Biomedical subjects

Judy R Kersten

Publications and source records attributed to Judy R Kersten.

58 records · Page 4Linked to original sources

PubMedDate not supplied

Antegrade iliac artery stent implantation for the temporal and spatial examination of stent-induced neointimal hyperplasia and alterations in regional fluid dynamics.

INTRODUCTION: Neointimal hyperplasia remains an important problem after stent implantation. Previous investigations examining vascular responses to stent implantation and effects of drugs have used a retrograde deployment approach that may inadvertently alter the local fluid dynamics surrounding the stent. We present a model of antegrade iliac artery stent implantation that facilitates the analysis of stent-induced alterations in neointimal hyperplasia and wall shear stress in vivo. METHODS: Stent delivery catheters were inserted through the left carotid artery in anesthetized rabbits (n=37). Catheters were advanced under fluoroscopic guidance to the distal iliac arteries, where the stent was deployed. Hemotoxylin and eosin (H&E) staining of unstented and stented vascular sections was performed 21 days after implantation. RESULTS: Selective unilateral stent implantation was successful in 32 of 37 rabbits. No histological abnormalities were observed in the aorta, contralateral unstented iliac, or distal femoral arteries. Neointimal hyperplasia was localized to the stented region. DISCUSSION: The model of stent implantation was relatively easy to perform and produced selective neointimal hyperplasia within the stented region without evidence of damage, cellular proliferation, or flow disruption in the surrounding normal arterial vessels. The model will allow detailed examination of the influence of stent implantation on indices of wall shear stress, neointimal hyperplasia, the mechanisms of cellular proliferation in vivo, and their modification by drugs.

Animals↗

PubMedDate not supplied

Cardioprotection by volatile anesthetics.

Preconditioning describes a very powerful endogenous mechanism by which the heart may be protected against ischemia and reperfusion injury. Transient administration of a volatile anesthetic before a prolonged ischemic episode reduces myocardial infarct size to a degree comparable to that observed during ischemic preconditioning. Many components of the signal transduction pathways responsible for cardioprotection are shared by anesthetic and ischemic preconditioning. Exposure to volatile anesthetics generates small "triggering" quantities of reactive oxygen species (ROS) by directly interacting with the mitochondrial electron transport chain or indirectly through a signaling cascade in which G-protein-coupled receptors, protein kinases, and mitochondrial ATP-sensitive potassium (K(ATP)) channels play important roles. Several clinical studies also suggest that preconditioning by volatile anesthetics exerts beneficial effects in patients undergoing cardiac surgery. This review summarizes some of the recent major developments in the understanding of cardioprotection by volatile anesthetics.

Anesthetics, Inhalation↗

PubMedDate not supplied

An intramyocardial catheter for repeated in vivo sampling of interstitial fluid.

INTRODUCTION: Coronary collateral development is an important adaptive response to chronic myocardial ischemia. Characterization of mitogenic factors responsible for collateral formation has been an elusive goal because these substances are difficult to sample from the myocardial interstitium at multiple times. We report the implantation of an exchange catheter capable of in vivo sampling of myocardial interstitial fluid in chronically instrumented dogs. METHODS: The catheter consisted of multiple perforations within a 2-cm segment of Micro-Renathane tubing that was implanted into the left ventricular myocardium between the left anterior descending (LAD) and left circumflex coronary artery (LCCA) perfusion territories and secured to the epicardium with a Silastic disk. Dogs (n=5) underwent brief (2 min) LAD occlusions once per hour, 8 times/day, 7 days/week for 2 weeks to stimulate coronary collateral growth. Another group of dogs (n=6) without repetitive coronary occlusions served as controls. Myocardial interstitial fluid was collected daily, and mitogenic activity was evaluated by the proliferative responses of growth-arrested, cultured vascular smooth muscle and endothelial cells. RESULTS: All dogs tolerated catheter implantation without complication. Each catheter functioned well throughout the duration of the experiment. Myocardial interstitial fluid obtained using the exchange catheter in this model of repetitive coronary occlusion produced marked proliferation of vascular smooth muscle and endothelial cells in vitro. DISCUSSION: The exchange catheter enables chronic in vivo sampling of myocardial interstitial fluid and may facilitate identification of mitogens involved in coronary collateral development.

Animals↗

PubMedDate not supplied

An automated coronary artery occlusion device for stimulating collateral development in vivo.

INTRODUCTION: Repetitive, brief coronary artery occlusions produce collateral development in experimental animals. This model causes coronary collateralization in a highly reproducible fashion, but the process is very labor intensive. We report the design and use of a fully automated hydraulic coronary occlusion device capable of producing repetitive coronary occlusions and enhancement of coronary collateral development in dogs. METHODS: The device consists of analog electronics that allow adjustment of occlusion number, frequency, pressure and duration, and mechanical components responsible for the coronary occlusion. The motor and piston of the device are coupled to a chronically implanted hydraulic vascular occluder placed around the left anterior descending coronary artery (LAD) of dogs instrumented for measurement of systemic and coronary hemodynamics. One group of dogs (n = 6) underwent brief (2 min) LAD occlusions once per hour, eight times per day, 5 days/week for 3 weeks to stimulate collateral development (measured using radioactive microspheres). Another group of dogs (n = 6) that did not receive repetitive occlusions served as controls. RESULTS: The device reproducibly produced repetitive LAD occlusions for the duration, frequency, and time interval initially programmed. A time-dependent increase in transmural collateral blood flow was observed in dogs undergoing repetitive occlusions using the device. Collateral blood flow was unchanged in dogs that did not undergo occlusions. DISCUSSION: The automated occluder device reliably produces repetitive coronary occlusions and may facilitate further study of coronary collateral development in response to chronic myocardial ischemia.

Animals↗