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To analyze whether the use of morphine, as initial treatment in acute cardiogenic pulmonary edema (ACPE), has an impact in clinical outcomes and mortality. A systematic review of the literature was performed, including all the studies comparing clinical outcomes in patients with ACPE OBJECTIVE
Morphine has been used for several decades in cases of acute pulmonary edema (APE) due to the anxiolytic and vasodilatory properties of the drug. The non-specific depression of the central nervous system is probably the most significant factor for the changes in hemodynamics in APE.
We compared four treatment protocols in 57 patients with presumed pre-hospital pulmonary edema. Group A patients were treated with nitroglycerin and furosemide, group B patients with morphine sulfate and furosemide, group C with all three agents, and group D with nitroglycerin and morphine, but
Intrathecal therapy [IT] has become an important modality for treatment of intractable cancer and noncancer pain although adverse events limit its effectiveness.
The purpose of this case series was to report and discuss the lower limb edema from IT hydromorphone and morphine therapy and its
We evaluated the anti-edema/antinociceptive effects of subcutaneous free and liposomal morphine in rats with carrageenan-induced inflammation of the paw. We assessed antinociception by the paw pressure test and edema by plethysmography. Unilamellar liposomes (150-200 nm) with 0.3% morphine
In order to assess possible renal mechanisms causing the as yet unexplained side-effects of peripheral edema, weight gain and swollen limbs seen during the chronic administration of opioids in patients, a rat study was designed, mimicking a constant infusion (24 h) of morphine (CAS 57-27-2) using
BACKGROUND
Nitrates are superior to furosemide in the management of acute pulmonary edema associated with myocardial infarction; however, their role in the absence of infarction is unclear.
RESULTS
A randomized comparison was undertaken of the relative effectiveness of primary therapy with either
Neurogenic inflammation, includes vasodilation, the increase of vasal permeability and edema due to the release of neuromediators from nerve endings. A modulation of the release of neurotransmitters, from nerve endings and neurogenic inflammation related phenomena, was observed with the
We report the case of an 11-yr-old boy who developed a non-cardiogenic pulmonary edema following inhalation of chlorine gas at a swimming pool. Rapid clinical improvement was noted after i.v. administration of morphine.
In order to compare the venodilation effect of morphine in normal individuals (22) with that in patients (13) with heart failure morphine sulfate (0.1 mg/kg) was administered to 13 patients with mild pulmonary edema. After morphine congestive symptoms improved and venodilation was induced as
The role of opioid receptors located in the central nervous system (CNS) and peripheral nervous system in inflammatory pain is well established. In contrast, although it is has been shown that mu agonists can reduce other manifestations of inflammation, such as edema, the mechanism of action remains
Standard treatment strategy for acute cardiogenic pulmonary edema includes noninvasive positive pressure ventilation as an alternative treatment for patients with acute cardiogenic pulmonary edema who require endotracheal intubation. Even in the improvement of hypoxemia, the beneficial effects
BACKGROUND
Morphine can inhibit inflammatory edema in experimental animals. The mechanisms and sites by which opioids exert this effect are still under debate. Since the spinal level is a site for modulation of the neurogenic component of inflammation, we investigated the effect of intrathecal
Recent studies suggest that peripheral morphine may represent a valuable treatment in inflammatory painful diseases. This study examined effects of intraplantar morphine against noxious pressure and paw edema in rats with repeated acute inflammation induced by two carrageenin injections 7 days
Morphine withdrawal response is associated with brain edema formation, blood-brain barrier (BBB) disruption, activation of glial cells and heat shock protein (HSP 72kDa) responses in the CNS. Thus, exploration of suitable therapeutic measures is the need of the hour to induce neuroprotection in