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Immediate and Long-Term Outcome of Acute H2S Intoxication Induced Coma in Unanesthetized Rats: Effects of Methylene Blue.

Sonobe T, Chenuel B, Cooper TK, Haouzi P - PLoS ONE (2015)

Bottom Line: The aim of our study was to 1--describe the immediate and long-term neurological effects following H2S-induced coma in un-anesthetized rats, and 2--determine the potential benefit of methylene blue (MB), a compound we previously found to counteract acute sulfide cardiac toxicity.The treated animals displayed a significantly higher occurrence of spatial search than the non-treated animals.However, a similar proportion of cortical necrosis was observed in both groups, with a milder clinical presentation following MB.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, Division of Pulmonary and Critical Care Medicine, Pennsylvania State University, College of Medicine, Hershey, PA, United States of America.

ABSTRACT

Background: Acute hydrogen sulfide (H2S) poisoning produces a coma, the outcome of which ranges from full recovery to severe neurological deficits. The aim of our study was to 1--describe the immediate and long-term neurological effects following H2S-induced coma in un-anesthetized rats, and 2--determine the potential benefit of methylene blue (MB), a compound we previously found to counteract acute sulfide cardiac toxicity.

Methods: NaHS was administered IP in un-sedated rats to produce a coma (n = 34). One minute into coma, the rats received MB (4 mg/kg i.v.) or saline. The surviving rats were followed clinically and assigned to Morris water maze (MWM) and open field testing then sacrificed at day 7.

Results: Sixty percent of the non-treated comatose rats died by pulseless electrical activity. Nine percent recovered with neurological deficits requiring euthanasia, their brain examination revealed major neuronal necrosis of the superficial and middle layers of the cerebral cortex and the posterior thalamus, with variable necrosis of the caudate putamen, but no lesions of the hippocampus or the cerebellum, in contrast to the typical distribution of post-ischemic lesions. The remaining animals displayed, on average, a significantly less effective search strategy than the control rats (n = 21) during MWM testing. Meanwhile, 75% of rats that received MB survived and could perform the MWM test (P<0.05 vs non-treated animals). The treated animals displayed a significantly higher occurrence of spatial search than the non-treated animals. However, a similar proportion of cortical necrosis was observed in both groups, with a milder clinical presentation following MB.

Conclusion: In conclusion, in rats surviving H2S induced coma, spatial search patterns were used less frequently than in control animals. A small percentage of rats presented necrotic neuronal lesions, which distribution differed from post-ischemic lesions. MB dramatically improved the immediate survival and spatial search strategy in the surviving rats.

No MeSH data available.


Related in: MedlinePlus

Example of the histopathology of the lung in a control rat and a rat exposed to H2S.Hematoxylin and eosin stained sections of perfused lungs from control and H2S-exposed rats, 100X magnification. Lungs of both rats are normal (top panels) with no evidence of lesions that would be expected to occur during inhaled sulfide exposure. As illustrated on the lower panels, both unexposed controls and H2S exposed rats displayed mild expansion of the peribronchial, peribronchiolar and perivascular interstitium by low to moderate numbers of lymphocytes and macrophages with fewer plasma cells consistent with chronic bronchus associated lymphoid tissue hyperplasia (BALT, see text for additional comments).
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pone.0131340.g015: Example of the histopathology of the lung in a control rat and a rat exposed to H2S.Hematoxylin and eosin stained sections of perfused lungs from control and H2S-exposed rats, 100X magnification. Lungs of both rats are normal (top panels) with no evidence of lesions that would be expected to occur during inhaled sulfide exposure. As illustrated on the lower panels, both unexposed controls and H2S exposed rats displayed mild expansion of the peribronchial, peribronchiolar and perivascular interstitium by low to moderate numbers of lymphocytes and macrophages with fewer plasma cells consistent with chronic bronchus associated lymphoid tissue hyperplasia (BALT, see text for additional comments).

Mentions: None of the rats exposed to H2S displayed any pulmonary lesions, including in the airways, compatible with sulfide toxicity, such as necrosis of the respiratory epithelium [56] or evidence for pulmonary edema [57] as shown in Fig 15. Of note is that most of the control and sulfide exposed rats displayed features consistent with chronic bronchus associated lymphoid tissue (BALT) hyperplasia which was regarded as nonspecific findings, common in rats with pulmonary colonization by various bacterial agents [58].


Immediate and Long-Term Outcome of Acute H2S Intoxication Induced Coma in Unanesthetized Rats: Effects of Methylene Blue.

Sonobe T, Chenuel B, Cooper TK, Haouzi P - PLoS ONE (2015)

Example of the histopathology of the lung in a control rat and a rat exposed to H2S.Hematoxylin and eosin stained sections of perfused lungs from control and H2S-exposed rats, 100X magnification. Lungs of both rats are normal (top panels) with no evidence of lesions that would be expected to occur during inhaled sulfide exposure. As illustrated on the lower panels, both unexposed controls and H2S exposed rats displayed mild expansion of the peribronchial, peribronchiolar and perivascular interstitium by low to moderate numbers of lymphocytes and macrophages with fewer plasma cells consistent with chronic bronchus associated lymphoid tissue hyperplasia (BALT, see text for additional comments).
© Copyright Policy
Related In: Results  -  Collection

License
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getmorefigures.php?uid=PMC4482667&req=5

pone.0131340.g015: Example of the histopathology of the lung in a control rat and a rat exposed to H2S.Hematoxylin and eosin stained sections of perfused lungs from control and H2S-exposed rats, 100X magnification. Lungs of both rats are normal (top panels) with no evidence of lesions that would be expected to occur during inhaled sulfide exposure. As illustrated on the lower panels, both unexposed controls and H2S exposed rats displayed mild expansion of the peribronchial, peribronchiolar and perivascular interstitium by low to moderate numbers of lymphocytes and macrophages with fewer plasma cells consistent with chronic bronchus associated lymphoid tissue hyperplasia (BALT, see text for additional comments).
Mentions: None of the rats exposed to H2S displayed any pulmonary lesions, including in the airways, compatible with sulfide toxicity, such as necrosis of the respiratory epithelium [56] or evidence for pulmonary edema [57] as shown in Fig 15. Of note is that most of the control and sulfide exposed rats displayed features consistent with chronic bronchus associated lymphoid tissue (BALT) hyperplasia which was regarded as nonspecific findings, common in rats with pulmonary colonization by various bacterial agents [58].

Bottom Line: The aim of our study was to 1--describe the immediate and long-term neurological effects following H2S-induced coma in un-anesthetized rats, and 2--determine the potential benefit of methylene blue (MB), a compound we previously found to counteract acute sulfide cardiac toxicity.The treated animals displayed a significantly higher occurrence of spatial search than the non-treated animals.However, a similar proportion of cortical necrosis was observed in both groups, with a milder clinical presentation following MB.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, Division of Pulmonary and Critical Care Medicine, Pennsylvania State University, College of Medicine, Hershey, PA, United States of America.

ABSTRACT

Background: Acute hydrogen sulfide (H2S) poisoning produces a coma, the outcome of which ranges from full recovery to severe neurological deficits. The aim of our study was to 1--describe the immediate and long-term neurological effects following H2S-induced coma in un-anesthetized rats, and 2--determine the potential benefit of methylene blue (MB), a compound we previously found to counteract acute sulfide cardiac toxicity.

Methods: NaHS was administered IP in un-sedated rats to produce a coma (n = 34). One minute into coma, the rats received MB (4 mg/kg i.v.) or saline. The surviving rats were followed clinically and assigned to Morris water maze (MWM) and open field testing then sacrificed at day 7.

Results: Sixty percent of the non-treated comatose rats died by pulseless electrical activity. Nine percent recovered with neurological deficits requiring euthanasia, their brain examination revealed major neuronal necrosis of the superficial and middle layers of the cerebral cortex and the posterior thalamus, with variable necrosis of the caudate putamen, but no lesions of the hippocampus or the cerebellum, in contrast to the typical distribution of post-ischemic lesions. The remaining animals displayed, on average, a significantly less effective search strategy than the control rats (n = 21) during MWM testing. Meanwhile, 75% of rats that received MB survived and could perform the MWM test (P<0.05 vs non-treated animals). The treated animals displayed a significantly higher occurrence of spatial search than the non-treated animals. However, a similar proportion of cortical necrosis was observed in both groups, with a milder clinical presentation following MB.

Conclusion: In conclusion, in rats surviving H2S induced coma, spatial search patterns were used less frequently than in control animals. A small percentage of rats presented necrotic neuronal lesions, which distribution differed from post-ischemic lesions. MB dramatically improved the immediate survival and spatial search strategy in the surviving rats.

No MeSH data available.


Related in: MedlinePlus