AI Article Synopsis
- The study investigated the effects of propofol on coronary and myocardial function in a rabbit heart model under normal and hyperoxic conditions.
- Hyperoxia caused significant coronary vasoconstriction, but propofol enhanced coronary vasodilation when hyperoxia was present.
- The findings suggest that while propofol's vasodilatory effects are amplified with increased oxygen levels, its overall impact on myocardial performance remains unchanged regardless of oxygen conditions.
Article Abstract
Unlabelled: We tested the hypothesis that in vitro coronary and myocardial effects of propofol (10-300 microM) should be significantly modified in an isolated and erythrocyte-perfused rabbit heart model in the absence (PaO(2) = 137 +/- 16 mm Hg, n = 12) or in the presence (PaO(2) = 541 +/- 138 mm Hg, n = 12) of hyperoxia. The induction of hyperoxia provoked a significant coronary vasoconstriction (-13% +/- 7%). Propofol induced increased coronary vasodilation in the presence of hyperoxia. Because high oxygen tension has been reported to induce a coronary vasoconstriction mediated by the closure of adenosine triphosphate-sensitive potassium channels, we studied the effects of propofol in 2 additional groups of hearts (n = 6 in each group) pretreated by glibenclamide (0.6 microM) and cromakalim (0.5 microM) in the absence and presence of hyperoxia, respectively. The pretreatment by glibenclamide induced a coronary vasoconstriction (-16% +/- 7%) which did not affect propofol coronary vasodilation. The pretreatment by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. Propofol induced a significant decrease in myocardial performance for a concentration >100 micro M both in the absence and presence of hyperoxia. We conclude that propofol coronary vasodilation is amplified in the presence of hyperoxia. This phenomenon is not explained by the previous coronary vasoconstriction induced by glibenclamide. However, the pretreatment of hearts by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. The myocardial effects of propofol were not affected by the presence of hyperoxia.
Implications: Propofol induced a coronary vasodilation that was amplified in the presence of hyperoxia. This phenomenon does not seem to be related to previous coronary vasoconstriction. The myocardial effects of propofol were not significantly modified in the presence of hyperoxia.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1213/01.ane.0000100681.15355.ac | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Aeromedical evacuation-relevant hypobaria following traumatic brain injury in rats contributes to cerebral blood flow depression, altered neurochemistry, and increased neuroinflammation.
J Cereb Blood Flow Metab
December 2024
Department of Anesthesiology and the Center for Shock Trauma and Anesthesiology Research (STAR), University of Maryland School of Medicine, Baltimore, MD, USA.
Aircraft cabins are routinely pressurized to the equivalent of 8000 ft altitude. Exposure of lab animals to aeromedical evacuation relevant hypobaria after traumatic brain injury worsens neurological outcomes, which is paradoxically exacerbated by hyperoxia. This study tested the hypothesis that exposure of rats to hypobaria following cortical impact reduces cerebral blood flow, increases neuroinflammation, and alters brain neurochemistry.
View Article and Find Full Text PDFCerebral capillary oxygen diffusion: exploring the concept of intracapillary hemoglobin conformational changes.
Intensive Care Med Exp
November 2024
The Ohio State University, Wexner Medical Center N411 Doan Hall, 410 West 10Th Avenue, Columbus, OH, 43210, USA.
The mechanisms of oxygen diffusion in brain capillaries have not been fully clarified to date. According to the laws of physics, the well-documented phenomenon of hyperoxemia-induced excessive increases in brain tissue oxygen pressure (PbtO2) contradicts traditional models of cerebral capillary oxygen diffusion. Circulating models predict a significant drop in oxygen pressure (PO2), and some of them foresee the presence of hypoxic or anoxic corners near the capillary end, regardless of high PbtO2 levels.
View Article and Find Full Text PDFLoss of Surfactant Protein A Alters Perinatal Lung Morphology and Susceptibility to Hyperoxia-Induced Bronchopulmonary Dysplasia.
Antioxidants (Basel)
October 2024
Department of Pediatrics, Division of Neonatal-Perinatal Medicine, Pulmonary Immunology and Physiology Laboratory, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.
Bronchopulmonary dysplasia (BPD) is a condition of poor alveolar formation that causes chronic breathing impairment in infants born prematurely. Preterm lungs lack surfactant and are vulnerable to oxidative injuries driving the development of BPD. Our recent studies reported that surfactant protein A (SP-A) genetic variants influence susceptibility to neonatal lung disease.
View Article and Find Full Text PDFHyperbaric oxygen rapidly produces intracellular bioenergetics dysfunction in human pulmonary cells.
Chem Biol Interact
December 2024
Department of Anesthesiology, The Ohio State University, Columbus, OH, 43210, USA; Center for Medical and Engineering Innovation, The Ohio State University, Columbus, OH, 43210, USA. Electronic address:
Hyperoxic exposure lasting days alters mitochondrial bioenergetic and dynamic functions in pulmonary cells as indices of oxygen toxicity. The aim of this study was to examine effects of short duration hyperbaric and hyperoxic exposures to induce oxygen toxicity similarly. Cultured human lung microvascular endothelial cells, human pulmonary artery endothelial cells and A549 cells were exposed to hyperoxia (∼5 % CO equivalent, balance O) under hyperbaric conditions (4.
View Article and Find Full Text PDFEumelanin and Pheomelanin Modelling in Optical Oximetry Using Pulse Oximetry (for 540 nm and 660 nm): DC Component.
Adv Exp Med Biol
October 2024
Division of Biomedical Engineering, School of Engineering, University of Glasgow, Glasgow, UK.
Oximetry is used to quantify the presence of oxygen in soft tissues. It can be expressed as, for example, tissue oxygen saturation (StO), arterial oxygen saturation (SaO) and pulsatile oxygen saturation (SpO), among others. Non-invasive medical devices are used to estimate (SaO).
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!