diazepam/nekroz

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Diazepam-induced coma with bullae and eccrine sweat gland necrosis.

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Bullous skin lesions that indicate sweat gland necrosis have been known to occur in drug-induced coma resulting from barbiturates and in carbon monoxide poisoning. To our knowledge, this is the first cases in which diazepam is implicated in causing bullous lesions over pressure points, and the first

Necrosis of the 4th and 5th digits after intra-articular injection of diazepam into the wrist.

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A 75-year-old woman presented with progressing pain, cyanosis, and hypaesthesia in her left hand after an intra-articular injection with diazepam into the wrist for osteoarthritis-related pain. Due to an iatrogenic intra-arterial injection, malperfusion of the ulnar digits developed. Angiography

Endogenous anxiogenic peptide, ODN-diazepam-binding inhibitor, and benzodiazepines enhance the production of interleukin-1 and tumor necrosis factor by human monocytes.

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Benzodiazepines (BZD) have been described to interact with specific peripheral-type receptors on phagocytes. The present study demonstrates that pico- to nanomolar concentrations of BZD compounds enhance the lipopolysaccharide (LPS)-induced production of tumor necrosis factor (TNF) and interleukin-1

Acute hepatic necrosis following treatment with amitriptyline and diazepam.

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Alterations in interleukin-6 production by LPS- and Con A-stimulated mixed splenocytes, spleen macrophages and lymphocytes in prenatally diazepam-exposed rats.

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Prenatal exposure to diazepam leads to a suppression of mitogen or allogen-induced lymphocyte proliferation as well as to a reduced production of tumour necrosis factor (TNF)-alpha from rat splenocytes during postnatal development of rats. We analysed the secretion of interleukin (IL)-6 which occurs

The effect of prenatal diazepam exposure on TNF-alpha production by rat splenocytes.

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Prenatal exposure to diazepam and other benzodiazepines (BDZ) has been found to result in a marked reduction of T-lymphocyte proliferation during postnatal development of rats. In search for pathogenic changes underlying this effect, we investigated the mitogen lipopolysaccharide (LPS) and

Poloxamer 188 as vehicle for injectable diazepam.

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The significant occurrence of thrombophlebitis in patients administered diazepam intravenously was described recently. This side effect has been attributed to the crystallization of diazepam and its subsequent precipitation upon contact with blood or intravenous fluids. The current study was

[An autopsied case of dementia with lewy bodies presenting with hemispheric cerebral cortical atrophy with selective neuronal necrosis after status epilepticus].

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We report on a 72-year-old-Japanese man with dementia with Lewy bodies (DLB) who presented with hemispheric cerebral cortical atrophy with selective neuronal necrosis after status epilepticus. His disease manifested with psychiatric symptoms, such as a "hot feeling" in the abdomen, at the age of 68

The anticonvulsive activity and toxicity of diazepam in three different formulations. An experimental study in mice.

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The anticonvulsive activity (ED50), acute toxicity (LD50), and minimal neurotoxicity (TD50) of diazepam in an emulsion form (Diazemuls) were compared with two different water-based diazepam solutions (Valium and Stesolid). The diazepam preparations were administered intravenously to male mice. After

Diazepam versus fentanyl for premedication during percutaneous coronary intervention: results from the Myocardial Protection by Fentanyl during Coronary Intervention (PROFIT) Trial.

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BACKGROUND Sedation is a cornerstone in the premedication for percutaneous coronary intervention (PCI). Benzodiazepines and opioids are frequently used. Previous results suggest that opioids mimic the adaptation to ischemia during repeated balloon inflations and may provide direct myocardial

Diazepam delays the death of hippocampal CA1 neurons following global ischemia.

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Although diazepam provides limited long term neuroprotection, it may be useful for expanding the therapeutic time window after stroke by delaying neuronal death. However, it is not known to what extent diazepam maintains normal cellular structure and function in the first few days after ischemia. We

Postischemic seizures and necrotizing ischemic brain damage: neuroprotective effect of postischemic diazepam and insulin.

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Insulin has recently been shown experimentally to modify ischemic brain damage when administered either before or after the episode of ischemia. In controlled studies in the rat, high doses of insulin (greater than or equal to 8 IU/kg) result in seizures and early death. The present study was

The role of diazepam in the treatment of nerve agent poisoning in a civilian population.

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The main site of action of diazepam, as with other benzodiazepines, is at the GABA(A) receptor, although it has been suggested that some of the potentially beneficial actions of diazepam in nerve agent poisoning are mediated through other means. It is likely that convulsions may have long-term

Necrosis of hippocampus and piriform lobe: clinical and neuropathological findings in two Italian cats.

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The present paper reports the clinical and neuropathological findings in two cats with a neuropathologically confirmed diagnosis of necrosis of the hippocampus and piriform lobe. The cats were presented because of acute onset of behavioural changes and complex partial seizures. The neurological

The effect of diazepam on myocardial function and coronary vascular tone after endotoxemia in the isolated rat heart model.

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OBJECTIVE Tumor necrosis factor alpha (TNF-α) has been implicated in the pathogenesis of cardiovascular disease and sepsis-associated cardiac dysfunction. Although initially described solely as a lipopolysaccharide (LPS)-induced macrophage product, evidence exists that cardiac myocytes themselves

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