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Biomedical subjects

S Levitsky

Publications and source records attributed to S Levitsky.

At least 19 recordsLinked to original sources
PubMed2002

Acoustic waves in cylindrical gap, filled by polymeric liquid.

Propagation of acoustic waves in thin-walled elastic tube with coaxial internal rigid rod is investigated in conjugated quasi-one-dimensional formulation. The cylindrical gap between the tube's wall and the central rod is filled by polymeric liquid, described by hereditary model with a discrete spectrum. Dynamics of the tube is treated within Kirchhoff-Love approximation. The dispersion equation accounting for viscoelastic effects in the fluid in coupling with inertia, radial and longitudinal deformations of the tube's wall has been obtained. Its analysis has showed strong influence of the liquid's rheological properties and geometrical parameters of the system on pressure signals dispersion and attenuation. The results can be used for rheological characterization of polymeric liquids by acoustic means.

Journal Article↗
PubMed2001

Opening of mitochondrial ATP-sensitive potassium channels enhances cardioplegic protection.

BACKGROUND: Mitochondrial and sarcolemmal ATP-sensitive potassium channels have been implicated in cardioprotection; however, the role of these channels in magnesium-supplemented potassium (K/Mg) cardioplegia during ischemia or reperfusion is unknown. METHODS: Rabbit hearts (n = 76) were used for Langendorff perfusion. Sham hearts were perfused for 180 minutes. Global ischemia hearts received 30 minutes of global ischemia and 120 minutes of reperfusion. K/Mg hearts received cardioplegia before ischemia. The role of ATP-sensitive potassium channels in K/Mg cardioprotection during ischemia and reperfusion was investigated, separately using the selective mitochondrial ATP sensitive potassium and channel blocker, 5-hydroxydecanoate, and the selective sarcolemmal ATP-sensitive potassium channel blocker HMR1883. Separate studies were performed using the selective mitochondrial ATP-sensitive potassium channel opener, diazoxide, and the nonselective ATP-sensitive potassium channel opener pinacidil. RESULTS: Infarct size was 1.9%+/-0.4% in sham, 3.7%+/-0.5% in K/Mg, and 27.8%+/-2.4% in global ischemia hearts (p < 0.05 versus K/Mg). Left ventricular peak-developed pressure (percent of equilibrium) at the end of 120 minutes of reperfusion was 91%+/-6% in sham, 92% +/-2% in K/Mg, and 47%+/-6% in global ischemia (p < 0.05 versus K/Mg). Blockade of sarcolemmal ATP-sensitive potassium channels in K/Mg hearts had no effect on infarct size or left ventricular peak-developed pressure. However, blockade of mitochondrial ATP-sensitive potassium channels before ischemia significantly increased infarct size to 23%+/-2% in K/Mg hearts (p < 0.05 versus K/Mg; no statistical significance [NS] as compared to global ischemia) and significantly decreased left ventricular peak-developed pressure to 69%+/-4% (p < 0.05 versus K/Mg). Diazoxide when added to K/Mg cardioplegia significantly decreased infarct size to 1.5%+/-0.4% (p < 0.05 versus K/Mg). CONCLUSIONS: The cardioprotection afforded by K/Mg cardioplegia is modulated by mitochondrial ATP-sensitive potassium channels. Diazoxide when added to K/Mg cardioplegia significantly reduces infarct size, suggesting that the opening of mitochondrial ATP-sensitive potassium channels with K/Mg cardioplegic protection would allow for enhanced myocardial protection in cardiac operations.

Adenosine Triphosphate↗
PubMed2001

Adenosine-enhanced ischemic preconditioning modulates necrosis and apoptosis: effects of stunning and ischemia-reperfusion.

BACKGROUND: Adenosine-enhanced ischemic preconditioning extends the protection of ischemic preconditioning by both significantly decreasing infarct size and significantly enhancing postischemic functional recovery. METHODS: The effects of adenosine-enhanced ischemic preconditioning on necrosis and apoptosis were investigated in the sheep heart using models of stunning (15 minutes regional ischemia, 120 minutes reperfusion) and ischemia-reperfusion (30 and 60 minutes regional ischemia, 120 minutes reperfusion). Ischemic preconditioned hearts received 5 minutes regional ischemia, 5 minutes reperfusion before ischemia. Adenosine-enhanced ischemic preconditioned hearts received a 10 mmol/L adenosine bolus (10 mL) through the left atrium coincident with ischemic preconditioning. Adenosine hearts received a 10 mmol/L bolus (10 mL) of adenosine. Regional ischemic hearts received no pretreatment. RESULTS: Minimal apoptosis (< 45 per 3,000 myocytes) was observed in the stunning models but was significantly increased with ischemia-reperfusion in regional ischemic hearts after 30 minutes (p < 0.05 versus ischemic preconditioning, adenosine, or adenosine-enhanced ischemic preconditioning) and in adenosine and ischemic preconditioned hearts after 60 minutes ischemia (p < 0.05 versus adenosine-enhanced ischemic preconditioning). DNA laddering was apparent after 60 minutes ischemia in regional ischemia, adenosine, and ischemic preconditioning but not in adenosine-enhanced ischemic preconditioned hearts. CONCLUSIONS: Adenosine-enhanced ischemic preconditioning significantly ameliorates necrosis and apoptosis in the regional ischemic blood-perfused heart.

Adenosine↗
PubMed2001

Effects of NHE-1 inhibition on cardioprotection and impact on protection by K/Mg cardioplegia.

BACKGROUND: Cardiac sodium hydrogen exchanger isoform-1 (NHE-1) activity during ischemia/reperfusion contributes to myocardial injury. The effects of NHE-1 inhibition during ischemia or reperfusion and on the protection afforded by K/Mg cardioplegia was unknown. METHODS: Rabbit hearts were used for Langendorff perfusion. Control hearts were perfused for 180 minutes. Global ischemia (GI) hearts received 30 minutes normothermic global ischemia and 120 minutes reperfusion. K/Mg hearts received cardioplegia 5 minutes before ischemia. Separate groups of GI and K/Mg hearts received the NHE-1 inhibitor, HOE-642, before ischemia (HOE-642-I), at the immediate start of reperfusion (HOE-642-R), or both before ischemia and at the immediate start of reperfusion (HOE-642-IR). RESULTS: Left ventricular peak developed pressure was significantly increased in HOE-I, HOE-R, and HOE-IR throughout reperfusion (p < 0.05 versus GI). Infarct size was significantly decreased (p < 0.05 versus GI) in all groups, but was significantly increased in HOE-R as compared with HOE-IR (p < 0.05). NHE-1 inhibition with K/Mg cardioplegia significantly decreased left ventricular peak developed pressure after 90 minutes of reperfusion (p < 0.05 versus K/Mg), with no significant effect on infarct size. CONCLUSIONS: NHE-1 inhibition used alone provides cardioprotection with optimal effects being observed with HOE-IR. NHE-1 inhibition with K/Mg cardioplegia decreases postischemic functional recovery during late reperfusion.

Animals↗
PubMed2001

Adenosine-enhanced ischemic preconditioning: adenosine receptor involvement during ischemia and reperfusion.

Adenosine-enhanced ischemic preconditioning (APC) extends the cardioprotection of ischemic preconditioning (IPC) by both significantly decreasing myocardial infarct size and significantly enhancing postischemic functional recovery. In this study, the role of adenosine receptors during ischemia-reperfusion was determined. Rabbit hearts (n = 92) were used for Langendorff perfusion. Control hearts were perfused for 180 min, global ischemia hearts received 30-min ischemia and 120-min reperfusion, and IPC hearts received 5-min ischemia and 5-min reperfusion before ischemia. APC hearts received a bolus injection of adenosine coincident with IPC. Adenosine receptor (A(1), A(2), and A(3)) antagonists were used with APC before ischemia and/or during reperfusion. GR-69019X (A(1)/A(3)) and MRS-1191/MRS-1220 (A(3)) significantly increased infarct size in APC hearts when administered before ischemia and significantly decreased functional recovery when administered during both ischemia and reperfusion (P < 0.05 vs. APC). DPCPX (A(1)) administered either before ischemia and/or during reperfusion had no effect on APC cardioprotection. APC-enhanced infarct size reduction is modulated by adenosine receptors primarily during ischemia, whereas APC-enhanced postischemic functional recovery is modulated by adenosine receptors during both ischemia and reperfusion.

Adenosine↗
PubMed2000

Anti-stunning and anti-infarct effects of adenosine-enhanced ischemic preconditioning.

BACKGROUND: Adenosine-enhanced ischemic preconditioning (APC) extends the protection afforded by ischemic preconditioning (IPC) by both significantly decreasing infarct size and significantly enhancing post-ischemic functional recovery. In this study, the anti-infarct effects and the anti-stunning effects of APC in contributing to enhanced post-ischemic functional recovery were determined and compared with IPC. METHODS AND RESULTS: Sheep (n=96) were subjected to 15, 30, 45, or 60 minutes of regional ischemia and 120 minutes of reperfusion. IPC hearts received 5 minutes of regional ischemia and 5 minutes of reperfusion before ischemia/reperfusion. APC hearts received a bolus injection of adenosine coincident with IPC. Adenosine hearts (ADO) received a bolus injection of adenosine before ischemia/reperfusion. Regional ischemia (RI) hearts received no pretreatment. Infarct size/area at risk was determined by tetrazolium staining. Regional myocardial function was determined by sonomicrometry. Segment shortening after 15 minutes of ischemia in which no infarct was incurred was 32. 1+/-10.6% in RI, 70.6+/-8.5% in IPC, and 77.4+/-6.0% in APC hearts. Segment shortening after 30 minutes of ischemia was 60.7+/-6.3% in APC hearts (P:<0.05 versus RI, ADO, IPC) but was <37% in all other groups. Infarct size/area at risk after 30 and 60 minutes of ischemia was, respectively, 25.8+/-5.7% and 49.8+/-6.0% in RI, 12. 9+/-3.0% and 29.2+/-5.0% in ADO, 11.6+/-2.4% and 24.6+/-2.7% in IPC, and 5.1+/-1.6% and 12.4+/-2.0% in APC hearts (P:<0.05 versus RI, ADO, IPC). CONCLUSIONS: APC and IPC exhibit anti-infarct and anti-stunning effects in the ovine heart, but these effects are rapidly diminished with IPC. APC significantly extends these effects, providing for significantly enhanced infarct size reduction and post-ischemic functional recovery (P:<0.05 versus IPC).

Adenosine↗
PubMed2000

Preconditioning with PKC and the ATP-sensitive potassium channels: a codependent relationship.

BACKGROUND: Both potassium channel openers and protein kinase C have been shown to independently elicit the myoprotective preconditioning response. However, the in vivo dependency between the two is unknown. METHODS: Thirty-seven sheep were divided into seven groups; animals received no pretreatment, pinacidil, pinacidil and potassium channel opener blocker glibenclamide, protein kinase C activator 4beta-phorbol-12,13-dibutyrate (PDBu), or PDBu and protein kinase C blocker chelerythrine. The last two groups underwent opposite blockade, chelerythrine + pinacidil, or glibenclamide + PDBu. All groups underwent 60 minutes of regional ischemia followed by 180 minutes of reperfusion. Regional function was assessed throughout the experiment, and at the conclusion of the study the infarct size (as a percentage of the area at risk) was determined. RESULTS: Infarct size decreased in the groups receiving only pinacidil or PDBu (control: 54%+/-3%, pinacidil: 25% +/-2%, PDBu: 21%+/-3%; p<0.05 pinacidil or PDBu versus control). This preconditioning protection was lost when the direct blocker was given (58%+/-5%, glibenclamide + pinacidil; 70%+/-6%, chelerythrine + PDBu; p = not significant versus control). The preconditioning response was again attenuated when the opposite blockers were given (64%+/-5%, chelerythrine + pinacidil; 63%+/-1%, glibenclamide + PDBu; p = not significant versus control). There was no significant difference in regional function. CONCLUSIONS: This study shows that both protein kinase C and potassium channels are necessary and codependent for preconditioning in the in vivo heart.

Animals↗
PubMed2000

Pharmacological preconditioning with the adenosine triphosphate-sensitive potassium channel opener pinacidil.

BACKGROUND: Ischemic preconditioning (IPC) decreases infarct size after global or regional ischemia. Potassium channel openers also precondition but are subject to dose-limiting vasodilation. We compared the mechanical and electrophysiological effects of ischemic and pharmacological preconditioning in an isolated rabbit heart model. METHODS: Rabbit hearts were preconditioned with either 10 micromol/L pinacidil alone (P-), 10 micromol/L pinacidil with 10 micromol/L phenylephrine (P+), or two cycles of global ischemia and reperfusion (IPC) before 1 hour of LAD occlusion. Left ventricular pressure, epicardial monophasic action potential duration (APD) and coronary flow were monitored throughout. Infarct size was determined at the end of reperfusion. RESULTS: Regional ischemia uniformly decreased APD (p<0.05). During reperfusion, APDs were prolonged beyond preischemic values in all preconditioned groups (p<0.05). P- and P+ reduced the incidence of fibrillation. P- significantly increased coronary flow (+15%, p = 0.001), whereas IPC and P+ did not. However, IPC and P- significantly decreased systolic function (p<0.05) but P+ did not. In addition, IPC depressed diastolic function (p<0.05) but P- and P+ did not. Infarct size was reduced by all methods (p<0.05). CONCLUSIONS: Pinacidil presents a safe and effective alternative to IPC for preserving the heart during regional ischemia. Its coronary vasodilatory effects are safely and effectively reversed by the addition of phenylephrine.

Action Potentials↗
PubMed2000

Predictors of 30-day hospital readmission after coronary artery bypass.

BACKGROUND: Risk factors for 30-day hospital readmission following coronary artery bypass grafting (CABG) have not been established. METHODS: We prospectively followed 485 consecutive patients who underwent isolated primary CABG at our institution in 1997. Patients were contacted by telephone at 30 days following operation to determine readmission status. RESULTS: The overall readmission rate was 16% (76 of 485). Female gender (25% versus 11%, p = 0.001) and diabetes (22% versus 12%, p = 0.005) were associated with significantly higher readmission rates. The relationship between female gender and readmission persisted after correcting for age and other comorbidities. Congestive heart failure trended towards a significant relationship with increased readmission rate (22% versus 14%, p = 0.09). There were no significant associations between 30-day readmission rate and age, hypertension, chronic obstructive pulmonary disease, history of myocardial infarction, peripheral vascular disease, creatinine level of > or = 1.4 mg/dL, or decreased left ventricular ejection fraction (< 40%). CONCLUSIONS: These data show that most of the classic risk factors for postoperative mortality are not necessarily associated with increased readmission. However, female gender and diabetes are associated with greater than twice the risk of 30-day readmission following CABG.

Aged↗
PubMed2000

Amrinone preconditioning in the isolated perfused rabbit heart.

BACKGROUND: Ischemic preconditioning (IPC) reduces infarct size in experimental preparations. IPC, however, is not without detrimental effects. We studied amrinone as a possible alternative to IPC. METHODS: Isolated perfused rabbit hearts were given a 5-minute infusion of 10 micromol/L amrinone followed by a 5-minute washout (n = 6). The anterior descending artery was then occluded for 1 hour and reperfused for 1 hour. Six hearts underwent IPC, with two episodes of 5-minute global ischemia followed by 5-minute reperfusion before LAD occlusion; eight control hearts received no preconditioning. Left ventricular pressure and ischemic zone epicardial monophasic action potentials were continuously monitored. RESULTS: IPC but not amrinone reduced peak pressure before anterior descending artery occlusion. Peak pressure fell significantly during ischemia and reperfusion in all hearts. End diastolic pressure rose significantly during reperfusion in control and IPC hearts but not in amrinone hearts. Action potentials shortened during ischemia in all hearts. They returned to preocclusion values in control hearts but lasted beyond preocclusion values in IPC and amrinone hearts. Both the incidences of ventricular fibrillation and infarct size were significantly reduced in amrinone hearts but not in IPC hearts. CONCLUSIONS: Amrinone is not only a useful inotropic agent but is also a superior preconditioning agent when compared to IPC.

Action Potentials↗
PubMed2000

Inhibition of RNA transcription modulates magnesium-supplemented potassium cardioplegia protection.

BACKGROUND: Previously we reported that decreased postischemic functional recovery was associated with increased DNA fragmentation in the aged myocardium. Magnesium-supplemented potassium (K/Mg) cardioplegia ameliorated DNA fragmentation and enhanced post-ischemic functional recovery. We hypothesized that K/Mg cardioprotection might involve either an RNA- or a protein-dependent mechanism. METHODS: Aged rabbit hearts underwent Langendorff perfusion. Global ischemia hearts (GI) received 30 minutes of global ischemia and 60 minutes of reperfusion; K/Mg hearts received cardioplegia before global ischemia. To investigate the role of RNA and protein synthesis, K/Mg hearts were treated with alpha-amanitin or cycloheximide to inhibit RNA or protein synthesis. We also determined the quantity of DNA fragmentation and RNA/DNA ratio. RESULTS: Inhibition of RNA but not protein synthesis significantly decreased K/Mg cardioprotection and was associated with significantly decreased postischemic functional recovery (p < 0.05 versus K/Mg), increased DNA fragmentation, and decreased RNA/DNA ratio (p < 0.05 versus K/Mg). CONCLUSIONS: These results indicate that K/Mg cardioprotection in the aged myocardium was modulated by an RNA-dependent mechanism.

Animals↗
PubMed2000

Acoustic waves in thin-walled elastic tube with polymeric solution

Acoustic waves in a pipe with polymeric liquid are investigated within a quasi-one-dimensional approach. Analysis of the dispersion equation has shown that rheological features lead to essential changes in both attenuation and speed of the sound. The results may find application in acoustic rheometry of polymeric liquids and for modeling of fast dynamic processes in polymer production technology.

Journal Article↗
PubMed2000

Attenuation of ultrasound in porous media with dispersed microbubbles

The dispersion relation for a granular bed with a small amount of fine bubbles is formulated and analyzed. It is assumed that the grain size is much larger than the bubble's radius and that their volume concentration is small. The study is motivated by the problem of acoustic diagnostics of fixed bed chemical reactors operating in multiphase flow regime.

Journal Article↗
PubMed2000

Differential role of sarcolemmal and mitochondrial K(ATP) channels in adenosine-enhanced ischemic preconditioning.

Adenosine-enhanced ischemic preconditioning (APC) extends the protection afforded by ischemic preconditioning (IPC) by both significantly decreasing infarct size and significantly enhancing postischemic functional recovery. The purpose of this study was to determine whether APC is modulated by ATP-sensitive potassium (K(ATP)) channels and to determine whether this modulation occurs before ischemia or during reperfusion. The role of K(ATP) channels before ischemia (I), during reperfusion (R), or during ischemia and reperfusion (IR) was investigated using the nonspecific K(ATP) blocker glibenclamide (Glb), the mitochondrial (mito) K(ATP) channel blocker 5-hydroxydecanoate (5-HD), and the sarcolemmal (sarc) K(ATP) channel blocker HMR-1883 (HMR). Infarct size was significantly increased (P < 0.05) in APC hearts with Glb-I, Glb-R, and 5-HD-I treatment and partially with 5-HD-R. Glb-I and Glb-R treatment significantly decreased APC functional recovery (P < 0.05 vs. APC), whereas 5-HD-I and 5-HD-R had no effect on APC functional recovery. HMR-IR significantly decreased postischemic functional recovery (P < 0.05 vs. APC) but had no effect on infarct size. These data indicate that APC infarct size reduction is modulated by mitoK(ATP) channels primarily during ischemia and suggest that functional recovery is modulated by sarcK(ATP) channels during ischemia and reperfusion.

Adenosine↗
PubMed1999

Alternatives for myocardial protection: adenosine-enhanced ischemic preconditioning.

Intrinsic to the development of new myoprotective protocols for use in cardiac surgery are the requirements of new protocols to be equal to or better than conventional cardioplegia in providing for enhanced post-ischemic functional recovery and decreased myocardial infarct size. Our data suggest that adenosine-enhanced ischemic preconditioning, in which a bolus injection of adenosine to the myocardium is used coincident with ischemic preconditioning, meets these requirements, providing equal cardioprotection as that of cold blood cardioplegia, significantly decreasing myocardial infarct size and significantly enhancing post-ischemic myocardial functional recovery in both the isolated perfused rabbit heart and in the in situ blood-perfused sheep heart. These results further suggest that adenosine-enhanced ischemic preconditioning may provide an effective, alternative myocardial protective protocol to reduce the morbidity and mortality in cardiac surgery.

Adenosine↗
PubMed1999

Adenosine-enhanced ischemic preconditioning provides myocardial protection equal to that of cold blood cardioplegia.

BACKGROUND: We recently described a novel myoprotective protocol-adenosine-enhanced ischemic preconditioning (APC)-that extends the protection of ischemic preconditioning (IPC) by both reducing myocardial infarct size and enhancing postischemic functional recovery in the isolated perfused heart. In the present report the efficacy of APC in the blood-perfused heart was investigated and compared with that of cold blood cardioplegia (CBC). METHODS: Cardiopulmonary bypass was instituted in 21 sheep hearts. The APC hearts (n = 6) received a bolus injection of adenosine through the aortic root at the immediate start of IPC (5 minutes of zero-flow global ischemia, followed by 5 minutes of reperfusion) before 30 minutes of global ischemia and 120 minutes of reperfusion. Nine other hearts received CBC. A control group (n = 6) received IPC only. RESULTS: Infarct size was significantly decreased (p<0.01) in the APC (3.0%+/-0.8%) and CBC (2.6%+/-0.2%) hearts compared with the IPC hearts (16.3%+/-1.6%). The preload recruitable stroke work relation, mean arterial pressure, and the time constant of pressure decay (tau) were significantly preserved (p<0.05) in APC and CBC hearts compared with IPC hearts. No significant differences were observed between APC and CBC hearts. CONCLUSIONS: Use of APC is as effective as CBC in significantly decreasing infarct size and enhancing post-ischemic functional recovery.

Adenosine↗
PubMed1999

Immediate vein graft thrombectomy for acute occlusion after coronary artery bypass grafting.

A 76-year-old man underwent coronary bypass grafting 3 days after exposure to heparin. Immediately after chest closure, he developed acute graft thrombosis and cardiac arrest in the setting of thrombocytopenia. Immediate graft thrombectomies were performed. Postoperative tests for heparin-induced thrombocytopenia and thrombosis (HITT) were positive. This case represents a dramatic example of HITT after coronary revascularization.

Aged↗