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11. ACTIVATED CHARCOAL ASPIRATION PRODUCES DIRECT PULMONARY INJURY

Author

Tenenbein, M, Shirota, K, and Pasterkamp, H

Subjects
Carbon, Activated -- Health aspects, Respiratory insufficiency -- Risk factors, Lungs -- Injuries, Environmental issues, Health, Pharmaceuticals and cosmetics industries
Abstract

Background: Aspiration of activated charcoal can produce mechanical airways obstruction but intra-pulmonary charcoal is considered inert. We present a patient who aspirated charcoal and went on to develop bronchiolitis obliterans and chronic respiratory failure. Case Report: A 15-year-old girl presented to the emergency department three hours after the ingestion of 4.0 g of nefazadone. She was alert and oriented with normal vital signs but was uncooperative. A nasogastric tube was passed and its location was confirmed by auscultation during air injection. After the administration of approximately one-half of a 50 g activated charcoal in water dose, she vomited, hyperventilated and removed the tube. There was a sudden onset of respiratory distress, stridor and peri-oral cyanosis. Bradypnea ([is less than] 10) and bradycardia ([is less than] 60) ensued, and she was intubated with difficulty. She was admitted to the ICU and bronchial lavage removed charcoal. After recovery from the acute insult, a progressive loss of pulmonary function ensued. Over a 90-day period, her FVC and [FEV.sub.1] declined from 90% and 60% of predicted to 40% and 30%, respectively. Bronchiolitis obliterans was diagnosed and supported by a CT scan of her chest. A second scan showed deterioration. Cyclosporine over 90 days (beginning on day 18) was given with the intent of decreasing the fibrotic process within the small airways. She became dependent upon supplemental oxygen 15 weeks after aspiration, and chronic hypercarbia ensued 7 months after aspiration. She is awaiting lung transplantation. Conclusion: Aspiration of stomach contents does not lead to bronchiolitis obliterans and direct instillation of charcoal into the lungs of animals produces pulmonary injury. This, along with our patient's clinical course and a previous case report of bronchiolitis obliterans, supports the hypothesis that aspiration of activated charcoal can produce direct pulmonary injury with progressive loss of lung function., Tenenbein M, Shirota K, Pasterkamp H. University of Manitoba, Winnipeg, Manitoba, [...]

Published
1999

13. Identification of a Unique Amyloid Sequence in AA Amyloidosis of a Pig Associated With Streptococcus Suis Infection.

Author

Kamiie, J., Sugahara, G., Yoshimoto, S., Aihara, N., Mineshige, T., Uetsuka, K., and Shirota, K.

Subjects
AMYLOIDOSIS, STREPTOCOCCUS suis, LABORATORY swine, INFLAMMATION, IMMUNOHISTOCHEMISTRY
Abstract

Here we report a pig with amyloid A (AA) amyloidosis associated with Streptococcus suis infection and identification of a unique amyloid sequence in the amyloid deposits in the tissue. Tissues from the 180-day-old underdeveloped pig contained foci of necrosis and suppurative inflammation associated with S. suis infection. Congo red stain, immunohistochemistry, and electron microscopy revealed intense AA deposition in the spleen and renal glomeruli. Mass spectrometric analysis of amyloid material extracted from the spleen showed serum AA 2 (SAA2) peptide as well as a unique peptide sequence previously reported in a pig with AA amyloidosis. The common detection of the unique amyloid sequence in the current and past cases of AA amyloidosis in pigs suggests that this amyloid sequence might play a key role in the development of porcine AA amyloidosis. An in vitro fibrillation assay demonstrated that the unique AA peptide formed typically rigid, long amyloid fibrils (10 nm wide) and the N-terminus peptide of SAA2 formed zigzagged, short fibers (7 nm wide). Moreover, the SAA2 peptide formed long, rigid amyloid fibrils in the presence of sonicated amyloid fibrils formed by the unique AA peptide. These findings indicate that the N-terminus of SAA2 as well as the AA peptide mediate the development of AA amyloidosis in pigs via cross-seeding polymerization. [ABSTRACT FROM AUTHOR]

Published
2017
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14. Direct compression of the failing heart reestablishes maximal mechanical efficiency

Author

Carrington, RAJ, Huang, Y, Kawaguchi, O, Yuasa, T, Shirota, K, Martin, D, and Hunyor, SN

Subjects
Sheep, Oxygen Consumption, Respiratory System, Pressure, Models, Cardiovascular, Animals, Heart, Blood Pressure, Heart-Assist Devices, Suction, Models, Theoretical
Abstract

BACKGROUND: In failing hearts, homeostatic mechanisms contrive to maximize stroke work and maintain normal arterial blood pressure at the expense of energetic efficiency. In contrast dobutamine reestablishes maximal mechanical efficiency by promoting energetically optimal loading conditions. However, dobutamine also wastefully increases nonmechanical oxygen consumption. We investigated whether direct mechanical cardiac compression would reestablish maximal mechanical efficiency without the oxygen-wasting effect. METHODS: The pressure-volume relationship and myocardial oxygen consumption were derived in sheep using left ventricular pressure and volume from manometer-tipped and conductance catheters, and coronary flow from Transonics flow probe. RESULTS: Propranolol hydrochloride and atropine sulfate were administered to reduce ejection fraction to 21% when ventricular elastance fell to 1.35 mm Hg/mL and mechanical efficiency to 79% of maximal. Low-pressure direct mechanical compression of the failing heart restored mechanical efficiency to 94% of maximal and realigned optimal left ventricular end-systolic pressure with operating left ventricular end-systolic pressure without altering nonmechanical oxygen consumption. CONCLUSIONS: We conclude that direct cardiac compression restores mechanical efficiency to normal maximum without wasting energy on additional nonmechanical activity.

Published
2003

36. Naturally Occurring Tyzzer's Disease in a Calf

Author

Ikegami, T., primary, Shirota, K., additional, Une, Y., additional, Nomura, Y., additional, Wada, Y., additional, Goto, K., additional, Takakura, A., additional, Itoh, T., additional, and Fujiwara, K., additional

Published
1999
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39. Renal Glomerular Fibrosis in a Cat

Author

Nakamura, S., primary, Shibata, S., additional, Shirota, K., additional, Abe, K., additional, Uetsuka, K., additional, Nakayama, H., additional, Goto, N., additional, and Doi, K., additional

Published
1996
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44. Renal Glomerular Fibrosis in Two Pigs

Author

Shirota, K., primary, Masaki, T., additional, Kitada, H., additional, Yanagi, M., additional, Ikeda, Y., additional, Une, Y., additional, Nokmura, Y., additional, and Jothy, S., additional

Published
1995
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