Pharmacotherapy of Neurochemical Imbalances
Sahab Uddin, Rashid Mamunur in Advances in Neuropharmacology, 2020
It is a highly toxic gas when breathed in large amount. However, it also functions as a neurotransmitter. Its function in the brain is still being clarified. In neurons, enzyme heme oxygenase (HO) degrades heme to form biliverdin, iron, and finally CO. CO stimulates soluble guanylyl cyclase enzyme like NO. In enteric nervous system and olfactory receptor neurons, CO acts as strong neurotransmitter. The neurons of the myenteric plexus contain HO2 and neuronal nitric oxide synthase (nNOS) in abundant amount. Any genetic deletion or pharmacologic inhibition of HO2 considerably decreases noradrenergic neurotransmission in the gut. Similarly, there is reduction in the generation of cGMP in olfactory neurons due to inhibition of heme oxygenase, which normally produce adequate CO to stimulate guanylyl cyclase. Production of CO also plays an important role in the conservation of circadian rhythms by influencing the DNA binding activity of key circadian transcription factors (Nestler et al., 2009; Baranano et al., 2001).
Scheme for Investigating Cases of Death due to Poisoning
Paul T. Jayaprakash in Crime Scene Investigation and Reconstruction, 2023
Major indications in the scene supporting accidental poisoning are evidence of lack of deliberation and willfulness on the part of the victim in exposure to the poison. Examples include carbon-monoxide-related fatalities involving family members sleeping in closed rooms that are connected to defective heating systems or fatalities of individuals relaxing inside cars parked in closed garages with engine and air conditioner turned on. Toxic-gas-related accidental poisoning occurs when individuals get into sewage tanks or into unused wells for cleaning them. In such instances, the SOCOs can tie a live chicken in a rope by its legs and let it go into the depth of the tank or well to verify if it becomes unconscious due to the noxious gases. Accidental poisoning may also be reported during drug and alcohol abuse. Mixing of methyl alcohol with other intoxicating liquors has been the cause for mass fatalities in some parts of India. This author examined a case wherein three friends consuming alcoholic drinks mistakenly mixed cyanide considering it to be chloral hydrate, and all of them died of cyanide poisoning.
The Toxic Environment and Its Medical Implications with Special Emphasis on Smoke Inhalation
Jacob Loke in Pathophysiology and Treatment of Inhalation Injuries, 2020
Carbon-containing material is ubiquitous in the environment. During the incomplete combustion of these materials and in the presence of a limited supply of air or ventilation, carbon monoxide is produced. Studies have shown that the most dangerous toxic gas produced in fires is carbon monoxide (Kimmerle, 1974; Gold et al., 1978; Pitt et ah, 1979;Mierley and Baker, 1983; Lowry et ah, 1985a)(Table 2). It is the predominant cause of death among fire victims at the scene of the fire or during the first 24 hours after the fire (Levine and Radford, 1977).
Liver transcriptome analysis reveals biological pathways and transcription factors in response to high ammonia exposure
Published in Inhalation Toxicology, 2022
Daojie Li, Shuangzhao Chen, Chun Liu, Baoxing Wei, Xiaoping Li
Ammonia is an air pollutant that can cause environmental problems, and it is also a toxic gas that can cause tissue damages in humans and animals. Ammonia in livestock farms can damage the respiratory system by direct inhalation (Wang, Wang, Chen, et al. 2020). Ammonia also affected many other organs through blood circulation system (An et al. 2019; Xing et al. 2019; Xu et al. 2020; Han et al. 2020a). Liver is an important organ for nutrient metabolism and detoxification (Reinke and Asher 2016). The pig liver is a suitable model to study the toxicity of ammonia to human liver (Lada et al. 2020). Transcriptomics is an important tool that can provide an effective information on the mechanisms of body response to environmental stresses. Through RNA extraction, fragmentation, capture, and sequencing, we can obtain the gene expression levels of the whole genome and find the key biological processes and key genes (Owens et al. 2019). Previous studies showed that a concentration of 20 ppm ammonia did not change hepatic gene expression in pigs (Cheng et al. 2014); however, ammonia at a concentration of 118–122 ppm caused liver damage and dysfunction by altering gene networks associated with oxidative stress and immune function in pigs (Zeng et al. 2021). In the present study, we explored hepatic transcriptional changes and identified some genes that may perform key biological functions in response to 80 ppm ammonia exposure in pigs.
Methods and Implementation of the 2019 EMS Practice Analysis
Published in Prehospital Emergency Care, 2022
Ashish R. Panchal, Madison K. Rivard, Rebecca E. Cash, John P. Corley, Marjorie Jean-Baptiste, Kirsten Chrzan, Mihaiela R. Gugiu
Events that had a disposition where no patient interaction occurred (e.g., no patient found or cancelled) were excluded. Events that had both a primary and a secondary impression of a “not value” (not applicable, not recorded, not reporting, not known, or not available) were considered uninformative and, thus, also excluded. Events that had only a primary or a secondary impression of a “not value”, however, were retained. Inhalation injury (toxic gas) and smoke inhalation impressions were combined. Respiratory distress and respiratory arrest impressions were also combined due to encompassing similar domains. Events were classified into categories by impression, with an event being included in the respective category if the primary or secondary impression included that impression. After the exclusion of “not value” impressions, there were a total of 25 impressions that were considered informative.
Comparisons of acute inflammatory responses of nose-only inhalation and intratracheal instillation of ammonia in rats
Published in Inhalation Toxicology, 2019
Linda Elfsmark, Lina Ågren, Christine Akfur, Elisabeth Wigenstam, Ulrika Bergström, Sofia Jonasson
Animals were placed in individual nose-only containers (EMMS, UK) and simultaneous exposed in an inhalation tower (Battelle) providing an equal air flow to each animal of 3 l/min of the NH3 (AGA gas, Sweden; compressed gas in gas cylinders: 25 mol-% NH3, 75 mol-% nitrogen) gas mixture. Rats were subjected to a single exposure of NH3-gas mixture (sub-lethal concentrations in the range of 9000–15 000 ppm, during 10 or 20 min) (Perkins et al. 2016). The NH3-concentration in the inhalation tower was monitored, using the Fix View 7.0 control system (Intellution inc., Norwood, MA), throughout the exposure time (air flow: 20 l/min, temperature: 22 °C and relative humidity 11–12%) and the experiments were conducted in a designated fume hood for toxic gas exposures. While animals were inhaling NH3, control animals were breathing room air in their cages on the bench next to the fume hood (relative humidity 14% in room air). Data regarding body weight-loss, the levels of fibrinogen in serum, total cells in bronchoalveolar lavage fluid (BALF), neutrophils in BALF are shown for NH3-exposure via nose-only inhalation at 24 h. One group of animals exposed to 13 000 ppm was also analyzed on day-14 post-exposure for long-term effects (data not shown).
Related Knowledge Centers
- Carbon Monoxide
- Nitrogen Dioxide
- Permissible Exposure Limit
- Threshold Limit Value
- Toxicity
- Median Lethal Dose
- Short-Term Exposure Limit
- Odor
- Chlorine
- Parts-Per Notation