| Farmacología clínica y experimental de propofol; un anestésico con propiedades neuroprotectoras |
The Experimental and Clinical Pharmacology of Propofol, an Anesthetic Agent with Neuroprotective Properties
Yoshinori Kotani, Masamitsu Shimazawa, Shinichi Yoshimura, Toru Iwama, Hideaki Hara.
CNS Neuroscience & Therapeutics 14 (2008) 95-10
Propofol (2,6-diisopropylphenol) is a versatile, short-acting, intravenous (i.v.) sedative-hypnotic agent initially marketed as an anesthetic, and now also widely used for the sedation of patients in the intensive care unit (ICU). At the room temperature propofol is an oil and is insoluble in water. It has a remarkable safety profile. Its most common side effects are dose-dependent hypotension and cardiorespiratory depression. Propofol is a global central nervous system (CNS) depressant. It activates γ-aminobutyric acid (GABAA) receptors directly, inhibits the N-methyl-D-aspartate (NMDA) receptor and modulates calcium influx through slow calcium-ion channels. Furthermore, at doses that do not produce sedation, propofol has an anxiolytic effect. It has also immunomodulatory activity, and may, therefore, diminish the systemic inflammatory response believed to be responsible for organ dysfunction. Propofol has been reported to have neuroprotective effects. It reduces cerebral blood flow and intracranial pressure (ICP), is a potent antioxidant, and has antiinflammatory properties. Laboratory investigations revealed that it might also protect brain from ischemic injury. Propofol formulations contain either disodium edetate (EDTA) or sodium metabisulfite, which have antibacterial and antifungal properties. EDTA is also a chelator of divalent ions such as calcium, magnesium, and zinc. Recently, EDTA has been reported to exert a neuroprotective effect itself by chelating surplus intracerebral zinc in an ischemia model. This article reviews the neuroprotective effects of propofol and its mechanism of action.
Keywords: Anesthesia; chelation; disodium edetate (EDTA); middle cerebral artery occlusion (MCAO); neuroprotection;propofol;zinc
Puede leer el artículo en PDF en este enlace: |
| Efectos neuroprotectores del propofol en el daño cerebral agudo |
Neuroprotective Effects of Propofol in Acute Cerebral Injury
Chiara Adembri, Luna Venturi, Domenico E. Pellegrini-Giampietro
Keywords: Cerebral ischemia; Neurodegeneration; Neuroprotection;Neuroresuscitation;Propofol;Traumatic brain injury
CNS Drug Reviews 2007;13:333-351
Abstract
Propofol (2,6-diisopropylphenol) is one of the most popular agents used for induction of anesthesia and long-term sedation, owing to its favorable pharmacokinetic profile, which ensures a rapid recovery even after prolonged administration. A neuroprotective effect, beyond that related to the decrease in cerebral metabolic rate for oxygen, has been shown to be present in many in vitro and in vivo established experimental models of mild/moderate acute cerebral ischemia. Experimental studies on traumatic brain injury are limited and less encouraging. Despite the experimental results and the positive effects on cerebral physiology (propofol reduces cerebral blood flow but maintains coupling with cerebral metabolic rate for oxygen and decreases intracranial pressure, allowing optimal intraoperative conditions during neurosurgical operations), no clinical study has yet indicated that propofol may be superior to other anesthetics in improving the neurological outcome following acute cerebral injury. Therefore, propofol cannot be indicated as an established clinical neuroprotectant per se, but it might play an important role in the so-called multimodal neuroprotection, a global strategy for the treatment of acute injury of the brain that includes preservation of cerebral perfusion, temperature control, prevention of infections, and tight glycemic control.
Lea el artículo completo en PDF en el siguiente enlace: |
|
No hay comentarios:
Publicar un comentario