABG participants in both PF and blood. INKT cells represented the only regulatory lymphocyte population reaching significantly higher concentration in PF than in blood. IL-6 and MCP1 level were elevated in PF compared to blood and MCP1 plasma level was markedly elevated in CABG group. CONCLUSIONS: Our study describes a comprehensive immunological analysis of PF in humans for the first time. We showed that the investigated lymphocyte populations and cardiovascular markers in PF have significantly different distribution compared to blood, and lymphocyte populations show different compartmentization in coronary disease and aortic stenosis.

Protective Effect of PACAP on Ischemia/Reperfusion-Induced Kidney Injury of Male and Female Rats: Gender Differences.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide that exerts general cytoprotective effects, including protection in different kidney disorders. The aim of our study was to investigate the ischemia/reperfusion-induced kidney injury of male and female rats to confirm the protective effects of PACAP in the kidney and to reveal possible gender differences.Male and female Wistar rats underwent unilateral renal artery clamping followed by 24-h, 48-h, or 14-day reperfusion. PACAP was administered intravenously before arterial clamping in half of the rats. Tubular damage, cytokine expression pattern, oxidative stress marker, antioxidative status and signaling pathways were evaluated using histology, immunohistology, cytokine array, PCR, and Western blot. Tubular damage was significantly less severe in the PACAP-treated male and female rats compared to controls. Results of female animals were significantly better in both treated and untreated groups. Cytokine expression, oxidative stress marker and antioxidative status confirmed the histological results. We also revealed that PACAP counteracted the decreased PKA phosphorylation, influenced the expression of BMP2 and BMP4, and increased the expression of the protein Smad1.We conclude that PACAP is protective in ischemia/reperfusion-induced kidney injury in both sexes, but females had markedly less pronounced injury after ischemia/reperfusion, possibly also involving further protective factors, the investigation of which could have future therapeutic value in treating ischemic kidney injuries.

Gastroesophageal Reflux Disease Might Induce Certain-Supposedly Adaptive-Changes in the Esophagus: A Hypothesis.

BACKGROUND: The increasing prevalence of GERD has become a major concern due to its major health and economic impacts. Beyond the typical unpleasant symptoms, reflux can also be the source of severe, potentially life-threatening complications, such as aspiration. AIM: Our aim was to support our hypothesis that the human body may in some cases develop various protective mechanisms to prevent these conditions. METHODS: Based on our experiences and review of the literature, we investigated the potential adaptive nature of seven reflux complications (hypertensive lower esophageal sphincter, achalasia, hypertensive upper esophageal sphincter, Zenker's diverticulum, Schatzki's ring, esophageal web, and Barrett's esophagus). RESULTS: Patients with progressive GERD may develop diverse structural and functional esophageal changes that narrow the lumen of the esophagus and therefore reduce the risk of regurgitation and protect the upper aerodigestive tract from aspiration. The functional changes (hypertensive lower esophageal sphincter, achalasia, hypertensive upper esophageal sphincter) seem to be adaptive reactions aimed at easing the unpleasant symptoms and reducing acid regurgitation. The structural changes (Schatzki's ring, esophageal web) result in very similar outcomes, but we consider these are rather secondary consequences and not real adaptive mechanisms. Barrett's esophagus is a special form of adaptive protection. In these cases, patients report significant relief of their previous heartburn as Barrett's esophagus develops because of the replacement of the normal squamous epithelium of the esophagus by acid-resistant metaplastic epithelium. CONCLUSION: We believe that GERD may induce different self-protective reactions in the esophagus that result in reduced acid regurgitation or decreased reflux symptoms.

Chronic adriamycin treatment impairs CGRP-mediated functions of meningeal sensory nerves.

Adriamycin is a potent anthracycline-type antitumor agent, but it also exerts potentially serious side effects due to its cardiotoxic and neurotoxic propensity. Multiple impairments in sensory nerve functions have been recently reported in various rat models. The present experiments were initiated in an attempt to reveal adriamycin-induced changes in sensory effector functions of chemosensitive meningeal afferents. Meningeal blood flow was measured with laser Doppler flowmetry in the parietal dura mater of adult male Wistar rats. The dura mater was repeatedly stimulated by topical applications of capsaicin, a transient receptor potential vanilloid 1 (TRPV1) receptor agonist, or acrolein, a transient receptor potential ankyrin 1 (TRPA1) receptor agonist, which induce the release of calcitonin gene-related peptide (CGRP) from meningeal afferents. The blood flow increasing effects of CGRP, histamine, acetylcholine and forskolin were also measured. Capsaicin- and acrolein-induced CGRP release was measured with enzyme-linked immunoassay in an ex vivo dura mater preparation. TRPV1 content of trigeminal ganglia and TRPV1-, CGRP- and CGRP receptor component-immunoreactive structures were examined in dura mater samples obtained from control and adriamycin-treated rats. The vasodilator effects of capsaicin, acrolein and CGRP were significantly reduced in adriamycin-treated animals while histamine-, acetylcholine- and forskolin-induced vasodilatation were unaffected. Measurements of CGRP release in an ex vivo dura mater preparation revealed an altered dynamic upon repeated stimulations of TRPV1 and TRPA1 receptors. In whole-mount dura mater preparations immunohistochemistry revealed altered CGRP receptor component protein (RCP)-immunoreactivity in adriamycin-treated animals, while CGRP receptor activity modifying protein (RAMP1)-, TRPV1- and CGRP-immunostaining were left apparently unaltered. Adriamycin-treatment slightly reduced TRPV1 protein content of trigeminal ganglia. The present findings demonstrate that adriamycin-treatment alters the function of the trigeminovascular system leading to reduced meningeal sensory neurogenic vasodilatation that may affect the local regulatory and protective mechanisms of chemosensitive afferents leading to alterations in tissue integrity.

Pneumoperitoneum induced ischemia-reperfusion injury of the peritoneum - Preconditioning may reduce the negative side-effects caused by carbon-dioxide pneumoperitoneum - Pilot study.

INTRODUCTION: Laparoscopy is more beneficial than the conventional open technique, however the pneumoperitoneum created may have an ischemic side effect. OBJECTIVE: Our aim was to evaluate the protective effects of preconditioning during laparoscopic cholecystectomies (LC). METHODS: 30 patients were randomized into 2 groups: I. PreC (preconditioning: 5 min. inflation, 5 min. deflation, followed by conventional LC), II: LC (conventional LC). Blood samples were taken before hospitalization (C = control), before surgery, after anaesthesia (B.S.), after surgery (A.S.) and 24 hours after the procedure (24 h). Measured parameters were: malondialdehyde (MDA), reduced glutathione (GSH), sulfhydril groups (-SH), superoxide-dismutase (SOD), catalase (CAT), myeloperoxidase (MPO), length of hospitalization and pain (VAS = visual analogue scale). RESULTS: Compared to the BS levels, no significant changes were detected in SOD's activity and MDA levels. GSH concentrations were significantly increased in the PreC group after operation. SH-, MPO, CAT and liver function enzymes were not significantly different. Hospitalization was shorter in the PreC group. Based on the VAS score patients had less pain in the PreC group. CONCLUSION: Significant differences concerning PreC group were found in GSH values. In the PreC group pain decreased by 2-2.5 units following the procedure, 24 h after surgery, and hospitalisation was also significantly shorter. In our pilot study the potential protective effect of preconditioning could be defined.

The role of GST polymorphism in reperfusion induced oxidative stress, inflammatory responses and clinical complications after surgical and percutaneous coronary intervention.

BACKGROUND: Patients having coronary artery disease treated by coronary bypass or PCI procedure are exposed to tissue damage because of the phenomenon called reperfusion injury. Reperfusion injury can be characterized/monitored by oxidative stress parameters, inflammatory markers and by post-operative complication rate. OBJECTIVE: Beyond the obvious factors determining its severity (affected myocardial mass, ischaemic time, collateral circulation etc.) we examined the GST enzyme group's most cardio selective member, GSTP1 and its genetic polymorphism if there is any genetically determined preventive effect on the above-mentioned parameters. MATERIALS AND METHODES: We have performed randomized prospective study in the Heart Institute of Pecs with 862 patients, treated by coronary bypass or PCI procedure. Blood samples were taken a day before, one hour, one day, one week after the operation. Leucocyte count (WBC), myeloperoxidase (MPO), thiol group (SH); Superoxide dismutase (SOD), malondialdehyde (MDA), reduced Glutathione (GSH) level was checked in different periods of time as a comparison. The onset of myocardial damage and the corresponding necro enzyme level changes were registered in the perioperative period. Our patient's GSTP1 allele pair combinations (A, B, or C) were determined by real time PCR method. RESULTS: In patients with GSTP1 AA genotype we have found significance level reaching plasma concentration rise in SOD and MDA, and drop in GSH, SH. The CKMB concentration rise in the post-operative 24 hours was significantly higher in the GSTP1 AA group. CONCLUSIONS: According to our results the AA allele combination can be considered as a risk factor. GSTP1-AA allele pair has negative effect on ischemia-reperfusion tolerance of the heart. In case of cardiovascular interventions, the study of GST enzyme polymorphisms can be an independent risk stratification factor in determining the perioperative risk in the future.

Diet-Induced Obesity Enhances TRPV1-Mediated Neurovascular Reactions in the Dura Mater.

OBJECTIVE: Exploring the pathophysiological changes in transient receptor potential vanilloid 1 (TRPV1) receptor of the trigeminovascular system in high-fat, high-sucrose (HFHS) diet-induced obesity of experimental animals. BACKGROUND: Clinical and experimental observations suggest a link between obesity and migraine. Accumulating evidence indicates that metabolic and immunological alterations associated with obesity may potentially modulate trigeminovascular functions. A possible target for obesity-induced pathophysiological changes is the TRPV1/capsaicin receptor which is implicated in the pathomechanism of headaches in a complex way. METHODS: Male Sprague-Dawley rats were fed a regular (n = 25) or HFHS diet (n = 26) for 20 weeks. At the end of the dietary period, body weight of the animals was normally distributed in both groups and it was significantly higher in animals on HFHS diet. Therefore, experimental groups were regarded as control and HFHS diet-induced obese groups. Capsaicin-induced changes in meningeal blood flow and release of calcitonin gene-related peptide (CGRP) from dural trigeminal afferents were measured in control and obese rats. The distribution of TRPV1- and CGRP-immunoreactive meningeal sensory nerves was also compared in whole mount preparations of the dura mater. Metabolic parameters of the animals were assessed by examining glucose and insulin homeostasis as well as plasma cytokine concentrations. RESULTS: HFHS diet was accompanied by reduced food consumption and greater fluid and energy intakes in addition to increased body weight of the animals. HFHS diet increased fasting blood glucose and insulin concentrations as well as levels of circulating proinflammatory cytokines interleukin-1ß and interleukin-6. In obese animals, dural application of the archetypal TRPV1 agonist capsaicin resulted in significantly augmented vasodilatory and vasoconstrictor responses as compared to controls. Diet-induced obesity was also associated with enhanced basal and capsaicin-induced CGRP release from meningeal afferents ex vivo. Except for minor morphological changes, the distribution of dural TRPV1- and CGRP-immunoreactive afferents was similar in control and obese animals. CONCLUSIONS: Our results suggest that obesity induced by long-term HFHS diet results in sensitization of the trigeminovascular system. Changes in TRPV1-mediated vascular reactions and CGRP release are pathophysiological alterations that may be of relevance to the enhanced headache susceptibility of obese individuals.

Pentoxifylline attenuates the local and systemic inflammatory response after infrarenal abdominal aortic ischemia-reperfusion.

AIMS: We studied the new anti-inflammatory effects of non-specific phosphodiesterase (PDE) inhibitor pentoxifylline (PTX) on ischaemia-reperfusion injury and postconditioning of the lower extremities. We aimed to examine the oxidative stress parameters (OSP), the inflammatory response and the changes in structure of skeletal muscle after revascularization surgery. METHODS: 50 Wistar rats in five groups underwent a 60 min infrarenal aortic cross clamping. After the ischaemia in IR+PC group ischemic postconditioning was performed, intermittent 15 seconds reperfusion, 15 seconds ischaemic periods were applied four times. The ischemic phase was followed by a 120 min of reperfusion. In IR+PTX group the animals were treated with PTX. In IR+PC+PTX group both ischemic postconditioning and PTX treatment were performed. Blood samples and biopsy from quadriceps muscle were collected. Plasma malondialdehyde, reduced glutathione, -SH-groups, TNF-alpha, IL-6 concentrations and superoxide dismutase enzyme activity were measured. RESULTS: The levels of OSP and the inflammatory proteins were significantly higher in the IR group. PTX treatment and PC could significantly decrease the levels of OSP and inflammatory proteins. When the animals were co-treated with PTX and PC the results were even better. CONCLUSIONS: Inhibition of PDE by PTX could markedly decrease the inflammatory response and moderate the ischaemia-reperfusion damages after lower limb ischemia and reperfusion. Administration of PTX could potentiate the beneficial effects of PC.

Sodium Pentosan Polysulfate Reduced Renal Ischemia-Reperfusion-Induced Oxidative Stress and Inflammatory Responses in an Experimental Animal Model.

Acute kidney injury (AKI) remains an independent risk factor for mortality and morbidity after vascular surgery (affecting the renal arteries) or aortic surgery (requiring suprarenal aortic clamping). These types of vascular surgery produce renal ischemia/reperfusion (I/R) injury, a common cause of AKI. The present studies aimed at monitoring the course of renal I/R injury at the cellular level and investigating the efficacy of long-term preoperative and single-shot intraoperative administration of sodium pentosan polysulfate (PPS) to protect renal tissue from acute I/R injury both in native and diabetic kidneys in rats. Western blot analyses of the proapoptotic (bax) and antiapoptotic (bcl-2) signaling pathways, as well as the extent of DNA damage (phospho-p53), were performed. Oxidative stress followed upon the termination of malondialdehyde, reduced glutathione, thiol group, and superoxide dismutase plasma levels. Inflammatory changes were measured by the determination of serum tumor necrosis factor-α and interleukin-1 levels. Morphological changes were detected by histological examinations. Our results showed that the long-term administration of PPS has an advantage in reducing I/R kidney injury in diabetic rats, while high-dose, single-shot parenteral administration of PPS prior to revascularization might be useful in nondiabetic rats.

Multiple impairments of cutaneous nociceptor function induced by cardiotoxic doses of Adriamycin in the rat.

Besides their deleterious action on cardiac muscle, anthracycline-type cytostatic agents exert significant neurotoxic effects on primary sensory neurons. Since cardiac sensory nerves confer protective effects on heart muscle and share common traits with cutaneous chemosensitive nerves, this study examined the effects of cardiotoxic doses of adriamycin on the function and morphology of epidermal nerves. Sensory neurogenic vasodilatation, plasma extravasation, and the neural CGRP release evoked by TRPV1 and TRPA1 agonists in vitro were examined by using laser Doppler flowmetry, the Evans blue technique, and ELISA, respectively. Carrageenan-induced hyperalgesia was assessed with the Hargreaves method. Immunohistochemistry was utilized to study cutaneous innervation. Adriamycin treatment resulted in profound reductions in the cutaneous neurogenic sensory vasodilatation and plasma extravasation evoked by the TRPV1 and TRPA1 agonists capsaicin and mustard oil, respectively. The in vitro capsaicin-, but not high potassium-evoked neural release of the major sensory neuropeptide, CGRP, was markedly attenuated after adriamycin treatment. Carrageenan-induced inflammatory hyperalgesia was largely abolished following the administration of adriamycin. Immunohistochemistry revealed a substantial loss of epidermal TRPV1-expressing nociceptive nerves and a marked thinning of the epidermis. These findings indicate impairments in the functions of TRPV1 and TRPA1 receptors expressed on cutaneous chemosensitive nociceptive nerves and the loss of epidermal axons following the administration of cardiotoxic doses of adriamycin. Monitoring of the cutaneous nociceptor function in the course of adriamycin therapy may well be of predictive value for early detection of the deterioration of cardiac nerves which confer protection against the deleterious effects of the drug.

[New approach in the surgical treatment of mitral regurgitation: beating heart transapical neochord implantation]. / A mitralis elégtelenség sebészi kezelésének új megközelítése: transapicalis ínhúrpótlás dobogó szíven.

Severe mitral regurgitation due to prolapse of the valve demands early surgical intervention. Recently artificial chord implantation is the prefered solution, which requires cardioplegia and application of cardiopulmonary bypass using the left atrial approach. Transoesophageal echocardiography guided transapical neochord implantation is an emerging new technique for the treatment of mitral regurgitation. It enables the operation through left minithoracotomy on beating heart using a special instrument introduced into the left ventricle. Acute procedural success rates in different centres vary between 86 and 100%. According to reports, 92% of the patients do not require additional intervention at the 3-month follow-up. Continuous integration of data resulting improved outcomes supports the hope that this novel, less-invasive technique will be applied widely for the treatment of mitral regurgitation.

Laparoszkópos hiatushernia-rekonstrukciót követo intraoesophagealis hálómigráció.

CASE PRESENTATION: The authors report the case of a 68-year-old patient who presented with dysphagia 4 months after a mesh-reinforced antireflux surgery. Examinations revealed partial penetration of the mesh into the esophagus. During an expedited surgery, the mesh was removed through thoraco-laparotomy. Distal esophagus and proximal gastric resections were carried out due to longitudinal perforation site and esophageal stricture, and the continuity of the alimentary tract was restored with jejunal interposition. At the 3-month follow-up visit the patient was asymptomatic and a swallow examination showed normal conditions after the surgery. DISCUSSION: Several studies have shown that primary closure of large hiatal hernias is associated with high recurrence rate. In order to reduce this ratio, mesh reinforcement of the crural repair was introduced to prevent reherniation. Therefore, the incidence of recurrence has indeed decreased, however, mesh-related complications have increased. Because of the special anatomical site, the mesh around the gastroesophageal junction is in continuous movement and this can potentially lead to complications such as esophageal erosion, perforation or extensive fibrosis and stenosis. These complications may cause severe, even life-threatening conditions that could only be treated with difficult surgeries. Based on the experience of our case and the review of the literature, we would like to highlight one of the potential, serious complications of mesh-reinforced hiatal repair.

Inhibition of Glutathione S-Transferase by Ethacrynic Acid Augments Ischemia-Reperfusion Damage and Apoptosis and Attenuates the Positive Effect of Ischemic Postconditioning in a Bilateral Acute Hindlimb Ischemia Rat Model.

AIMS: We studied the effects of the inhibition of the endogene antioxidant glutathione-S-transferase (GST) by ethacrynic acid (EA) on ischemia-reperfusion (IR) injury and postconditioning (PC) in the lower extremities. We aimed to examine the oxidative stress parameters (OSP), inflammatory response and activation of proapoptotic signaling proteins (PSP) after revascularization surgery. METHODS: Sixty Wistar rats were divided into 6 groups: control, IR, PC, EA-control, IR and administration of EA (IR/EA) and PC and administration of EA (PC/EA). The IR, PC, IR/EA and PC/EA groups underwent 60 min of infrarenal aortic cross-clamping. After that, PC was performed in the PC and PC/EA groups. In 3 of the groups, the animals were treated with EA (EA-control, IR/EA and PC/EA groups) as well. The ischemia was followed by 120 min of reperfusion. Blood samples and biopsy specimens were collected from the quadriceps muscle. Plasma malondialdehyde, reduced glutathione, thiol/sulfhydryl group levels, TNF-α and IL-6 concentrations and superoxide-dismutase enzyme activity were measured. RESULTS: The levels of the OSP and the inflammatory proteins were higher in the EA-administered groups. The ratio of phosphorylated PSP was higher in the EA-administered groups and the protective effect of PC did not develop. CONCLUSIONS: Inhibition of GST by EA augmented the IR damage. GST inhibition was associated with a different activation of the mitogen-activated protein kinases and the PSP, regulating these pathways in the process of apoptosis and PC.

[Dilemmas of the reconstruction of the major pelvic artery due to infectious aortic graft complication]. / A medencei veroér helyreállításának dilemmái szeptikus aortagraft esete kapcsán.

INTRODUCTION: In the pelvic region thrombendarterectomy and bypass procedures are the most commonly performed procedures to treat peripheral artery occlusive diseases with chronic, severe circulation failure caused by atherosclerosis. Biologic and synthetic grafts can also be used in bypass surgeries. Application of synthetic grafts can acutely increase the development of the infectious graft complication and its mortality is still between 70 and 75% in pelvic processes. We describe the difficulties and dilemmas of an infectious aortobifemoral graft. CASE PRESENTATION: 58-year-old female patient with right lower limb trophic ulcer underwent a DSA examination showing a bilateral iliac occlusion and aortobifemoral bypass surgery with Dacron graft implantation was performed. Re-occlusion and infection of the graft led to an in situ silver Dacron graft replacement. Due to the one-sided re-occlusion, a femoro-femoral crossover bypass surgery applying silver graft was performed. Despite the previously described procedures the infectious process got worse and autologous deep vein reconstruction was required beside the removal of the infectious synthetic grafts at the same time. DISCUSSION: There are local and extraanatomical solutions to reduce infectious graft complication. In pelvic infections bypass surgeries using autologous deep vein can show the best results. This procedure is the trustworthiest but also the most straining technique due to the extension of surgical time and increased blood loss. The proper surgical strategy should be selected on individual bases including cardiopulmonary load ability, patient age and technical/infrastructural possibilities.

Molecular mechanisms underlying the Nephroprotective effects of PACAP in diabetes.

Diabetic nephropathy is the leading cause of end-stage renal failure and accounts for 30-40 % of patients entering renal transplant programmes. The nephroprotective effects of the neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP38) against diabetes have been shown previously, but the molecular mechanisms responsible for these effects remain unknown. In the present study, we showed that PACAP treatment counteracted the diabetes-induced increase in the level of the proapoptotic pp38MAPK and cleaved caspase-3 and also decreased the p60 subunit of NFκB. The examined antiapoptotic factors, including pAkt and pERK1/2, showed a slight increase in the diabetic kidneys, while PACAP treatment resulted in a notable elevation of these proteins. PCR and Western blot revealed the downregulation of fibrotic markers, like collagen IV and TGF-ß1 in the kidney. PACAP treatment resulted in increased expression of the antioxidant glutathione. We conclude that the nephroprotective effect of PACAP in diabetes is, at least partly, due to its antiapoptotic, antifibrotic and antioxidative effect in addition to the previously described antiinflammatory effect.

Polymorphisms in glutathione S-transferase are risk factors for perioperative acute myocardial infarction after cardiac surgery: a preliminary study.

In the present study we explored glutathione S-transferase (GST) polymorphisms in selected patients who experienced accelerated myocardial injury following open heart surgery and compared these to a control group of patients without postoperative complications. 758 Patients were enrolled from which 132 patients were selected to genotype analysis according to exclusion criteria. Patients were divided into the following groups: Group I: control patients (n = 78) without and Group II.: study patients (n = 54) with evidence of perioperative myocardial infarction. Genotyping for GSTP1 A (Ile105Ile/Ala113Ala), B (Ile105Val/Ala113Ala) and C (Ile105Val/Ala113Val) alleles was performed by using real-time-PCR. The heterozygous AC allele was nearly three times elevated (18.5 vs. 7.7 %) in the patients who suffered postoperative myocardial infarction compared to controls. Contrary, we found allele frequency of 14.1 % for homozygous BB allele in the control group whereas no such allele combination was present in the study group. These preliminary results may suggest the protective role for the B and C alleles during myocardial oxidative stress whereas the A allele may represent predisposing risk for cellular injury in patients undergoing cardiac surgery.

[Endovascular treatment of subclavian artery pseudoaneurysm as a delayed complication after surgery for aorto-bifemoral graft infection]. / Aortobifemoralis graft gennyedés megoldásának kései szövodményeként jelentkezo subclavia álaneurysma endovascularis kezelése.

CASE REPORT: In this article we present a relatively rare vascular surgical complication and an uncommon treatment of it. In this case we used an aorto-bifemoral bypass on a patient with Leriche syndrome. The implanted Y-graft got infected and we were forced to remove it. Having inserted the abdominal aortic graft, an axillobifemoral bypass was also applied to secure the circulation of the lower limbs. However, the graft occluded later on, and 37 months after the inital surgery a rather large pseudoaneurysm developed at the origin of the graft in the right subclavian artery. Another surgical intervention was indicated to prevent embolisation, rupture and compression. Instead of the conventional surgical method (resection, interposition) we did an endovascular procedure. We removed the false aneurysm by inserting a covered stent, using catheter technique, into the right brachial artery and therefore prevented the previously mentioned complications. DISCUSSION: This minimal invasive method is very useful for high risk patients to prevent the injury of neighbouring anatomical structures in the region as well as minimize blood loss and potential complications of long term anaesthesia when open surgery is done.

[Pathology and diagnostic opportunities of lower limb compartment syndrome]. / Az alsó végtagi compartment-syndroma kórtana és diagnosztikai lehetoségei.

BACKGROUND: The indication for the surgical treatment of lower limb compartment syndrome mostly depends on the clinical signs, which can be uncertain and often delayed, resulting in a late and insufficient intervention. AIM: In this study, the progression of compartment syndrome was monitored with the measurement of intracompartmental pressure and tissue oxygen saturation. MATERIALS AND METHODS: 16 patients (12 male and 4 female; mean age: 62,7 years) underwent acute lower limb revascularization surgery due to critical (more than 4 hour) limb ischaemia. The indications were the following: 5 iliac artery embolisms and 11 femoral artery occlusions. After revascularization, significant lower limb oedema and swelling were detected. To monitor the elevated intracompartmental pressure (ICP), KODIAG pressure meter was used. Tissue oxygen saturation (StO2) was measured with near-infrared-spectroscopy. RESULTS: In 12 cases the IPC exceeded the critical 40 mmHg. In these patients, StO2 was 50-53%, in spite of the successful re-canalisation. An urgent, semi-open fasciotomy was performed in these cases. In four patients, the clinical picture suggested compartment syndrome. However, the measured parameters did not indicate surgical intervention (ICP: 25-35 mmHg, StO2: normal). SUMMARY: In addition to the empirical guidelines, we describe an evidence based surgical intervention strategy for lower limb compartment syndrome. Our results and advised parameter intervals help the clinicians to decide between conservative and operative treatment of the disease.