چاپ صفحه |  صفحه نخست سامانه |  چکیده مقاله |  نویسندگان |  دانلود مقاله | دانشگاه علوم پزشکی تبریز |
| Once admired for its supposed safety, nitrous oxide is presently blamed to increase adverse cardiovascular effects through augmenting plasma homocysteine concentrations (1, 2). Hemodynamic alterations following the administration of nitrous oxide are extremely complicated and sometimes contradictory. Enhanced venous return, arterial pressure, pulmonary and systemic vascular resistance, cardiac output, pupillary dilation and diaphoresis occur under nitrous oxide administration consistent with sympathomimetic properties of nitrous oxide (3). Conversely, reductions in arterial pressure are also probable, especially in patients with coronary artery disease. Nitrous oxide can also depress myocardial contractility due to decreased availability of Ca2+ for contractile activation; yet, myocardial relaxation kinetics remains intact (4). In the presence of a volatile anesthetic, nitrous oxide decreases MVO2 (Myocardial oxygen consumption) and myocardial O2 extraction which may exacerbate myocardial ischemia during concomitant reductions in arterial pressure in patients with coronary artery disease. Consequently, it could be conjectured that probable adverse cardiovascular effects following nitrous oxide administration are variable and consequent of a multi-variable phenomenon rather than a single variable such as increased levels of homocysteine. Studied purely focusing on the effects of nitrous oxide are difficult to conduct due to the numerous confounding factors. |
| نویسنده | نفر چندم مقاله |
|---|---|
| عطا محمودپور | اول |
| صمد اسلام جمال گلزاری | دوم |
| نام فایل | تاریخ درج فایل | اندازه فایل | دانلود |
|---|---|---|---|
| E-Cardiovascular Nitrous Oxide.pdf | 1398/09/04 | 220916 | دانلود |
