Respiratory inhibitors effect

Efflux is blocked by compounds such as respiratory inhibitors that decrease levels of ATP. Apparently the influx-efflux mechanism is dependent on intracellular ATP, which is utilized by the plasma membrane ATPase and thus drives the efflux process (36). The synergistic effects of respiratory inhibitors could serve as the basis for using a combination of inhibitors. This also brings up the possibility that through the use of respiratory inhibitors, fungi that are normally insensitive or only slightly sensitive to fenarimol or imazalil due to efflux systems could be controlled. 

Interactions. Morphine (also pethidine and possibly other opioids) is potentiated by monoamine oxidase inhibitors. Any central nervous system depressant (including alcohol) will have additive effects. Patients recently exposed to neuromuscular blocking agents (unless this is adequately reversed, e.g. by neostigmine) are particularly at risk from the respiratory depressant effects of morphine. The effect of diuretic drugs may be reduced by release of antidiuretic hormone by morphine. Useful interactions include the potientating effect on pain relief of tricyclic antidepressants and of dexamfetamine. 

Glinn, M., Ernster, L. and Lee, C.P. (1991) Initiation of lipid peroxidation in submitochondrial particles effect of respiratory inhibitors. Arch. Biochem. Biophys. 290 57-65. 

V 1 1 IM/IV. Diffuses away from endplate, hydrolyzed by plasma pseudocholinesterase and acetylcholinesterase. T intraocular pressure (contraindicated open eye wounds) and gastric pressure (caution reflux during intubation), dysrhythmias. Postoperative muscle pain (myoglobin release and hyperkalemia). May trigger malignant hyperthermia. 1. Fasciculations in chest and abdomen 2. Neck, arms, legs 3. Facial, phaiynx, larynx 4. Respiratory muscles Effects not reversed by acetylcholinesterase inhibitors. Effects are poorly reversed by electrical stimulation. 

FIGURE 20.20 The effect of respiratory inhibitors, (a) No inhibitor present. Schematic view of electron transport. The red arrows indicate the flow of electrons, (b) Inhibitor present. The flow of electrons from carrier 2 to carrier 3 is blocked by the respiratory inhibitor. Reduced carrier 2 accumulates, as does oxidized carrier 3, because they cannot react with each other. 

By studying the effect of Bryophyllum leaf section thickness on respiration, Kinraide and Behan (1975) noted that as sections decreased in size, O2 uptake increased, and organic acid accumulation was depressed. The specific inhibitors of the citric acid cycle, malonate and fluoroacetate, inhibited the increased oxygen consumption and restored acid accumulation in the thin, 1-mm leaf sections. Other respiratory inhibitors, not specific for the citric acid cycle, did not restore acid accumulation. Hence, they concluded that respiration competes with acid synthesis. 

No As(V) was bioaccumulated by a cell which had been pretreaied with dinitrophenol (respiratory inhibitor) or with heat. Little effect of sodium azide (photosynthesis inhibitor) on bioaccumulation was observed. 

The thiazolidinediones have also been reported to act as inhibitors of the respiratory chain at high concentrations, and this appears to account for their ability to activate AMGPK in cultured cells. However, the primary target of the thiazolidinediones appears to be the peroxisome proliferator-activated receptor-y ( PPAR-y), a member of the nuclear receptor superfamily expressed in adipocytes. One of the major effects of stimulation of PPAR-y in adipocytes is the release ofthe... 

Inhaled NO has been used for treatment of persistent pulmonary hypertension of newborn infants, critical respiratory failure of preterm infants, and acute hypertension of adult cardiac surgery patients. PDE-5 inhibitors such as sildenafil are also effective for treatment of pulmonary hypertension. The combination of PDE-5 and NO inhalation yields additive beneficial effects on pulmonary hemodynamics. On the other hand, measurement of exhaled NO is a noninvasive and reproducible test that is a surrogate measure of airway inflammation in patients with bronchial asthma. 

The indications for these agents are in principle identical to those of the non-selective NSAIDs although the substances have not yet received approval for the whole spectrum of indications of the conventional NSAIDs. Because they lack COX-1-inhibiting properties, COX-2-selective inhibitors show fewer side effects than conventional NSAIDs. However, they are not free of side effects because COX-2 has physiological functions that are blocked by the COX-2 inhibitors. The most frequently observed side effects are infections of the upper respiratory tract, diarrhoea, dyspepsia, abdominal discomfort and headache. Peripheral oedema is as frequent as with conventional NSAIDs. The frequency of gastrointestinal complications is approximately half that observed with conventional NSAIDs. 

Ephedra (sea grape, ma-huang, yellow horse) ephedra sinica Relieves colds, improves respiratory function, headaches, diuretic effects 3heart rate, psychosis l hedra should only be used after consulting with the physician. Many restrictions apply and the herb can cause serious reactions. Do not use with cardiac glycosides, monoamine oxidase inhibitor halothane, guanethidine, (MAOIs) or oxytocin. Do not use with 3. John s wort or in weight loss formulas. 

The precise mechanism of dimethylhydrazine toxicity is uncertain. In addition to the contact irritant effects, the acute effects of dimethylhydrazine exposure may involve the central nervous system as exemplified by tremors and convulsions (Shaffer and Wands 1973) and behavioral changes at sublethal doses (Streman et al. 1969). Back and Thomas (1963) noted that the deaths probably involve respiratory arrest and cardiovascular collapse. The central nervous system as a target is consistent with the delayed latency in response reported for dimethylhydrazine (Back and Thomas 1963). There is some evidence that 1,1-dimethylhydrazine may act as an inhibitor of glutamic acid decarboxylase, thereby adversely affecting the aminobutyric acid shunt, and could explain the latency of central-nervous-system effects (Back and Thomas 1963). Furthermore, vitamin B6 analogues that act as coenzymes in the aminobutyric acid shunt have been shown to be effective antagonists to 1,1-dimethylhydrazine toxicity (reviewed in Back and Thomas 1963). 

Researchers at SRMLSC recently developed a HTS that allowed the identification of potential inhibitors of the severe acute respiratory syndrome coronavirus (SARS CoV) from large compound libraries [34], The luminescent-based assay, which measured the inhibition of SARS CoV-induced cytopathic effects (CPE) in Vero E6 cells, was validated with two different diversity sets of compounds against the SARS CoV. The hit rate for both libraries was approximately 0.01%. 

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