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Günter Janetschek - One of the best experts on this subject based on the ideXlab platform.

  • PARTIAL NEPHRECTOMY USING RENAL ARTERY PERFUSION FOR Cold Ischemia: FUNCTIONAL AND ONCOLOGICAL OUTCOMES
    The Journal of Urology, 2008
    Co-Authors: Christophe Ghysel, Faisal Nassar, Avi Beri, Jean-baptiste Lattouf, Karl Leeb, Günter Janetschek
    Abstract:

    Purpose: We present our series on the safety and long-term oncologic and functional outcomes of laparoscopic partial nephrectomy using renal artery perfusion for Cold Ischemia. Patients and Methods: Of 94 patients who underwent laparoscopic partial nephrectomy at our center between August 2000 and September 2006, 28 procedures were performed using Cold Ischemia and are included in this review. Mean age was 57.8 years (range 22–80 yrs). Mean tumor size was 2.67 cm (range 1.5–5 cm). Five patients had an imperative indication for partial nephrectomy. Eight tumors were hilar. Cold Ischemia was achieved through renal artery catheterization followed by intraoperative artery clamping and perfusion with 4°C lactated Ringer solution with mannitol. Results: Mean Ischemia time was 40.8 min (range 25–101 min). Mean estimated blood loss was 241 mL (range 50–1000 mL). Three patients underwent conversion to open surgery, but their procedures were still completed under Cold perfusion. Segmental artery penetration and ven...

  • Long-term functional outcome of renal units after laparoscopic nephron-sparing surgery under Cold Ischemia.
    Journal of endourology, 2006
    Co-Authors: Firas Abukora, Karl Leeb, Nasser Albqami, Thiagarajan Nambirajan, Johann Ziegerhofer, Günter Janetschek
    Abstract:

    Background and Purpose: Renal-artery occlusion is used to control bleeding during laparoscopic nephronsparing surgery, but there are worries about ischemic damage. We compared the functional outcomes of kidneys treated under warm and Cold Ischemia. Patients and Methods: Twelve patients treated with warm Ischemia and 14 treated with Cold Ischemia had renal function investigation 3 to 6 months postoperatively. Four and ten patients, respectively, also had preoperative studies. Results: In patients treated with warm Ischemia, two kidneys had evidence of possible damage, but the kidney with the longest Ischemia (56 minutes) was normal. Among patients treated with Cold Ischemia, function was lost in one case. Parenchymal transit time was prolonged in five patients, but in four cases, this probably was attributable to performance of a contrast-enhanced CT scan the same day. In the fifth patient, an ischemic injury is possible. Conclusion: The parenchymal transit time is a good indicator of ischemic damage. Neph...

  • laparoscopic partial nephrectomy in Cold Ischemia renal artery perfusion
    The Journal of Urology, 2004
    Co-Authors: Günter Janetschek, Karl Leeb, Alaa Abdelmaksoud, Fariborz Bagheri, Hassan M Alzahrani, Manfred Gschwendtner
    Abstract:

    ABSTRACTPurpose: Laparoscopic partial nephrectomy represents a feasible option for patients with small renal masses. We describe our initial experience with laparoscopic partial nephrectomy in Cold Ischemia achieved by renal artery perfusion.Materials and Methods: From November 2001 to March 2003 laparoscopic partial nephrectomy in Cold Ischemia was performed in 15 patients with renal cell carcinoma. Cold Ischemia was achieved by continuous perfusion of Ringers lactate at 4C through the renal artery, which was clamped. Tumor excision was performed in a bloodless field with biopsy taken from the tumor bed. The collecting system was repaired if needed. Renal reconstruction was performed by suturing over hemostatic bolsters.Results: All procedures were successfully completed laparoscopically by our new technique. Mean operative time was 185 minutes (range 135 to 220). Mean Ischemia time was 40 minutes (range 27 to 101). Estimated mean intraoperative blood loss was 160 ml (range 30 to 650). Entry to the colle...

Walter Mark - One of the best experts on this subject based on the ideXlab platform.

  • Mitochondrial defects and heterogeneous cytochrome c release after cardiac Cold Ischemia and reperfusion.
    American journal of physiology. Heart and circulatory physiology, 2003
    Co-Authors: Andrey V. Kuznetsov, Stefan Schneeberger, Gerald Brandacher, Raimund Margreiter, Walter Mark, Rüdiger Seiler, Wolfgang Steurer, Valdur Saks, Yves Usson, Erich Gnaiger
    Abstract:

    Mitochondria play a critical role in myocardial Cold Ischemia-reperfusion (CIR) and induction of apoptosis. The nature and extent of mitochondrial defects and cytochrome c (Cyt c) release were dete...

  • Gene expression profiling of prolonged Cold Ischemia and reperfusion in murine heart transplants
    Transplantation, 2002
    Co-Authors: Albert Amberger, Stefan Schneeberger, Gerald Hernegger, Gerald Brandacher, Peter Obrist, Peter Lackner, Raimund Margreiter, Walter Mark
    Abstract:

    Background. Heart transplantation causes complex changes in the biological homeostasis of the graft. Current knowledge is restricted to a few genes and regulation of certain factors involved in Ischemia-reperfusion (I/R) injury. Efficient strategies to prevent I/R injury, however, require a better understanding of its mechanisms. Using cDNA microarrays, we investigated gene expression profiles of murine cardiac isografts. Methods. For microarray hybridization experiments, chips with 8,734 individual target sequences were used. Messenger RNA was extracted from hearts subjected to warm Ischemia and different time periods of reperfusion or to prolonged Cold Ischemia or warm Ischemia and transplantation. Native hearts served as controls. Results. A set of 68 sequences was regulated in all hearts. In addition, grafts without Cold Ischemia showed differential expression of 65 sequences, which were not found in hearts transplanted after Cold storage, and which in turn had 38 sequences regulated and not detected in grafts without Cold Ischemia. Overall, approximately 50% of regulated transcripts are expressed sequence tags (ESTs) with unknown function. Annotated genes encoded immune modulators (20% of sequences), receptor proteins, structural proteins, and proteins involved in metabolism. Conclusion. Our data demonstrate expression profiles of hearts subjected to prolonged Cold Ischemia or transplantation in an isogeneic setting. We have defined functional complexes and detected a substantial amount of ESTs encoding novel proteins. These studies may provide a molecular basis for further functional experiments and may help identify potential targets for modulation of postischemic inflammation.

Atsunori Nakao - One of the best experts on this subject based on the ideXlab platform.

  • amelioration of rat cardiac Cold Ischemia reperfusion injury with inhaled hydrogen or carbon monoxide or both
    Journal of Heart and Lung Transplantation, 2010
    Co-Authors: Atsunori Nakao, David J. Kaczorowski, Yinna Wang, Jon Cardinal, Bettina M. Buchholz, Ryujiro Sugimoto, Kimimasa Tobita, Sungsoo Lee, Yoshiya Toyoda, Timothy R. Billiar
    Abstract:

    Background Recent advances in novel medical gases, including hydrogen and carbon monoxide (CO), have demonstrated significant opportunities for therapeutic use. This study was designed to evaluate the effects of inhaled hydrogen or CO, or both, on Cold Ischemia/reperfusion (I/R) injury of the myocardium. Methods Syngeneic heterotopic heart transplantation was performed in rats after 6 or 18 hours of Cold Ischemia in Celsior solution. Survival, morphology, apoptosis and marker gene expression were assessed in the grafts after in vivo inhalation of hydrogen (1% to 3%), CO (50 to 250 ppm), both or neither. Both donors and recipients were treated for 1 hour before and 1 hour after reperfusion. Results After 6-hour Cold Ischemia, inhalation of hydrogen (>2%) or CO (250 ppm) alone attenuated myocardial injury. Prolonged Cold Ischemia for 18 hours resulted in severe myocardial injury, and treatment with hydrogen or CO alone failed to demonstrate significant protection. Dual treatment with hydrogen and CO significantly attenuated I/R graft injury, reducing the infarcted area and decreasing in serum troponin I and creatine phosphokinase (CPK). Hydrogen treatment alone significantly reduced malondialdehyde levels and serum high-mobility group box 1 protein levels as compared with air-treated controls. In contrast, CO only marginally prevented lipid peroxidation, but it suppressed I/R-induced mRNA upregulation for several pro-inflammatory mediators and reduced graft apoptosis. Conclusions Combined therapy with hydrogen and CO demonstrated enhanced therapeutic efficacy via both anti-oxidant and anti-inflammatory mechanisms, and may be a clinically feasible approach for preventing Cold I/R injury of the myocardium.

  • Amelioration of rat cardiac Cold Ischemia/reperfusion injury with inhaled hydrogen or carbon monoxide, or both.
    The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 2009
    Co-Authors: Atsunori Nakao, David J. Kaczorowski, Yinna Wang, Jon Cardinal, Bettina M. Buchholz, Ryujiro Sugimoto, Kimimasa Tobita, Sungsoo Lee, Yoshiya Toyoda, Timothy R. Billiar
    Abstract:

    Background Recent advances in novel medical gases, including hydrogen and carbon monoxide (CO), have demonstrated significant opportunities for therapeutic use. This study was designed to evaluate the effects of inhaled hydrogen or CO, or both, on Cold Ischemia/reperfusion (I/R) injury of the myocardium. Methods Syngeneic heterotopic heart transplantation was performed in rats after 6 or 18 hours of Cold Ischemia in Celsior solution. Survival, morphology, apoptosis and marker gene expression were assessed in the grafts after in vivo inhalation of hydrogen (1% to 3%), CO (50 to 250 ppm), both or neither. Both donors and recipients were treated for 1 hour before and 1 hour after reperfusion. Results After 6-hour Cold Ischemia, inhalation of hydrogen (>2%) or CO (250 ppm) alone attenuated myocardial injury. Prolonged Cold Ischemia for 18 hours resulted in severe myocardial injury, and treatment with hydrogen or CO alone failed to demonstrate significant protection. Dual treatment with hydrogen and CO significantly attenuated I/R graft injury, reducing the infarcted area and decreasing in serum troponin I and creatine phosphokinase (CPK). Hydrogen treatment alone significantly reduced malondialdehyde levels and serum high-mobility group box 1 protein levels as compared with air-treated controls. In contrast, CO only marginally prevented lipid peroxidation, but it suppressed I/R-induced mRNA upregulation for several pro-inflammatory mediators and reduced graft apoptosis. Conclusions Combined therapy with hydrogen and CO demonstrated enhanced therapeutic efficacy via both anti-oxidant and anti-inflammatory mechanisms, and may be a clinically feasible approach for preventing Cold I/R injury of the myocardium.

  • Role of NF-κB on liver Cold Ischemia-reperfusion injury
    American journal of physiology. Gastrointestinal and liver physiology, 2002
    Co-Authors: Yoshihito Takahashi, Raymond W. Ganster, Andrea Gambotto, Lifang Shao, Takashi Kaizu, Gautam P. Yagnik, Atsunori Nakao, George Tsoulfas, Takashi Ishikawa
    Abstract:

    The role of NF-κB, the rapid-response transcription factor for multiple genes, in Cold Ischemia-reperfusion (I/R) injury was examined after syngeneic transplantation of liver grafts. Lewis rat reci...

Andrey V. Kuznetsov - One of the best experts on this subject based on the ideXlab platform.

  • Impact of Cold Ischemia on Mitochondrial Function in Porcine Hearts and Blood Vessels
    International journal of molecular sciences, 2013
    Co-Authors: Dominik Wiedemann, Thomas Schachner, Nikolaos Bonaros, Melissa Dorn, Martin Andreas, Alfred Kocher, Andrey V. Kuznetsov
    Abstract:

    The effects of Cold storage using Custodiol® (Histidine-Tryptophan-Ketoglutarate, HTK) or isotonic saline solution on mitochondrial function in hearts (left and rights ventricles) and various blood vessels of pigs were investigated. Hearts, saphenous veins, internal-mammary-arteries and aortas of male landrace pigs were harvested and exposed to Cold Ischemia in either saline or Custodiol-HTK solution. Mitochondrial function was measured in situ in permeabilized fibers by high-resolution respirometry. Mitochondrial respiratory capacities (maximal respiration rates) were similar in the right and left ventricle in controls and after 14 h of Cold storage were significantly better preserved in Custodiol-HTK than in saline solution. Mitochondrial respiration rates in various blood vessels including aorta, arteries and veins were less than 5% of myocardium rates. In contrast to the pig heart, in some blood vessels, like veins, mitochondrial function remained stable even after 24 h of Cold Ischemia. HTK-Custodiol protection of mitochondrial function after prolonged Cold Ischemia was observed in the myocardium but not in blood vessels. HTK-Custodiol solution thus offers significant protection of myocardial mitochondria against Cold ischemic injury and can be used as efficient preservation solution in organ transplantation but probably has no benefit for blood vessels preservation. Analysis of mitochondrial function can be used as a valuable approach for the assessment of Cold ischemic injury in various tissues including pig heart and various blood vessels.

  • Mitochondrial defects and heterogeneous cytochrome c release after cardiac Cold Ischemia and reperfusion.
    American journal of physiology. Heart and circulatory physiology, 2003
    Co-Authors: Andrey V. Kuznetsov, Stefan Schneeberger, Gerald Brandacher, Raimund Margreiter, Walter Mark, Rüdiger Seiler, Wolfgang Steurer, Valdur Saks, Yves Usson, Erich Gnaiger
    Abstract:

    Mitochondria play a critical role in myocardial Cold Ischemia-reperfusion (CIR) and induction of apoptosis. The nature and extent of mitochondrial defects and cytochrome c (Cyt c) release were dete...

Timothy R. Billiar - One of the best experts on this subject based on the ideXlab platform.

  • amelioration of rat cardiac Cold Ischemia reperfusion injury with inhaled hydrogen or carbon monoxide or both
    Journal of Heart and Lung Transplantation, 2010
    Co-Authors: Atsunori Nakao, David J. Kaczorowski, Yinna Wang, Jon Cardinal, Bettina M. Buchholz, Ryujiro Sugimoto, Kimimasa Tobita, Sungsoo Lee, Yoshiya Toyoda, Timothy R. Billiar
    Abstract:

    Background Recent advances in novel medical gases, including hydrogen and carbon monoxide (CO), have demonstrated significant opportunities for therapeutic use. This study was designed to evaluate the effects of inhaled hydrogen or CO, or both, on Cold Ischemia/reperfusion (I/R) injury of the myocardium. Methods Syngeneic heterotopic heart transplantation was performed in rats after 6 or 18 hours of Cold Ischemia in Celsior solution. Survival, morphology, apoptosis and marker gene expression were assessed in the grafts after in vivo inhalation of hydrogen (1% to 3%), CO (50 to 250 ppm), both or neither. Both donors and recipients were treated for 1 hour before and 1 hour after reperfusion. Results After 6-hour Cold Ischemia, inhalation of hydrogen (>2%) or CO (250 ppm) alone attenuated myocardial injury. Prolonged Cold Ischemia for 18 hours resulted in severe myocardial injury, and treatment with hydrogen or CO alone failed to demonstrate significant protection. Dual treatment with hydrogen and CO significantly attenuated I/R graft injury, reducing the infarcted area and decreasing in serum troponin I and creatine phosphokinase (CPK). Hydrogen treatment alone significantly reduced malondialdehyde levels and serum high-mobility group box 1 protein levels as compared with air-treated controls. In contrast, CO only marginally prevented lipid peroxidation, but it suppressed I/R-induced mRNA upregulation for several pro-inflammatory mediators and reduced graft apoptosis. Conclusions Combined therapy with hydrogen and CO demonstrated enhanced therapeutic efficacy via both anti-oxidant and anti-inflammatory mechanisms, and may be a clinically feasible approach for preventing Cold I/R injury of the myocardium.

  • Amelioration of rat cardiac Cold Ischemia/reperfusion injury with inhaled hydrogen or carbon monoxide, or both.
    The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 2009
    Co-Authors: Atsunori Nakao, David J. Kaczorowski, Yinna Wang, Jon Cardinal, Bettina M. Buchholz, Ryujiro Sugimoto, Kimimasa Tobita, Sungsoo Lee, Yoshiya Toyoda, Timothy R. Billiar
    Abstract:

    Background Recent advances in novel medical gases, including hydrogen and carbon monoxide (CO), have demonstrated significant opportunities for therapeutic use. This study was designed to evaluate the effects of inhaled hydrogen or CO, or both, on Cold Ischemia/reperfusion (I/R) injury of the myocardium. Methods Syngeneic heterotopic heart transplantation was performed in rats after 6 or 18 hours of Cold Ischemia in Celsior solution. Survival, morphology, apoptosis and marker gene expression were assessed in the grafts after in vivo inhalation of hydrogen (1% to 3%), CO (50 to 250 ppm), both or neither. Both donors and recipients were treated for 1 hour before and 1 hour after reperfusion. Results After 6-hour Cold Ischemia, inhalation of hydrogen (>2%) or CO (250 ppm) alone attenuated myocardial injury. Prolonged Cold Ischemia for 18 hours resulted in severe myocardial injury, and treatment with hydrogen or CO alone failed to demonstrate significant protection. Dual treatment with hydrogen and CO significantly attenuated I/R graft injury, reducing the infarcted area and decreasing in serum troponin I and creatine phosphokinase (CPK). Hydrogen treatment alone significantly reduced malondialdehyde levels and serum high-mobility group box 1 protein levels as compared with air-treated controls. In contrast, CO only marginally prevented lipid peroxidation, but it suppressed I/R-induced mRNA upregulation for several pro-inflammatory mediators and reduced graft apoptosis. Conclusions Combined therapy with hydrogen and CO demonstrated enhanced therapeutic efficacy via both anti-oxidant and anti-inflammatory mechanisms, and may be a clinically feasible approach for preventing Cold I/R injury of the myocardium.