Lisa Clark
Duke University
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Lisa Clark.
Annals of Surgical Oncology | 2002
Matthew F. Kalady; Bryan M. Clary; Lisa Clark; Marcia R. Gottfried; Eric M. Rohren; R. Edward Coleman; Theodore N. Pappas; Douglas S. Tyler
Background This study examined the effect that 18-fluorodeoxyglucose positron emission tomography (18FDG-PET) imaging had on the clinical management of patients with suspected periampullary malignancy.
Resuscitation | 1993
Peter Rhee; Kenneth Waxman; Lisa Clark; C.Jeffrey Kaupke; Nosratola D. Vaziri; Gail T. Tominaga; Gianna Scannell
Tumor necrosis factor (TNF) is a key mediator involved in many physiologic processes including immunity, inflammation, and metabolism. A relationship between TNF and hemorrhagic shock has not been clearly demonstrated. To help understand the role of TNF in hemorrhagic shock we developed a hemorrhagic shock model to measure TNF and monocyte levels during hemorrhage and resuscitation. Male Sprague-Dawley rats were anesthetized and subjected to a 50% blood loss (30 ml/kg) over 2 min and left in shock for 58 min. The animals were then resuscitated with two times blood loss (60 ml/kg) using lactated Ringers over 1 h. This model results in 75% mortality within 3 days (LD 75). Blood samples (2 ml) were obtained at intervals during shock and resuscitation, and assayed for TNF concentrations and white blood cell counts. Despite a marked fall in total leukocytes (24,600 pre-hemorrhage to 11,300 post-hemorrhage, P < 0.005), monocytes increased in percentage and in total count. Blood levels of TNF were initially undetectable but rose within 10 min after hemorrhage, peaked at 30 min after hemorrhage, and then became undetectable during resuscitation. In this model, macrophages and TNF are released into the circulation after hemorrhagic shock. TNF may play a role as a mediator in the pathophysiology of hemorrhagic shock.
Critical Care Medicine | 1991
Kenneth Waxman; Lisa Clark; Mohammed H. Soliman; Steven Parazin
BackgroundPentoxifylline improves survival in animal models of hemorrhagic shock. The purpose of this study was to determine the physiologic effects of pentoxifylline in hemorrhagic shock that may be responsible for improved survival. MethodsRandomized, prospective, blinded trials in Sprague-Dawley rats subjected to hemorrhage and resuscitation, with or without pentoxifylline. ResultsPentoxifylline had no effect on BP or cardiac output. However, tissue oxygenation and oxygen consumption were increased with pentoxifylline resuscitation. Pentoxifylline resuscitation also significantly decreased polymorphonuclear leukocyte adhesiveness. ConclusionsPentoxifylline improves tissue oxygenation and oxygen consumption posthemorrhage and this effect is not due to increased cardiac output. Therefore, it must be due to improved microcirculatory blood flow. This effect may be due to decreased polymorphonuclear leukocyte adhesiveness induced by pentoxifylline resuscitation. (Crit Care Med 1991; 19:728)
Resuscitation | 1992
Gianna Scannell; Lisa Clark; Kenneth Waxman
UNLABELLED BACKGROUND AND METHODS. Rapid changes in cardiac output (CO) and organ perfusion occur with hemorrhagic shock and fluid resuscitation. To assess regional alterations of flow, 40 Sprague-Dawley male rats were subjected to hemorrhagic shock and crystalloid resuscitation under halothane anesthesia. Polyethylene microspheres were injected before and after hemorrhage and after resuscitation. At sacrifice, brain, lungs, heart, liver, intestine, spleen and kidneys were harvested, weighed and radioactivity counted. Changes in mean arterial pressure, oxygen consumption, organ flow and CO were also measured. RESULTS Cardiac output decreased during hemorrhage (P less than 0.01), it increased with resuscitation but did not return to baseline even with infusion of fluid volumes of three times the blood loss. Flow decreased during hemorrhage in all organs, but the difference was not statistically significant in the liver (P greater than 0.05), since a larger percentage of CO was maintained as hepatic perfusion. During resuscitation, flow to brain and kidneys increased over the percentage values expected by increased CO (P less than 0.01), but flow to the liver did not increase significantly. Flow to small bowel remained depressed (P less than 0.005). CONCLUSIONS Following hemorrhage there is hypoperfusion of all splanchnic organs; however, flow to the liver decreases least. Crystalloid resuscitation in our model failed to return CO to baseline. Blood supply to intestine remained depressed in disproportion to CO both after hemorrhage and resuscitation and hepatic blood flow remained decreased after resuscitation.
Seminars in Surgical Oncology | 1999
E. G. Chekan; Lisa Clark; Justin J. Wu; Theodore N. Pappas; Steve Eubanks
Very few patients with a periampullary neoplasm present with resectable disease. Consequently, various operative and non-operative techniques have been developed to palliate patients with unresectable periampullary disease. Laparoscopic biliary (cholecystojejunostomy) and enteric bypass (gastrojejunostomy) are reasonable options as compared to their open counterparts for operative palliation. However, only a limited number of carefully selected patients meet selection criteria for laparoscopic palliation.
Journal of Surgical Oncology | 1999
Lisa Clark; Edward Ritter; Katie Glazebrook; Douglas S. Tyler
A case report is presented of a woman with recurrent DCIS occurring several years following a total mastectomy, the diagnosis of which was aided by a subpectoral saline implant. A discussion of factors associated with recurrence and a review of the literature is provided. A role for selective use of mammography in screening postmastectomy reconstructed breasts in patients at high risk for recurrence is suggested. J. Surg. Oncol. 1999;71:182–185.
Archive | 1990
Kenneth Waxman; Lisa Clark; Mohammed H. Soliman; Steven Parazin
AbstractWe have previously shown that pentoxifylline (PTF) improves survival in an animal model of hemorrhagic shock. This paper reports upon physiologic effects of PTF in this model which might be responsible for its benefit. In a standardized model of hemorrhagic shock and resuscitation in rats, the effects of PTF added to resuscitation upon blood pressure, cardiac output, tissue oxygenation, and total body oxygen consumption were compared to placebo controls. In addition, the effects of PTF resuscitation upon polymorphonuclear leukocyte (PMN) adhesiveness was measured. PTF had no effect upon blood pressure or cardiac output. However, tissue oxygenation and oxygen consumption were increased with PTF resuscitation. PTF resuscitation also significantly decreased PMN adhesiveness. These data show that PTF improves tissue oxygenation and oxygen consumption following hemorrhage, and that this effect is not due to increased cardiac output. It must therefore be due to improved microcirculatory blood flow and tissue utilization of oxygen. This effect may be due to decreased PMN adhesiveness induced by PTF resuscitation.
American Journal of Roentgenology | 1998
Mary T. Keogan; Douglas S. Tyler; Lisa Clark; Malcolm S. Branch; V G McDermott; David M. DeLong; R.E. Coleman
Respiratory Care Clinics of North America | 1999
Lisa Clark; Richard E. Moon
American Surgeon | 1991
Rhee P; Kenneth Waxman; Lisa Clark; Gail T. Tominaga; Mohammed H. Soliman