scispace - formally typeset
Search or ask a question
Author

Rebecca J. Dignan

Bio: Rebecca J. Dignan is an academic researcher from VCU Medical Center. The author has contributed to research in topics: Artery & Myograph. The author has an hindex of 9, co-authored 14 publications receiving 413 citations.

Papers
More filters
Journal ArticleDOI
TL;DR: The detailed evaluation of left ventricular chamber mechanics suggests that dynamic cardiomyoplasty may have a role in ameliorating the functional and mechanical derangements associated with progression of dilatedCardiomyopathy both by augmenting cardiac performance and by diminishing determinants of myocardial oxygen consumption.

94 citations

Journal ArticleDOI
TL;DR: Prevention of platelet-, adrenergic-, or potassium-induced contraction may be more important when the gastroepiploic artery is used as an alternate conduit for coronary artery bypass, reinforcing consideration of nitrovasodilators and platelet inhibitors in the perioperative interval.

63 citations

Journal ArticleDOI
TL;DR: Pentafraction lessened weight gain and fluid requirements during cardiopulmonary bypass, favorably influencing the percent tissue water of certain organs, including heart, lung, liver, spleen, skin, or brain.

57 citations

Journal ArticleDOI
TL;DR: It is hypothesized that coronary artery endothelial cell function and smooth muscle function are modified by global myocardial ischemia and bradykinin-induced secretion of endothelium-derived relaxing factor as a marker of endothelialcell function is used.

54 citations

Journal ArticleDOI
TL;DR: This study suggests that triiodothyronine supplementation significantly enhances postischemic left ventricular functional recovery and that this recovery is due to mechanisms other than enhanced availability of myocardial high-energy phosphates.

40 citations


Cited by
More filters
Journal ArticleDOI
TL;DR: The molecular responses of neutrophils to ischemia-reperfusion are described, the cellular and tissue damage inflicted either directly or indirectly by these white cells are discussed, and the physiological impact of interdiction ofNeutrophil-mediated interactions with myocardial cells at various levels on lethal post-ischemic injury are discussed.
Abstract: Neutrophils respond to myocardial ischemia-reperfusion in a manner similar to the bacterial invasion of a host. The inflammatory-like response that follows the onset of reperfusion involves intense interactions with the coronary vascular endothelium, arterial wall, and cardiomyocytes in a very well-choreographed manner. Neutrophils have been implicated as primary and secondary mediators of lethal injury after reperfusion to coronary vascular endothelium and cardiomyocytes. The involvement of neutrophils in the pathogenesis of lethal myocardial injury has been inferred from (1) their presence and accumulation in reperfused myocardium in temporal agreement with injury induced, (2) the armamentarium of toxic agents such as oxidants and proteases that are released by neutrophils in reperfused myocardium, (3) responsivity to (recruitment by and/or activation by) inflammatory factors released by reperfused myocardium, and (4) inhibition of lethal post-ischemic myocyte or endothelial cell injury by strategies that interdict neutrophil interactions at any number of stages. However, whether neutrophils are directly involved in the pathogenesis of lethal reperfusion injury in the myocardium, are just pedestrian (first) responders to inflammatory signals released after the onset of reperfusion, or are important to an early but not clinically important phase of pathology are still points of controversy. As with the general area of myocardial protection itself, the failure to reproduce the salubrious effects of anti-neutrophil therapeutic strategies and to successfully translate these strategies into clinical practice has not only fueled the debate, but has jeopardized the further pursuit of myocardial protection therapeutics to improve post-ischemic outcomes. This review will describe the molecular responses of neutrophils to ischemia-reperfusion, discuss the cellular and tissue damage inflicted either directly or indirectly by these white cells, and discuss the physiological impact of interdiction of neutrophil-mediated interactions with myocardial cells at various levels on lethal post-ischemic injury. In addition, it will discuss the arguments for and against the involvement of neutrophils in responses to ischemia-reperfusion in experimental models, and the failure to translate experimentally successful therapy into clinical practice.

636 citations

Journal ArticleDOI
TL;DR: The understanding of the molecular processes regulating actions of neutrophils in ischemic-reperfusion injury may be applicable to other clinical situations, such as trauma, shock and organ or tissue (i.e. vascular conduits) transplantation.
Abstract: Reperfusion of ischemic myocardium is necessary to salvage tissue from eventual death. However, reperfusion after even brief periods of ischemia is associated with pathologic changes that represent either an acceleration of processes initiated during ischemia per se, or new pathophysiological changes that were initiated after reperfusion. This 'reperfusion injury' shares many characteristics with inflammatory responses in the myocardium. Neutrophils feature prominently in this inflammatory component of postischemic injury. Ischemia-reperfusion prompts a release of oxygen free radicals, cytokines and other proinflammatory mediators that activate both the neutrophils and the coronary vascular endothelium. Activation of these cell types promotes the expression of adhesion molecules on both the neutrophils and endothelium, which recruits neutrophils to the surface of the endothelium and initiate a specific cascade of cell-cell interactions, leading first to adherence of neutrophils to the vascular endothelium, followed later by transendothelial migration and direct interaction with myocytes. This specific series of events is a prerequisite to the phenotypic expression of reperfusion injury, including endothelial dysfunction, microvascular collapse and blood flow defects, myocardial infarction and apoptosis. Pharmacologic therapy can target the various components in this critical series of events. Effective targets for these pharmacologic agents include: (a) inhibiting the release or accumulation of proinflammatory mediators, (b) altering neutrophil or endothelial cell activation and (c) attenuating adhesion molecule expression on endothelium, neutrophils and myocytes. Monoclonal antibodies to adhesion molecules (P-selectin, L-selectin, CD11, CD18), complement fragments and receptors attenuate neutrophil-mediated injury (vascular injury, infarction), but clinical application may encounter limitations due to antigen-antibody reactions with the peptides. Humanized antibodies and non-peptide agents, such as oligosaccharide analogs to sialyl Lewis, may prove effective in this regard. Both nitric oxide and adenosine exhibit broad spectrum effects against neutrophil-mediated events and, therefore, can intervene at several critical points in the ischemic-reperfusion response, and may offer greater benefit than agents that interdict at a single point in the cascade. The understanding of the molecular processes regulating actions of neutrophils in ischemic-reperfusion injury may be applicable to other clinical situations, such as trauma, shock and organ or tissue (i.e. vascular conduits) transplantation.

592 citations

Patent
23 Jan 1997
TL;DR: In this paper, a method for less-invasive repair or replacement of a cardiac valve comprises placing an instrument through an intercostal access port and through a penetration in a wall of a vessel in communication with the heart.
Abstract: Systems and methods are disclosed for performing less-invasive surgical procedures within the heart. A method for less-invasive repair or replacement of a cardiac valve comprises placing an instrument through an intercostal access port and through a penetration in a wall of a vessel in communication with the heart, advancing the instrument into the heart, and using the instrument to perform a surgical intervention on a cardiac valve in the heart under visualization through an intercostal access port. The surgeons hands are kept outside of the chest during each step. The surgical intervention may comprise replacing the cardiac valve with a prosthetic valve, wherein the native valve is removed using a tissue removal instrument, the native valve annulus is sized with a specialized sizing device, a prosthetic valve is introduced through an intercostal access port and through the penetration in the vessel, and the prosthetic valve is secured at the native valve position, all using instruments positioned through intercostal access ports without placing the hands inside the chest. Systems and devices for performing these procedures are also disclosed.

482 citations

Patent
19 Oct 2001
TL;DR: In this paper, a port-access coronary artery bypass (CABG) surgery is performed through small incisions or access ports made through the intercostal spaces between the patient's ribs, resulting in greatly reduced pain and morbidity.
Abstract: Surgical methods and instruments are disclosed for performing port-access or closed-chest coronary artery bypass (CABG) surgery in multivessel coronary artery disease. In contrast to standard open-chest CABG surgery, which requires a median sternotomy or other gross thoracotomy to expose the patient's heart, port-access CABG surgery is performed through small incisions or access ports made through the intercostal spaces between the patient's ribs, resulting in greatly reduced pain and morbidity to the patient. In situ arterial bypass grafts, such as the internal mammary arteries and/or the right gastroepiploic artery, are prepared for grafting by thoracoscopic or laparoscopic takedown techniques. Free grafts, such as a saphenous vein graft or a free arterial graft, can be used to augment the in situ arterial grafts. The graft vessels are anastomosed to the coronary arteries under direct visualization through a cardioscopic microscope inserted through an intercostal access port. Retraction instruments are provided to manipulate the heart within the closed chest of the patient to expose each of the coronary arteries for visualization and anastomosis. Disclosed are a tunneler and an articulated tunneling grasper for rerouting the graft vessels, and a finger-like retractor, a suction cup retractor, a snare retractor and a loop retractor for manipulating the heart. Also disclosed is a port-access topical cooling device for improving myocardial protection during the port-access CABG procedure. An alternate surgical approach using an anterior mediastinotomy is also described.

335 citations

Journal ArticleDOI
TL;DR: It is concluded that intravascular volume replacement with 6% HES 130/0.4 improved tissue oxygenation during and after major surgical procedures compared with a crystalloid-based volume replacement strategy.
Abstract: UNLABELLED The effects of intravascular volume replacement regimens on tissue oxygen tension (ptiO(2)) are not definitely known. Forty-two consecutive patients scheduled for elective major abdominal surgery were prospectively randomized to receive either 6% hydroxyethyl starch (HES) (mean molecular weight 130 kd, degree of substitution 0.4, n = 21) or lactated Ringer's solution (RL, n = 21) for intravascular volume replacement. Fluids were administered perioperatively and continued for 24 h on the intensive care unit to keep central venous pressure between 8 and 12 mm Hg. The ptiO(2) was measured continuously in the left deltoid muscle by using microsensoric implantable partial pressure of oxygen catheters after the induction of anesthesia (baseline, T0), 60 min (T1) and 120 min thereafter (T2), at the end of surgery (T3), and on the morning of the first postoperative day on the intensive care unit (T4). HES 130/0.4 2920 +/- 360 mL and 11,740 +/- 2,630 mL of RL were given to the patients within the study period. Systemic hemodynamics and oxygenation (PaO(2), PaCO(2)) did not differ significantly between the two volume groups throughout the study. From similar baseline values, ptiO(2) increased significantly in the HES-treated patients (a maximum of 59% at T4), whereas it decreased in the RL group (a maximum of -23% at T4, P < 0.05). The largest differences of ptiO(2) were measured on the morning of the first postoperative day. We conclude that intravascular volume replacement with 6% HES 130/0.4 improved tissue oxygenation during and after major surgical procedures compared with a crystalloid-based volume replacement strategy. Improved microperfusion and less endothelial swelling may be responsible for the increase in ptiO(2) in the HES 130/0.4-treated patients. IMPLICATIONS In patients undergoing major abdominal surgery, a colloid-based (with hydroxyethyl starch [HES] 130/0.4) and a crystalloid-based (with lactated Ringer's solution [RL]) volume replacement regimen was compared regarding tissue oxygen tension (ptiO(2)) measured continuously by microsensoric implantable catheters. The ptiO(2) increased in the HES-treated (+59%) but decreased in the RL-treated (-23%) patients. Improved microcirculation may be the mechanism for the better ptiO(2) in the HES group.

266 citations