Caudoputamen is damaged by hypocapnia during mechanical ventilation in a rat model of chronic cerebral hypoperfusion

Etsuko Miyamoto, Hidekazu Tomimoto, Shin Ichi Nakao, Hideaki Wakita, Ichiro Akiguchi, Katsuichi Miyamoto, Koh Shingu

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Background and Purpose - Postoperative brain dysfunction, such as delirium, is a common complication of anesthesia and is sometimes prolonged, especially in patients with cerebrovascular disease. In the present study we investigated the effect of hypocapnia during anesthesia on neuronal damage using a rat model of chronic cerebral hypoperfusion. Methods - Chronic cerebral hypoperfusion was induced by clipping the bilateral common carotid arteries in male Wistar rats. Fourteen days after the operation, these animals were mechanically ventilated for 2 hours and then kept in suitable conditions for an additional 14 days. Twenty-four rats were assigned to 4 groups: those with chronic cerebral hypoperfusion with either hypocapnia or normocapnia during anesthesia, and those given sham operation with either hypocapnia or normocapnia. White matter lesions in the brain sections were evaluated with Klüver-Barrera staining. Proliferation of glial cells was estimated with the use of immunohistochemistry of glial fibrillary acidic protein, a marker for astroglia, and CD11b, a marker for microglia. Computer-assisted morphometry was applied to the immunohistochemical results of microtubule-associated protein 2 to evaluate the loss of neurons. Results - The histological damage was localized almost exclusively in the white matter in the rats subjected to chronic cerebral hypoperfusion but without hypocapnia. Neuronal damage and astroglial proliferation occurred with aggravated white matter lesions in the caudoputamen in the rats with chronic cerebral hypoperfusion and hypocapnia. No lesions were observed in sham-operated rats with either hypocapnia or normocapnia. Conclusions - These results indicate that hypocapnia during anesthesia causes tissue damage in the caudoputamen, which may be responsible for long-lasting postoperative delirium in patients with stroke and/or dementia.

Original languageEnglish
Pages (from-to)2920-2925
Number of pages6
JournalStroke
Volume32
Issue number12
DOIs
Publication statusPublished - 01-01-2001

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Hypocapnia
Artificial Respiration
Anesthesia
Delirium
Cerebrovascular Disorders
Microtubule-Associated Proteins
Common Carotid Artery
Glial Fibrillary Acidic Protein
Brain
Microglia
Neuroglia
Astrocytes
Dementia
Wistar Rats
Immunohistochemistry
Stroke
Staining and Labeling
Neurons

All Science Journal Classification (ASJC) codes

  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine
  • Advanced and Specialised Nursing

Cite this

Miyamoto, E., Tomimoto, H., Nakao, S. I., Wakita, H., Akiguchi, I., Miyamoto, K., & Shingu, K. (2001). Caudoputamen is damaged by hypocapnia during mechanical ventilation in a rat model of chronic cerebral hypoperfusion. Stroke, 32(12), 2920-2925. https://doi.org/10.1161/hs1201.100216
Miyamoto, Etsuko ; Tomimoto, Hidekazu ; Nakao, Shin Ichi ; Wakita, Hideaki ; Akiguchi, Ichiro ; Miyamoto, Katsuichi ; Shingu, Koh. / Caudoputamen is damaged by hypocapnia during mechanical ventilation in a rat model of chronic cerebral hypoperfusion. In: Stroke. 2001 ; Vol. 32, No. 12. pp. 2920-2925.
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Miyamoto, E, Tomimoto, H, Nakao, SI, Wakita, H, Akiguchi, I, Miyamoto, K & Shingu, K 2001, 'Caudoputamen is damaged by hypocapnia during mechanical ventilation in a rat model of chronic cerebral hypoperfusion', Stroke, vol. 32, no. 12, pp. 2920-2925. https://doi.org/10.1161/hs1201.100216

Caudoputamen is damaged by hypocapnia during mechanical ventilation in a rat model of chronic cerebral hypoperfusion. / Miyamoto, Etsuko; Tomimoto, Hidekazu; Nakao, Shin Ichi; Wakita, Hideaki; Akiguchi, Ichiro; Miyamoto, Katsuichi; Shingu, Koh.

In: Stroke, Vol. 32, No. 12, 01.01.2001, p. 2920-2925.

Research output: Contribution to journalArticle

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T1 - Caudoputamen is damaged by hypocapnia during mechanical ventilation in a rat model of chronic cerebral hypoperfusion

AU - Miyamoto, Etsuko

AU - Tomimoto, Hidekazu

AU - Nakao, Shin Ichi

AU - Wakita, Hideaki

AU - Akiguchi, Ichiro

AU - Miyamoto, Katsuichi

AU - Shingu, Koh

PY - 2001/1/1

Y1 - 2001/1/1

N2 - Background and Purpose - Postoperative brain dysfunction, such as delirium, is a common complication of anesthesia and is sometimes prolonged, especially in patients with cerebrovascular disease. In the present study we investigated the effect of hypocapnia during anesthesia on neuronal damage using a rat model of chronic cerebral hypoperfusion. Methods - Chronic cerebral hypoperfusion was induced by clipping the bilateral common carotid arteries in male Wistar rats. Fourteen days after the operation, these animals were mechanically ventilated for 2 hours and then kept in suitable conditions for an additional 14 days. Twenty-four rats were assigned to 4 groups: those with chronic cerebral hypoperfusion with either hypocapnia or normocapnia during anesthesia, and those given sham operation with either hypocapnia or normocapnia. White matter lesions in the brain sections were evaluated with Klüver-Barrera staining. Proliferation of glial cells was estimated with the use of immunohistochemistry of glial fibrillary acidic protein, a marker for astroglia, and CD11b, a marker for microglia. Computer-assisted morphometry was applied to the immunohistochemical results of microtubule-associated protein 2 to evaluate the loss of neurons. Results - The histological damage was localized almost exclusively in the white matter in the rats subjected to chronic cerebral hypoperfusion but without hypocapnia. Neuronal damage and astroglial proliferation occurred with aggravated white matter lesions in the caudoputamen in the rats with chronic cerebral hypoperfusion and hypocapnia. No lesions were observed in sham-operated rats with either hypocapnia or normocapnia. Conclusions - These results indicate that hypocapnia during anesthesia causes tissue damage in the caudoputamen, which may be responsible for long-lasting postoperative delirium in patients with stroke and/or dementia.

AB - Background and Purpose - Postoperative brain dysfunction, such as delirium, is a common complication of anesthesia and is sometimes prolonged, especially in patients with cerebrovascular disease. In the present study we investigated the effect of hypocapnia during anesthesia on neuronal damage using a rat model of chronic cerebral hypoperfusion. Methods - Chronic cerebral hypoperfusion was induced by clipping the bilateral common carotid arteries in male Wistar rats. Fourteen days after the operation, these animals were mechanically ventilated for 2 hours and then kept in suitable conditions for an additional 14 days. Twenty-four rats were assigned to 4 groups: those with chronic cerebral hypoperfusion with either hypocapnia or normocapnia during anesthesia, and those given sham operation with either hypocapnia or normocapnia. White matter lesions in the brain sections were evaluated with Klüver-Barrera staining. Proliferation of glial cells was estimated with the use of immunohistochemistry of glial fibrillary acidic protein, a marker for astroglia, and CD11b, a marker for microglia. Computer-assisted morphometry was applied to the immunohistochemical results of microtubule-associated protein 2 to evaluate the loss of neurons. Results - The histological damage was localized almost exclusively in the white matter in the rats subjected to chronic cerebral hypoperfusion but without hypocapnia. Neuronal damage and astroglial proliferation occurred with aggravated white matter lesions in the caudoputamen in the rats with chronic cerebral hypoperfusion and hypocapnia. No lesions were observed in sham-operated rats with either hypocapnia or normocapnia. Conclusions - These results indicate that hypocapnia during anesthesia causes tissue damage in the caudoputamen, which may be responsible for long-lasting postoperative delirium in patients with stroke and/or dementia.

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