Showing papers by "Volkmar Falk published in 2001"

Influence of three-dimensional vision on surgical telemanipulator performance

Abstract: Background: Different viewing conditions (two- and three-dimensional National Television Standard Committee [2D-NTSC and 3D-NTSC] and two-dimensional high-definition television [2D-HDTV]) on telemanipulator performance were evaluated. Methods: Six taskes were performed by 15 endoscopic surgeons using the daVinci telemanipulation system. Performance time and errors were measured. Encoder data from the system were used for kinematic analysis of motion. A self-evaluation questionnaire regarding performance under various viewing conditions was obtained. Results: Resolution was better with 2D-HDTV. The estimate of relative distance was not influenced by the different visualization systems. Motor skill tasks were performed faster with binocular vision (3D-NTSC) than with monocular vision (2D-NTSC, 2D-HDTV). For both 2D settings, the deceleration phase of motion was prolonged (p < 0.05 vs 3D). Peak velocity was reduced with 2D-HDTV as compared with 3D-NTSC (p = 0.01). The surgeons tended to favor the 3D system despite their use of 2D systems in their own practice. Conclusions: Three-dimensional vision enhances telemanipulator performance as compared with a 2D system at the same or higher level of resolution. Because it allows faster and more precise movement, future surgical systems should focus on 3D visualization.

Upregulation of Bcl-2 Through Caspase-3 Inhibition Ameliorates Ischemia/Reperfusion Injury in Rat Cardiac Allografts

Abstract: Background Oxidative stress after ischemia/reperfusion of cardiac allografts leads to cytokine production. Bcl-2, an inhibitor of apoptosis, also has strong antioxidant properties. Caspase-3 is known to cleave bcl-2. This study tests the hypothesis that bcl-2 is downregulated while tumor necrosis factor-α (TNF-α) levels increase after cardiac transplantation. Furthermore, the use of caspase-3 inhibition was investigated as a strategy for preserving myocardial bcl-2 and mitochondrial cytochrome c after transplantation. Methods and Results PVG-to-ACI rat heterotopic cardiac transplantations were performed in 4 groups designed with 30 minutes’ ischemia and 4 or 8 hours of reperfusion (n=4 per group). Treatment consisted of DEVD-CHO 500 μg IP per animal to donor and recipient 2 hours before transplantation and 250 μg IC into allograft. Controls were treated with saline. Grafts were analyzed by reverse transcription–polymerase chain reaction for bcl-2 mRNA, by ELISA for TNF-α, for myeloperoxidase activity, and by Western blot for cytochrome c. In untreated groups, bcl-2 mRNA decreased significantly over time, whereas TNF-α increased significantly at 4 hours ( P =0.003) and returned to baseline after 8 hours’ reperfusion ( P =NS compared with normal hearts). Treatment with caspase-3 inhibitor showed significant upregulation of bcl-2 mRNA expression after 4 and 8 hours of reperfusion ( P <0.001 versus control), with a concomitant decrease in TNF-α to baseline levels. Myeloperoxidase activity in all groups was no different from that of normal hearts. Mitochondrial cytochrome c release increased in both control and treatment groups. Conclusions Bcl-2 is actively downregulated and TNF-α is upregulated in this model of cardiac allograft ischemia/reperfusion. Furthermore, the caspase-3 pathway is linked to this process, and blockade of caspase-3 can ameliorate reperfusion injury by upregulating bcl-2 and inhibiting TNF-α without affecting cytochrome c release.

Regression of Left Ventricular Hypertrophy After Surgical Therapy for Aortic Stenosis Is Associated With Changes in Extracellular Matrix Gene Expression

Abstract: Background Regression of left ventricular hypertrophy (LVH) after surgical correction for aortic stenosis is not fully understood on the molecular level. The aim of this study was to examine whether there is an association between LVH regression and extracellular matrix (ECM) gene expression. Methods and Results A standard model of controlled LVH induction by supracoronary banding (A=baseline) was applied in 44 growing sheep (age, 6 to 8 months). Surgical correction to release the pressure gradient was performed 8.3±1 months later (B). The animals were killed after another 10.1±2 months (C). At all time points, hemodynamic evaluations and quantitative analysis of mRNA and protein expression for matrix metalloproteinases (MMP) and their tissue inhibitors (TIMP) was performed. Left ventricular mass index was 82±21 (A) versus 150±33 (B), P<0.01, and 78±18 g/m2 (C), P<0.01. Left ventricular function and cardiac index remained stable. Myocardial fiber diameter index was 9.1±1.2 (A) versus 12.3±1.4 (B), P<0.01,...

Extracellular matrix gene expression correlates to left ventricular mass index after surgical induction of left ventricular hypertrophy.

Abstract: The cardiac extracellular matrix (ECM) is a dynamic entity maintaining the structural and functional properties of the myocardium. Little is known about alterations in ECM regulation during controlled induction of compensated left ventricular hypertrophy (LVH) using experimental aortic stenosis. Fifteen growing sheep received supra-coronary banding at an age of 7 ± 1 months whereas 10 age-matched sheep served as the control group (C). Explantation of the hearts was performed 8.3 ± 1 months after banding. Gene sequences for sheep matrix metalloproteinase (MMP)-1,-2,-3,-9 and tissue inhibitors (TIMP)-1,-2,-3 were isolated and cloned. Then mRNA and protein gene expression analyses were performed. Concentric LVH with no evidence of heart failure was diagnosed at explantation. Left ventricular mass index (LVMI) was 150 ± 33 g/m2 (LVH) versus 88 ± 23 (C) and 82 ± 21 (baseline) (p < 0.01 versus LVH). Parallel to LVH there was a significant increase in mRNA and protein expression for MMP-1,-2,-3,-9 and for TIMP-1,-2 whereas there was a significant decrease in TIMP-3 gene expression. A close correlation between changes in LVMI and ECM gene expression was found. Compensated LVH goes along with a significant modification of MMP and TIMP gene expression. Alterations in ECM gene expression may be part of the adaptive process during left ventricular remodeling.

Up-regulation of Bcl-2 through hyperbaric pressure transfection of TGF-β1 ameliorates ischemia-reperfusion injury in rat cardiac allografts

Abstract: Background: Oxidative stress after ischemia-reperfusion of cardiac allografts leads to activation of cardiomyocytes and production of cytokines. Bcl-2, an inhibitor of the apoptotic pathway, also has strong antioxidant properties. Ischemia-reperfusion injury after transplantation leads to decreased bcl-2 and increased tumor necrosis factor (TNF)-a levels. Transforming growth factor (TGF)-β 1 is known to attenuate ischemia-reperfusion injury and inhibits apoptosis of myofibroblasts. We hypothesize that TGF-β 1 , prevents bcl-2 cleavage and increased TNF-a production. Methods: Rat PVG donor hearts were heterotopically transplanted into ACI recipients. Donor hearts were procured and assigned to groups: (1) intracoronary TGF-β 1 (200 ng/ml) perfusion and pressure at 78 psi for 45 minutes (n = 4); (2) intracoronary TGF-β 1 perfusion and incubation for 45 minutes without pressure (n = 4), (3) saline perfusion and incubation for 45 minutes without pressure (n = 4). Hearts were procured 4 hours after transplantation and analyzed by reverse transcriptase-polymerase chain reaction for bcl-2 mRNA expression, ELISA for TNF-a, and for myeloperoxidase activity (MPO). Results: Bcl-2 decreased in untreated animals (bcl-2:G3PDH ratio = 0.85 ± 0.73 vs 1.16 ± 0.11, not significant [NS]), whereas TNF-a increased to 669.99 ± 127.09 vs 276.84 ± 73.65 pg/mg total protein in controls (p < 0.003). In TGF-β 1 pressure-treated hearts, bcl-2 was up-regulated (2.49 ± 0.6 vs 1.16 ± 0.11, controls, p < 0.005), whereas TNF-a was unchanged (396.1 ± 100.38 vs 276.84 ± 73.65 pg/mg, NS). Hearts treated with TGF-β 1 and pressure showed significant up-regulation of bcl-2 compared with hearts treated with TGF-β 1 without pressure (2.49 ± 0.6 vs 1.17 ± 0.6, p < 0.02). MPO showed no differences. Conclusions: Bcl-2 is down-regulated and TNF-a up-regulated in this model of ischemia-reperfusion injury. Furthermore, TGF-β 1 is linked to this process and ameliorates reperfusion injury by up-regulating bcl-2 and inhibiting TNF-a. Therapeutic overexpression of myocardial TGF-β 1 may be clinically useful to control ischemia-reperfusion injury associated with cardiac transplantation.

Floating thrombus on an ASD occluder device in a patient with hemophilia A.

Abstract: The case presented is that of a 29-year-old man with a history of hemophilia A who was admitted with recurrent onsets of transient cerebrovascular ischemia; he had undergone a transvenous closure of an atrial septal defects with an occluder device (Cardioseal Starflex) two months ago. Due to a factor-VIII deficiency, no further anticoagulation therapy was initiated. On admission, transesophageal echocardiography revealed a floating thrombus on the left atrial side of the umbrella. The device was explanted via a right minithoracotomy, and the atrial septal defect was closed. The patient had an uneventful recovery.