Professor, Anesthesiology, Medical College of Wisconsin
Anesthesiology
Dr. David Stowe, MD
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David Stowe works in the field of Anesthesiology. He attended Medical College of Wisconsin. Medical College of Wisconsin is ranked 54/62 in Research/PrimaryCare. David Stowe is also a published MD. He has 101 publication published. The most recent publication is: Matching of vertebrate cardiac energy demand to energy metabolism.
Publications
- Computational Analysis of Ca2+ Dynamics in Isolated Cardiac Mitochondria Predicts Two Distinct Modes of Ca2+ Uptake.
- Isoflurane modulates cardiac mitochondrial bioenergetics by selectively attenuating respiratory complexes.
- Genetically Determined Mitochondrial Preservation and Cardioprotection against Myocardial Ischemia-Reperfusion Injury in a Consomic Rat Model.
- Extra-matrix Mg(2+) limits Ca (2+) uptake and modulates Ca (2+) uptake-independent respiration and redox state in cardiac isolated mitochondria.
- Mitochondrial handling of excess Ca(2+) is substrate-dependent with implications for reactive oxygen speciesgeneration.
- Protection against cardiac injury by small Ca(2+)-sensitive K(+) channels identified in guinea pig cardiac inner mitochondrial membrane.
- Safety and Efficacy of Ranolazine for the Treatment of Chronic Angina Pectoris.
- Differential effects of buffer pH on Ca(2+)-induced ROS emission with inhibited mitochondrial complexes I and III.
- Reversible Blockade of Complex I or Inhibition of PKCβ Reduces Activation and Mitochondria Translocation of p66Shc to Preserve Cardiac Function after Ischemia.
- Mitochondrial targets for volatile anesthetics against cardiac ischemia-reperfusion injury.
- Matching of vertebrate cardiac energy demand to energy metabolism.
- Volatile anesthetics attenuate sympathomimetic actions on the guinea pig SA node.
- Autonomic hyperreflexia in spinal cord injured patients during extracorporeal shock wave lithotripsy.
- Partial attenuation of hemodynamic responses to rapid sequence induction and intubation with labetalol.
- Cardiac cell action potential duration is dependent upon induced changes in free Ca2+ activity during pH changes in vitro.
- Effects of nitrous oxide on contractile function and metabolism of the isolated heart.
- Differential protective effects of halothane and isoflurane against hypoxic and reoxygenation injury in the isolated guinea pig heart.
- A comparison of epidural narcotics, with and without a test dose, to epidural lidocaine for extracorporeal shock wave lithotripsy.
- Direct comparative effects of halothane, enflurane, and isoflurane on oxygen supply and demand in isolated hearts.
- Opposing effects of diacetyl monoxime on contractility and calcium transients in isolated myocardium.
- Additive depressant effects of amiodarone given with halothane in isolated hearts.
- Chronic verapamil treatment depresses automaticity and contractility in isolated cardiac tissues.
- Amrinone reverses cardiac depression and augments coronary vasodilation with isoflurane in the isolated heart.
- Depression of atrial rate, atrioventricular nodal conduction, and cardiac contraction by diltiazem and volatile anesthetics in isolated hearts.
- Attenuation of hemodynamic responses to rapid sequence induction and intubation in healthy patients with a single bolus of esmolol.
- Comparison of halothane, enflurane, and isoflurane with nitrous oxide on contractility and oxygen supply and demand in isolated hearts.
- Comparative cardiac effects of KT-362 and verapamil in isolated heart--correlation to calcium channel current depression.
- Direct comparative effects of isoflurane and desflurane in isolated guinea pig hearts.
- Comparison of etomidate, ketamine, midazolam, propofol, and thiopental on function and metabolism of isolated hearts.
- Halothane reduces dysrhythmias and improves contractile function after global hypoperfusion in isolated hearts.
- Damage to mitochondrial complex I during cardiac ischemia reperfusion injury is reduced indirectly by anti-anginal drug ranolazine.
- Enhanced charge-independent mitochondrial free Ca(2+) and attenuated ADP-induced NADH oxidation by isoflurane: Implications for cardioprotection.
- Reduced Mitochondrial Ca2+ Loading and Improved Functional Recovery after Ischemia Reperfusion Injury in Old vs. Young Guinea Pig Hearts.
- Ranolazine reduces Ca2+ overload and oxidative stress and improves mitochondrial integrity to protect against ischemia reperfusion injury in isolated hearts.
- Mitochondrial approaches to protect against cardiac ischemia and reperfusion injury.
- Adding ROS Quenchers to Cold K+ Cardioplegia Reduces Superoxide Emission During 2-Hour Global Cold Cardiac Ischemia.
- Mitochondrial free [Ca2+] increases during ATP/ADP antiport and ADP phosphorylation: exploration of mechanisms.
- Mitochondrial matrix K+ flux independent of large-conductance Ca2+-activated K+ channel opening.
- Potential therapeutic benefits of strategies directed to mitochondria.
- Comparison of cumulative planimetry versus manual dissection to assess experimental infarct size in isolated hearts.
- Modulation of mitochondrial bioenergetics in the isolated Guinea pig beating heart by potassium and lidocaine cardioplegia: implications for cardioprotection.
- Mitochondrial reactive oxygen species production in excitable cells: modulators of mitochondrial and cell function.
- Enhanced Na+/H+ exchange during ischemia and reperfusion impairs mitochondrial bioenergetics and myocardial function.
- Low-flow perfusion of guinea pig isolated hearts with 26 degrees C air-saturated Lifor solution for 20 hours preserves function and metabolism.
- KATP channel openers have opposite effects on mitochondrial respiration under different energetic conditions.
- Differential increase of mitochondrial matrix volume by sevoflurane in isolated cardiac mitochondria.
- Inhibited mitochondrial respiration by amobarbital during cardiac ischaemia improves redox state and reduces matrix Ca2+ overload and ROS release.
- Isoflurane activates human cardiac mitochondrial adenosine triphosphate-sensitive K+ channels reconstituted in lipid bilayers.
- Reverse electron flow-induced ROS production is attenuated by activation of mitochondrial Ca2+-sensitive K+ channels.
- beta-Blockade abolishes anesthetic preconditioning: impact on clinical applicability.
- Ten-hour preservation of guinea pig isolated hearts perfused at low flow with air-saturated Lifor solution at 26{degrees}C: comparison to ViaSpan solution.
- Mitochondrial inner membrane electrophysiology assessed by rhodamine-123 transport and fluorescence.
- ROS scavenging before 27 degrees C ischemia protects hearts and reduces mitochondrial ROS, Ca2+ overload, and changes in redox state.
- Modulation of electron transport protects cardiac mitochondria and decreases myocardial injury during ischemia and reperfusion.
- Anesthetic preconditioning enhances Ca2+ handling and mechanical and metabolic function elicited by Na+-Ca2+ exchange inhibition in isolated hearts.
- Mitochondrial Ca2+-induced K+ influx increases respiration and enhances ROS production while maintaining membrane potential.
- A comparison of three phosphodiesterase type III inhibitors on mechanical and metabolic function in guinea pig isolated hearts.
- Ischemia reperfusion dysfunction changes model-estimated kinetics of myofilament interaction due to inotropic drugs in isolated hearts.
- Characterization of human cardiac mitochondrial ATP-sensitive potassium channel and its regulation by phorbol ester in vitro.
- Increasing heart size and age attenuate anesthetic preconditioning in guinea pig isolated hearts.
- Ischemia-reperfusion injury changes the dynamics of Ca2+-contraction coupling due to inotropic drugs in isolated hearts.
- Reactive oxygen species as mediators of cardiac injury and protection: the relevance to anesthesia practice.
- Cardiac mitochondrial preconditioning by Big Ca2+-sensitive K+ channel opening requires superoxide radical generation.
- Improved mitochondrial bioenergetics by anesthetic preconditioning during and after 2 hours of 27 degrees C ischemia in isolated hearts.
- Cardioprotection with volatile anesthetics: mechanisms and clinical implications.
- Warm ischemic preconditioning improves mitochondrial redox balance during and after mild hypothermic ischemia in guinea pig isolated hearts.
- Anesthetic preconditioning: the role of free radicals in sevoflurane-induced attenuation of mitochondrial electron transport in Guinea pig isolated hearts.
- Reactive oxygen species and cardiac preconditioning: many questions remain.
- Dual exposure to sevoflurane improves anesthetic preconditioning in intact hearts.
- Attenuation of mitochondrial respiration by sevoflurane in isolated cardiac mitochondria is mediated in part by reactive oxygen species.
- Cardiac pharmacological preconditioning with volatile anesthetics: from bench to bedside?
- Negative inotropic drugs alter indexes of cytosolic [Ca(2+)]-left ventricular pressure relationships after ischemia.
- Comparison of hyperkalemic cardioplegia with altered [CaCl2] and [MgCl2] on [Ca2+]i transients and function after warm global ischemia in isolated hearts.
- Cardiac preconditioning by volatile anesthetic agents: a defining role for altered mitochondrial bioenergetics.
- Reduced reactive O2 species formation and preserved mitochondrial NADH and [Ca2+] levels during short-term 17 degrees C ischemia in intact hearts.
- Hypothermia augments reactive oxygen species detected in the guinea pig isolated perfused heart.
- Effect of low [CaCl2] and high [MgCl2] cardioplegia and moderate hypothermic ischemia on myoplasmic [Ca2+] and cardiac function in intact hearts.
- Ischemic preconditioning: triggering role of nitric oxide-derived oxidants in isolated hearts.
- Cardiotonic drugs differentially alter cytosolic [Ca2+] to left ventricular relationships before and after ischemia in isolated guinea pig hearts.
- How inotropic drugs alter dynamic and static indices of cyclic myoplasmic [Ca2+] to contractility relationships in intact hearts.
- Reactive oxygen species precede the epsilon isoform of protein kinase C in the anesthetic preconditioning signaling cascade.
- Anesthetic preconditioning: effects on latency to ischemic injury in isolated hearts.
- Anesthetic preconditioning improves adenosine triphosphate synthesis and reduces reactive oxygen species formation in mitochondria after ischemia by a redox dependent ...
- Na+/H+ exchange inhibition with cardioplegia reduces cytosolic [Ca2+] and myocardial damage after cold ischemia.
- Sevoflurane exposure generates superoxide but leads to decreased superoxide during ischemia and reperfusion in isolated hearts.
- Preconditioning with sevoflurane reduces changes in nicotinamide adenine dinucleotide during ischemia-reperfusion in isolated hearts: reversal by 5-hydroxydecanoic acid.
- Cross-bridge kinetics modeled from myoplasmic [Ca2+] and LV pressure at 17 degrees C and after 37 degrees C and 17 degrees C ischemia.
- Anesthetic preconditioning attenuates mitochondrial Ca2+ overload during ischemia in Guinea pig intact hearts: reversal by 5-hydroxydecanoic acid.
- Ischemic preconditioning alters real-time measure of O2 radicals in intact hearts with ischemia and reperfusion.
- Sevoflurane preconditioning before moderate hypothermic ischemia protects against cytosolic [Ca(2+)] loading and myocardial damage in part via mitochondrial K(ATP) cha...
- Differences in cardiotoxicity of bupivacaine and ropivacaine are the result of physicochemical and stereoselective properties.
- Altered NADH and improved function by anesthetic and ischemic preconditioning in guinea pig intact hearts.
- Anesthetic preconditioning: triggering role of reactive oxygen and nitrogen species in isolated hearts.
- Cardiac preconditioning with 4-h, 17 degrees C ischemia reduces [Ca(2+)](i) load and damage in part via K(ATP) channel opening.
- Inhibition of Na(+)/H(+) isoform-1 exchange protects hearts perfused after 6-hour cardioplegic cold storage.
- Sevoflurane before or after ischemia improves contractile and metabolic function while reducing myoplasmic Ca(2+) loading in intact hearts.
- Blocking Na(+)/H(+) exchange reduces [Na(+)](i) and [Ca(2+)](i) load after ischemia and improves function in intact hearts.
- Ischemic and anesthetic preconditioning reduces cytosolic [Ca2+] and improves Ca(2+) responses in intact hearts.
- Volatile anaesthetics restore bradykinin and serotonin-induced coronary vasodilation after blocking nitric oxide synthase: lack of anaesthetic effects on KATP channels...
- Changes in [Na(+)](i), compartmental [Ca(2+)], and NADH with dysfunction after global ischemia in intact hearts.
Schools
Medical College of Wisconsin
Med College Wi Affil Hosps
Doctors Specialties
- Anesthesiology
Accepted Insurances
Education
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Medical College of Wisconsin Affiliated Hospitals -
Medical College of Wisconsin
Drug Facts
| NPI NUMBER | 1629043286 | |
| NPPES Provider LastName | STOWE | |
| NPPES Provider FirstName | DAVID | |
| NPPES Provider ZIPCode | 064573654 | |
| NPPES Provider State | CT | |
| Specialty Description | Physician Assistant | |
| Total Claim Count | 83.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1629043286 |
| Last Name Of The Provider | STOWE |
| First Name Of The Provider | DAVID |
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