Disease relevance of Rattrack

• The relationship between right duct lymph flow and extravascular lung water was studied in 3 normal dogs and 15 dogs with pulmonary edema induced by alpha-naphthylthiourea (ANTU) [1].
• The detailed topography of filtration and of accumulation of the tracer dextran 75 was studied in 3 control dogs and in 9 experimental dogs in which edema was induced with 27 mg/kg alpha-naphthylthiourea [2].
• We compared the effect of 7 ml/kg body weight tidal volume mechanical ventilation for 2 min with that of 25 (HV25), 33(HV33), and 45(HV45) ml/kg body weight HV in anesthetized rats previously exposed or not exposed to alpha-naphthylthiourea (ANTU) [3].
• This interpretation is supported by a markedly increased leakage of CC16 in experimental exudates induced by ANTU and the finding of high CC16 concentrations in human transudates associated with congestive heart failure, two conditions wherein PF has been shown to arise from the interstitial spaces of the lung [4].
• ANTU specifically increases pulmonary vascular permeability in adult rats and causes acute pulmonary oedema and pleural effusion [5].

High impact information on Rattrack

• The relationship between right duct lymph flow and extravascular lung water in dogs given alpha-naphthylthiourea [1].
• Anionic and cationic ferritin was also perfused through the pulmonary circulation of lungs isolated from control rats and rats previously injected with alpha-naphthylthiourea, which produces permeability pulmonary edema [6].
• In lungs with alpha-naphthylthiourea pulmonary edema, perfused for 2-15 minutes, anionic ferritin leaked from pulmonary capillaries into the alveolar interstitium and alveolar space, while cationic ferritin remained within the capillary lumen [6].
• In alpha-naphthylthiourea lungs perfused for 45-60 minutes, cationic ferritin also leaked through the injured endothelium and bound twice as much to the alveolar as the capillary basement membranes [6].
• Rats were given intraperitoneal injections of 20 mg/kg alpha-naphthylthiourea (ANTU), resulting in an increased permeability edema with alveolar flooding [7].

Chemical compound and disease context of Rattrack

• Potentiation by piperonyl butoxide of alpha-naphthylthiourea toxicity in the isolated, perfused rat lung [8].
• 1. The hydrolysis of adenosine di- and monophosphate (ADP, AMP) was studied in perfused lungs isolated from rats treated with alpha-naphthylthiourea (ANTU) to induce acute lung injury [9].
• Administration of alpha-naphthylthiourea (ANTU) to rats causes damage to pulmonary endothelial cells and possibly mesothelial lining cells that together may account for the massive pleural effusion characteristic of thiourea toxicity [10].
• Whereas PEEP had no consistent effect on extravascular thermal volume in ANTU edema, there was a reversible increase in ETV during PEEP in animals with HCl or OA injury and underestimation of ELM [11].
• Fluorescein-labeled dextran concentration is increased in BAL fluid after ANTU-induced edema in rats [12].

Biological context of Rattrack

• Lung microvascular permeability to dextran in alpha-naphthylthiourea-induced edema. Sites of filtration, patterns of accumulation, and effects of fixation [2].
• Inhibition of drug toxicity to the lungs by tachyphylaxis, specific antimetabolites or iodides did not abolish the effect of ANTU on CFE [5].
• The pharmacokinetics of [3H]PGE2 were significantly altered after ANTU and these changes persisted beyond the time when both lung weight ratio and 99mTcDTPA clearance had recovered to normal values [13].
• Hydrostatic edema (HE) was induced by raising the venous pressure, and permeability edema (PE) was induced with alpha-naphthylthiourea [14].
• 2. S-oxidation was inhibited by 1-(1-naphthyl)-2-thiourea and thiobenzamide, known inhibitors of FMO, but was not enhanced by n-octylamine, a known enhancer of FMO [15].

Anatomical context of Rattrack

• Between 4 and 48 hours after ANTU, the fluid removal rate from both compartments was much slower, and interstitial fluid was removed at a faster rate than alveolar fluid [7].
• Keratinocyte growth factor (KGF) prevents alpha-naphthylthiourea (ANTU)-induced permeability edema ex vivo [16].
• CC16 was also studied in serum and PF of normal rats and in rats with pleural exudate induced by alpha-naphthyl-thiourea (ANTU) [4].
• INTERVENTIONS: The effects of granulocyte colony-stimulating factor given alone or after alpha-naphthylthiourea used to induce acute lung injury were investigated [17].
• Metabolism of alpha-naphthylthiourea by rat liver and rat lung microsomes [18].

Associations of Rattrack with other chemical compounds

• CC16 concentration (mean+/-sD in microg x L(-1)), measured by a sensitive latex immunoassay, was significantly reduced in BALF of all treated groups (IPO 380+/-100; MMT 730+/-200; ANTU 1,070+/-200; controls 1,700+/-470) [19].
• We injured the LLL via the airway by instilling either 0.1 N HCl or a mixture of glucose and glucose oxidase or via the pulmonary vessels by injecting either alpha-naphthylthiourea or oleic acid into the LLL pulmonary artery [20].
• Data from our laboratory show that scavengers such as superoxide dismutase, dimethylsulfoxide, and catalase as well as leukocyte depletion provide partial protection to the very caustic alpha-naphthylthiourea [21].
• We compared the hydrolysis of radiolabelled chylomicrons from rat mesenteric lymph by perfused lungs isolated from rats pretreated with ANTU; with the vehicle, Tween 80, alone; or untreated control rats [22].
• To study the value of indexes of endothelial cell function in experimentally induced pulmonary microvascular injury, lung damage was produced in anesthetized dogs by intravenous injection of oleic acid (OA; n = 6), alpha-naphthylthiourea (ANTU; n = 5), or phorbol myristate acetate (PMA; n = 6) [23].

Gene context of Rattrack

• Acute effect of endothelin-1 on lung oedema induced by alpha-naphthylthiourea (ANTU) [24].
• Phosphoramidon, an inhibitor of endothelin converting enzyme, did not alter the oedema producing effect of alpha-naphthylthiourea indicating the lack of the participation of endothelin-peptide cascade to this pathological event [24].
• However, a linear relationship was obtained between the pulmonary uptake of (18)F-FHBG and in vitro assays of TK activity in rats treated with ANTU [25].
• Lipoprotein lipase activity in homogenates of lungs from ANTU and Tween treated rats did not differ [22].

Analytical, diagnostic and therapeutic context of Rattrack

• DESIGN: To reproduce a routine situation in cancer patients receiving chemotherapy, we investigated the mechanisms underlying granulocyte colony-stimulating factor-induced exacerbation of alpha-naphthylthiourea-related pulmonary edema [17].
• MEASUREMENTS AND MAIN RESULTS: The alpha-naphthylthiourea produced an acute permeability pulmonary edema detected by lung leak over the 180-min ex vivo period of monitoring the isolated perfused lung (leak = 8+/-mL; wet/dry weight ratio 14.7+/-2; lavage protein 3.1+/-1 mg/mL) [26].
• To determine if the polyamines are involved in a well-characterized animal model of acute lung injury, the present experiments assessed the relation between changes in polyamine synthesis and development of edema in lungs from rats treated with alpha-naphthylthiourea (ANTU) [27].
• To determine the effect of the type of lung injury on the thermodilution estimation of extravascular lung water, we produced pulmonary edema in 25 anesthetized dogs by injection of alloxan or alpha-naphthylthiourea (ANTU) into the pulmonary circulation or by instillation of hydrochloric acid (HCI) into the airway [28].

References