Xylazine

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Andy Mauromoustakos - One of the best experts on this subject based on the ideXlab platform.

  • Biochemical and morphological alterations in Xylazine-induced pulmonary edema.
    Toxicologic pathology, 1993
    Co-Authors: C.w. Qualls, John H. Wyckoff, Gladstone K. Dzata, S. Sangiah, Andy Mauromoustakos, Larry E. Stein
    Abstract:

    Sprague-Dawley rats were given 42 mg/kg Xylazine intramuscularly, and lungs were lavaged with phosphate-buffered saline 3, 6, and 12 hr later. Total protein, lactate dehydrogenase (LDH), xanthine oxidase (XO), tumor necrosis factor (TNF), and interleukin 1 (IL-1) were measured in bronchoalveolar lavage fluid (BALF). Protein concentration, LDH, XO, and TNF levels were increased (p < 0.05) in the BALF from Xylazine-treated rats as compared to controls. IL-1 level was unchanged at 3 and 6 hr and was reduced (p < 0.05) at 12 hr. Another group of rats was given 42 mg/kg Xylazine intramuscularly, and lungs were fixed 0.5 and 12 hr later. Histologically, severe pulmonary edema (PE) involving the alveoli and perivascular stroma was observed. Fibrin, increased numbers of eosinophils, and macrophages with foamy cytoplasm were present in the alveoli of all treated animals. Ultrastructurally, endothelial damage, characterized by thinning, detachment from basement membranes, or bleb formation, was observed. The lesions were similar in both Xylazine groups, differing mainly in severity with the 12-hr group having more severe lesions than the 0.5-hr group. To determine whether endothelial injury is caused by direct toxicity of Xylazine, bovine pulmonary artery endothelial cells (BPAECs) were incubated with Xylazine (0.3, 3, and 30 micrograms) for 0.5 or 3 hr. Xylazine did not have any effects on BPAECs, as indicated by phase-contrast microscopy and dye-exclusion viability assay. These results indicate that Xylazine-induced PE is due to increased permeability resulting from endothelial injury, which is not caused by direct effect of Xylazine on pulmonary endothelium. While oxygen radicals and TNF are possibly involved, IL-1 does not appear to play a role in Xylazine-induced PE.

  • Xylazine-induced pulmonary edema in rats.
    Toxicology and applied pharmacology, 1991
    Co-Authors: S. Sangiah, C.w. Qualls, Rick L. Cowell, Andy Mauromoustakos
    Abstract:

    Inhibitors of cytochrome P450, such as SK&F 525-A, prolong the duration of Xylazine-ketamine anesthesia and cause pulmonary edema (PE) and death in rats. To determine the cause of PE, Sprague-Dawley rats were given a single dose of Xylazine (21 mg/kg, im) alone or in combination with ketamine (45 mg/kg, im) and/or SK&F 525-A (50 mg/kg, ip) and percentage lung to body weight (%LWBW) ratios (as an indicator of PE) were compared. The results indicated that Xylazine caused PE which was independent of ketamine and was enhanced by SK&F 525-A. Subsequently, it was determined that 42 mg/kg Xylazine, im, is an optimal edemagenic dose. Xylazine (42 mg/kg, im) increased the %LWBW ratio as compared to control. Pleural effusion (PLE) of various amounts was observed in 75% of the animals. The pleural fluid to serum protein ratio for Xylazine was similar to that obtained for α-naphthylthiourea (5 mg/kg, ip). Extensive serous PLE and alveolar edema with hemorrhage were found at necropsy in Xylazine-treated rats. Pretreatment with yohimbine (4.2 mg/kg), prazosin (20 mg/kg), tolazoline (20 mg/kg), yohimbine (4.2 mg/kg) plus prazosin (20 mg/kg), atropine (20 mg/kg), dimethyl sulfoxide (DMSO) (7.8 g/kg), allopurinol (50 mg/kg), superoxide dismutase (20,000 U/kg), catalase (20,000 U/kg), BW755C (50 mg/kg), ibuprofen (50 mg/kg), cystathionine (100 mg/kg) plus taurine (100 mg/kg) did not affect the %LWBW ratio. PLE was increased by yohimbine, yohimbine plus prazosin, and allopurinol, reduced by DMSO, and not changed in other groups. The results indicate that Xylazine caused increased-permeability PE characterized by rapid onset, cellular damage and protein-rich pleural fluid. PE may not be mediated by adverse cardiovascular effects of Xylazine and oxygen radicals are possibly involved in its etiology.

S. Sangiah - One of the best experts on this subject based on the ideXlab platform.

  • Biochemical and morphological alterations in Xylazine-induced pulmonary edema.
    Toxicologic pathology, 1993
    Co-Authors: C.w. Qualls, John H. Wyckoff, Gladstone K. Dzata, S. Sangiah, Andy Mauromoustakos, Larry E. Stein
    Abstract:

    Sprague-Dawley rats were given 42 mg/kg Xylazine intramuscularly, and lungs were lavaged with phosphate-buffered saline 3, 6, and 12 hr later. Total protein, lactate dehydrogenase (LDH), xanthine oxidase (XO), tumor necrosis factor (TNF), and interleukin 1 (IL-1) were measured in bronchoalveolar lavage fluid (BALF). Protein concentration, LDH, XO, and TNF levels were increased (p < 0.05) in the BALF from Xylazine-treated rats as compared to controls. IL-1 level was unchanged at 3 and 6 hr and was reduced (p < 0.05) at 12 hr. Another group of rats was given 42 mg/kg Xylazine intramuscularly, and lungs were fixed 0.5 and 12 hr later. Histologically, severe pulmonary edema (PE) involving the alveoli and perivascular stroma was observed. Fibrin, increased numbers of eosinophils, and macrophages with foamy cytoplasm were present in the alveoli of all treated animals. Ultrastructurally, endothelial damage, characterized by thinning, detachment from basement membranes, or bleb formation, was observed. The lesions were similar in both Xylazine groups, differing mainly in severity with the 12-hr group having more severe lesions than the 0.5-hr group. To determine whether endothelial injury is caused by direct toxicity of Xylazine, bovine pulmonary artery endothelial cells (BPAECs) were incubated with Xylazine (0.3, 3, and 30 micrograms) for 0.5 or 3 hr. Xylazine did not have any effects on BPAECs, as indicated by phase-contrast microscopy and dye-exclusion viability assay. These results indicate that Xylazine-induced PE is due to increased permeability resulting from endothelial injury, which is not caused by direct effect of Xylazine on pulmonary endothelium. While oxygen radicals and TNF are possibly involved, IL-1 does not appear to play a role in Xylazine-induced PE.

  • Xylazine-induced pulmonary edema in rats.
    Toxicology and applied pharmacology, 1991
    Co-Authors: S. Sangiah, C.w. Qualls, Rick L. Cowell, Andy Mauromoustakos
    Abstract:

    Inhibitors of cytochrome P450, such as SK&F 525-A, prolong the duration of Xylazine-ketamine anesthesia and cause pulmonary edema (PE) and death in rats. To determine the cause of PE, Sprague-Dawley rats were given a single dose of Xylazine (21 mg/kg, im) alone or in combination with ketamine (45 mg/kg, im) and/or SK&F 525-A (50 mg/kg, ip) and percentage lung to body weight (%LWBW) ratios (as an indicator of PE) were compared. The results indicated that Xylazine caused PE which was independent of ketamine and was enhanced by SK&F 525-A. Subsequently, it was determined that 42 mg/kg Xylazine, im, is an optimal edemagenic dose. Xylazine (42 mg/kg, im) increased the %LWBW ratio as compared to control. Pleural effusion (PLE) of various amounts was observed in 75% of the animals. The pleural fluid to serum protein ratio for Xylazine was similar to that obtained for α-naphthylthiourea (5 mg/kg, ip). Extensive serous PLE and alveolar edema with hemorrhage were found at necropsy in Xylazine-treated rats. Pretreatment with yohimbine (4.2 mg/kg), prazosin (20 mg/kg), tolazoline (20 mg/kg), yohimbine (4.2 mg/kg) plus prazosin (20 mg/kg), atropine (20 mg/kg), dimethyl sulfoxide (DMSO) (7.8 g/kg), allopurinol (50 mg/kg), superoxide dismutase (20,000 U/kg), catalase (20,000 U/kg), BW755C (50 mg/kg), ibuprofen (50 mg/kg), cystathionine (100 mg/kg) plus taurine (100 mg/kg) did not affect the %LWBW ratio. PLE was increased by yohimbine, yohimbine plus prazosin, and allopurinol, reduced by DMSO, and not changed in other groups. The results indicate that Xylazine caused increased-permeability PE characterized by rapid onset, cellular damage and protein-rich pleural fluid. PE may not be mediated by adverse cardiovascular effects of Xylazine and oxygen radicals are possibly involved in its etiology.

C.w. Qualls - One of the best experts on this subject based on the ideXlab platform.

  • Biochemical and morphological alterations in Xylazine-induced pulmonary edema.
    Toxicologic pathology, 1993
    Co-Authors: C.w. Qualls, John H. Wyckoff, Gladstone K. Dzata, S. Sangiah, Andy Mauromoustakos, Larry E. Stein
    Abstract:

    Sprague-Dawley rats were given 42 mg/kg Xylazine intramuscularly, and lungs were lavaged with phosphate-buffered saline 3, 6, and 12 hr later. Total protein, lactate dehydrogenase (LDH), xanthine oxidase (XO), tumor necrosis factor (TNF), and interleukin 1 (IL-1) were measured in bronchoalveolar lavage fluid (BALF). Protein concentration, LDH, XO, and TNF levels were increased (p < 0.05) in the BALF from Xylazine-treated rats as compared to controls. IL-1 level was unchanged at 3 and 6 hr and was reduced (p < 0.05) at 12 hr. Another group of rats was given 42 mg/kg Xylazine intramuscularly, and lungs were fixed 0.5 and 12 hr later. Histologically, severe pulmonary edema (PE) involving the alveoli and perivascular stroma was observed. Fibrin, increased numbers of eosinophils, and macrophages with foamy cytoplasm were present in the alveoli of all treated animals. Ultrastructurally, endothelial damage, characterized by thinning, detachment from basement membranes, or bleb formation, was observed. The lesions were similar in both Xylazine groups, differing mainly in severity with the 12-hr group having more severe lesions than the 0.5-hr group. To determine whether endothelial injury is caused by direct toxicity of Xylazine, bovine pulmonary artery endothelial cells (BPAECs) were incubated with Xylazine (0.3, 3, and 30 micrograms) for 0.5 or 3 hr. Xylazine did not have any effects on BPAECs, as indicated by phase-contrast microscopy and dye-exclusion viability assay. These results indicate that Xylazine-induced PE is due to increased permeability resulting from endothelial injury, which is not caused by direct effect of Xylazine on pulmonary endothelium. While oxygen radicals and TNF are possibly involved, IL-1 does not appear to play a role in Xylazine-induced PE.

  • Xylazine-induced pulmonary edema in rats.
    Toxicology and applied pharmacology, 1991
    Co-Authors: S. Sangiah, C.w. Qualls, Rick L. Cowell, Andy Mauromoustakos
    Abstract:

    Inhibitors of cytochrome P450, such as SK&F 525-A, prolong the duration of Xylazine-ketamine anesthesia and cause pulmonary edema (PE) and death in rats. To determine the cause of PE, Sprague-Dawley rats were given a single dose of Xylazine (21 mg/kg, im) alone or in combination with ketamine (45 mg/kg, im) and/or SK&F 525-A (50 mg/kg, ip) and percentage lung to body weight (%LWBW) ratios (as an indicator of PE) were compared. The results indicated that Xylazine caused PE which was independent of ketamine and was enhanced by SK&F 525-A. Subsequently, it was determined that 42 mg/kg Xylazine, im, is an optimal edemagenic dose. Xylazine (42 mg/kg, im) increased the %LWBW ratio as compared to control. Pleural effusion (PLE) of various amounts was observed in 75% of the animals. The pleural fluid to serum protein ratio for Xylazine was similar to that obtained for α-naphthylthiourea (5 mg/kg, ip). Extensive serous PLE and alveolar edema with hemorrhage were found at necropsy in Xylazine-treated rats. Pretreatment with yohimbine (4.2 mg/kg), prazosin (20 mg/kg), tolazoline (20 mg/kg), yohimbine (4.2 mg/kg) plus prazosin (20 mg/kg), atropine (20 mg/kg), dimethyl sulfoxide (DMSO) (7.8 g/kg), allopurinol (50 mg/kg), superoxide dismutase (20,000 U/kg), catalase (20,000 U/kg), BW755C (50 mg/kg), ibuprofen (50 mg/kg), cystathionine (100 mg/kg) plus taurine (100 mg/kg) did not affect the %LWBW ratio. PLE was increased by yohimbine, yohimbine plus prazosin, and allopurinol, reduced by DMSO, and not changed in other groups. The results indicate that Xylazine caused increased-permeability PE characterized by rapid onset, cellular damage and protein-rich pleural fluid. PE may not be mediated by adverse cardiovascular effects of Xylazine and oxygen radicals are possibly involved in its etiology.

Larry E. Stein - One of the best experts on this subject based on the ideXlab platform.

  • Biochemical and morphological alterations in Xylazine-induced pulmonary edema.
    Toxicologic pathology, 1993
    Co-Authors: C.w. Qualls, John H. Wyckoff, Gladstone K. Dzata, S. Sangiah, Andy Mauromoustakos, Larry E. Stein
    Abstract:

    Sprague-Dawley rats were given 42 mg/kg Xylazine intramuscularly, and lungs were lavaged with phosphate-buffered saline 3, 6, and 12 hr later. Total protein, lactate dehydrogenase (LDH), xanthine oxidase (XO), tumor necrosis factor (TNF), and interleukin 1 (IL-1) were measured in bronchoalveolar lavage fluid (BALF). Protein concentration, LDH, XO, and TNF levels were increased (p < 0.05) in the BALF from Xylazine-treated rats as compared to controls. IL-1 level was unchanged at 3 and 6 hr and was reduced (p < 0.05) at 12 hr. Another group of rats was given 42 mg/kg Xylazine intramuscularly, and lungs were fixed 0.5 and 12 hr later. Histologically, severe pulmonary edema (PE) involving the alveoli and perivascular stroma was observed. Fibrin, increased numbers of eosinophils, and macrophages with foamy cytoplasm were present in the alveoli of all treated animals. Ultrastructurally, endothelial damage, characterized by thinning, detachment from basement membranes, or bleb formation, was observed. The lesions were similar in both Xylazine groups, differing mainly in severity with the 12-hr group having more severe lesions than the 0.5-hr group. To determine whether endothelial injury is caused by direct toxicity of Xylazine, bovine pulmonary artery endothelial cells (BPAECs) were incubated with Xylazine (0.3, 3, and 30 micrograms) for 0.5 or 3 hr. Xylazine did not have any effects on BPAECs, as indicated by phase-contrast microscopy and dye-exclusion viability assay. These results indicate that Xylazine-induced PE is due to increased permeability resulting from endothelial injury, which is not caused by direct effect of Xylazine on pulmonary endothelium. While oxygen radicals and TNF are possibly involved, IL-1 does not appear to play a role in Xylazine-induced PE.

Max C Lang - One of the best experts on this subject based on the ideXlab platform.

  • cardiovascular and respiratory effects of tiletamine zolazepam
    Pharmacology Biochemistry and Behavior, 1993
    Co-Authors: Ronald P Wilson, Ian S Zagon, David R. Larach, Max C Lang
    Abstract:

    Abstract The combination of tiletamine and zolazepam is an important dissociative anesthetic-tranquilizer. However, little is known about the effects of this combination on the heart and respiration in rats. Adult, male rats anesthetized with tiletamine-zolazepam alone or tiletamine-zolazepam combined with Xylazine or butorphanol were evaluated for changes in heart rate, mean arterial blood pressure, arterial blood pH, and blood gases during a 75-min period of anesthesia. Rats anesthetized with tiletamine-zolazepam had increased mean arterial blood pressure and less respiratory depression than did rats anesthetized with sodium pentobarbital. Tiletamine-zolazepam combined with Xylazine at either dose produced bradycardia and a marked hypotension that persisted throughout the 75-min period. This combination produced respiratory depression comparable to tiletamine-zolazepam alone. The addition of butorphanol to tiletamine-zolazepam caused a transient hypotension and bradycardia. Tiletamine-zolazepam plus butorphanol produced a mild to severe respiratory depression that was dose and time dependent. These results demonstrate that: a) Tiletamine-zolazepam is cardiostimulatory, a property consistent with the known cardiovascular effects of other dissociative anesthetics; b) xylaxine plus tiletamine-zolazepam is a potent cardiovascular depressant combination; and c) tiletamine-zolazepam plus butorphanol at specific doses is an anesthetic-analgesic combination with minimal effects on cardiovascular and respiratory function.