antidote/hypoxia

Paraoxon in doses of one LD50 (0.426 mg/kg), eight times and eighty times LD 50 was applied s.c. to female Sprague-Dawley rats. After 3, 6, 10, 24 and 36--48 h the activities of enzymes GOT, GPT, GLDH, SDH, CPK and ChE were measured, once after i.m. antidote application of Toxogonin only, of

BACKGROUND Current management of acute inhalational carbon monoxide (CO) toxicity includes hyperbaric or normobaric O2 therapy. However, efficacy has not been established. The purpose of this study was to establish therapeutic proof of concept for a novel injectable antidote consisting of the

Cyanide is a rapidly acting and highly toxic chemical. It inhibits cytochrome c oxidase in the mitochondrial electron transport chain, resulting in cellular hypoxia, cytotoxic anoxia and potentially death. In order to overcome challenges associated with current cyanide antidotes, dimethyl trisulfide

The authors carried out studies on 18 nonanesthetised and anesthetised cats under the conditions of complete imobilization with tricuran and under artificial respiration and examined the temporary consequence of the effects on the spontaneous and induced cerebral activity after poisoning with lethal

OBJECTIVE Hydrogen sulfide (H2S) is a highly toxic gas for which no effective antidotes exist. It acts, at least in part, by binding to cytochrome c oxidase, causing cellular asphyxiation and anoxia. We investigated the effects of three different ligand forms of cobinamide, a vitamin B12 analog, to

Isolated perfused livers from rats fasted 16 h before surgery showed a strong decrease in oxygen consumption as well as hepatotoxic responses when subjected to 30 min of hypoxia (95%, N2/5% CO2) followed by 90 min of reoxygenation (95% O2/5% CO2). Toxicity was evident by a release of enzymes (LDH,

Acetaminophen (APAP) overdose represents the most frequent cause of acute liver failure, resulting in death or liver transplantation in more than one-third of patients in the United States. The effectiveness of the only antidote, N-acetylcysteine (NAC), declines rapidly after APAP ingestion, long

Physiological metabolism of cyanide takes place by a single major pathway that forms non-toxic thiocyanate that is subsequently excreted. Rhodanese is the primary enzyme to execute metabolism of cyanide with minor pathways from other sulfurtransferases in vivo. The rhodanese enzyme depends on sulfur

Aluminum phosphide (ALP) poisoning is one of the major causes of suicidal deaths. Toxicity by ALP is caused by the liberation of phosphine gas, which rapidly causes cell hypoxia due to inhibition of oxidative phosphorylation, leading to circulatory failure. Treatment of ALP toxicity is mainly

The toxicity of a combination of isopropyl methylphosphonofluoridate (sarin; GB) and cyclohexyl methylphosphonofluoridate (GF) and the efficacy of various oxime reactivators in combination with atropine against the combined GB/GF challenge were evaluated in mice. The 24-h s.c. LD50 of the GB/GF

Cyanide is a toxic compound which inhibits the cellular utilization of oxygen. A number of substances can give rise to cyanide intoxication, which in some cases may have a delayed onset. The symptoms are non-specific and reflect cellular hypoxia. Several strategies may be employed in the treatment.

Carbon monoxide and cyanide are toxins that induce cellular hypoxia; both can be produced in the context of domestic fires and may have a synergistic effect. We present the case of a man, victim of a house fire, who was initially diagnosed as having carbon monoxide poisoning, but that afterwards

Cyanide poisoning is a life threatening condition. But specific antidotes exist and can be easily prepared from available substances in hospital. Administration of antidotes will produce methemoglobin, which itself causes hypoxia. Nitrite induced methemoglobin can be extremely dangerous and even

Respiratory tract injuries caused by inhalation of smoke or chemical products are related to significant morbidity and mortality. While many strategies have been built up to manage cutaneous burn injuries, few logical diagnostic strategies for patients with inhalation injuries exist and almost all

Combustion toxicology is complex so, although victims exposed to combustion products are mainly treated symptomatically, it is important to identify those situations when specific therapeutic measures might be of importance. Victims presenting respiratory symptoms including severe cough,