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Original Articles
- Flush Perfusion, Preservation and Reperfusion Effects in Lung Transplantation: Light Microscopic and Ultrastructural Study.
- Kun Young Kwon, Young Keun Lim, Jae Hoon Bae, Chang Kwon Park
- Korean J Pathol. 1998;32(11):967-977.
- 1,545 View
- 10 Download
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Abstract
- This study was undertaken to investigate the morphologic changes following flushing, preservation and reperfusion procedures in a canine lung allotransplantation model. Donor lungs were flushed with modified Euro-Collins (MEC) solution, low potassium dextran glucose (LPDG) solution or University of Wisconsin (UW) solution, then stored at 10oC for 20 hours. Light microscopic and electron microscopic features of the lungs were examined after flushing, preservation and 2 hours after reperfusion. After flushing light microscopy showed focal mild alveolar collapse and interstitial edema. After preservation the lung tissue showed multiple foci of alveolar collapse, consolidation, and alveolar epithelial cell damage. After reperfusion the lung tissue showed diffuse alveolar collapse, consolidation and many destroyed cellular debris in the alveolar lumina. After flushing electron microscopy showed focal alveolar collapse and mild swelling of type I epithelial cells. After preservation both type I epithelial cells and endothelial cells were swollen and destroyed focally. Some type I epithelial cells were detached from the basal lamina. The endothelial cells showed luminal protrusion of tactile-like structure and vacuoles of the cytoplasm. After reperfusion the lung tissue showed fibrin material in the alveoli, prominent type I epithelial cell swelling with fragmented cytoplasmic debris and marked endothelial cell swelling with vacuoles or tactile-like projections. The alveolar macrophages showed active phagocytosis. After preservation scanning electron microscopic examination of the pulmonary arteries showed multiple patchy areas of swelling or conglomerated lesions in the inner surface of the pulmonary arteries. In conclusion, the ultrastructural changes associated with flushing were mild in severity, the donor lungs were injured during the preservation, and further damage occurred during the reperfusion.
- Distribution of Free Radicals in Reperfusion Injury after Transient Brain Ischemia.
- Eunkyoung Kwak, Hyungho Suh, Jiyoung Park, Yunsup Kum, Taein Park, Jungwan Kim, Yoonkyung Sohn
- Korean J Pathol. 2000;34(11):893-900.
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Abstract
PDF - Free radicals are known as an important factor which may act on reperfusion injury after transient or permanent brain ischemia. Numerous studies about cytotoxic function of free radical have been done. Most of these studies demonstrate the function of free radical in reperfusion injury by using radical scavenger or antioxidant as inhibitor of radicals. We used a modification of Karnovsky's Mn2 /diaminobenzidine (DAB) technique to demonstrate intravascular free radicals following transient occlusion and reperfusion of one middle cerebral artery in Sprague-Dawley rats. The MCA was occluded for 2 hours using an intraluminal suture method. The reperfusion time after transient ischemia was 1 hour, 6 hours, and 24 hours, respectively. Animals were perfused transcardially with solution containing Mn2 and DAB. After DAB perfusion, the brains were removed promptly, sectioned in frozen, and stained with methylene blue for light microscopic examination. Upon light microscopic examination, free radicals were confined within intravascular lumen and the amount of deposits increased according to the duration of reperfusion. Upon electron microscopic examination, free radicals were located in nuclear membrane and membrane of mitochondria and RER, and demonstrated as electron dense deposits. In addition, cell processes of the neuron revealed an electron dense deposits beneath the inner side of the membrane. In conclusion, free radicals demonstrated in the reperfusion injury area indicate that free radical acts as an important cytotoxic factor. Intracellular localization of free radicals may explain the relationship between free radical and delayed neuronal injury.
- The Effect of Ischemic Preconditioning in Rat Liver: The Expression of Interleukin-1 and Nuclear Factor-B.
- Kum Yoon Seup, Soo Kyoung Lee, Sun zoo Kim, Eun Kyoung Kwak, Ji Young Park, Tae In Park, Han Ik Bae, Yoon Kyung Sohn, In Soo Suh
- Korean J Pathol. 2002;36(4):238-242.
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Abstract
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- BACKGROUND
A short period of ischemia and reperfusion, called ischemic preconditioning, protects various tissues against subsequent sustained ischemic insult. Apoptosis of hepatocytes and sinusoidal endothelial cells are a critical mechanisms of injury in the ischemic liver. Because nuclear factor-B (NF-B) has a significant role in the cell survival, we hypothesized that ischemic preconditioning protects by inhibition of apoptosis through the expression of NF-B, induced by interleukin-1 (IL-1), which is known for enhancement of its transcription and activation.
METHODS
We induced ischemia and reperfusion on rat liver, and performed in situ terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labelling assay and polymerase chain reaction for IL-1 mRNA and NF-B mRNA.
RESULTS
Apoptosis of hepatocytes and sinusoidal endothelial cells, assessed by in situ TUNEL assay, was significantly reduced with preconditioning. The expression of IL-1 mRNA and NF-B mRNA are seen on discrete monoclonal bands around 344 and 356 base pairs, in comparison with normal rat liver, but, there was no significant difference between the ischemia-reperfusion group and the preconditioning group.
CONCLUSIONS
We suggest that ischemic preconditioning confers dramatic protection against prolonged ischemia via inhibition of apotosis through the expression of IL-1 inducing NF-B and its activation. However, we need further study in the activity of NF-B, such as nucleotide shift assay, because the activity of NF-B is regulated by binding of the inhibitory protein, IB.
- Correlation Between Neuronal Apoptosis and Expression of Inducible Nitric Oxide Synthase after Transient Focal Cerebral Ischemia.
- Byoung Yuk Yi, Sung Kyoo Hwang, Ku Seong Kang, Hong Hua Quan, Young Mi Lee, Jung Wan Kim, Eun Kyoung Kwak, Ji Young Park, Yoon Kyung Sohn
- Korean J Pathol. 2004;38(6):364-371.
- 1,692 View
- 13 Download
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Abstract
PDF
- BACKGROUND
Neuronal death in acute-phase cerebral ischemic injury is caused by necrosis. However, neuronal injury after reperfusion can be associated with apoptosis.
METHODS
We used Sprague-Dawley rats whose brains were reperfused after middle cerebral artery occlusion for either 30 min or 2 h. We examined a relationship between apoptosis and the expression of inducible nitric oxide synthase (iNOS) in the brain tissue from 3 h to 14 days after reperfusion in both groups.
RESULTS
TUNEL and iNOS positivity were closely related in both groups. The 2-h ischemia group exhibited increases in the amount of TUNEL and iNOS-positive cells for up to 3 days after reperfusion, at which the TUNEL and iNOS-positive cells decreased. The 30-min ischemia group exhibited peak positivity 24 h after reperfusion, followed by a similar decrease. iNOS mRNA expression peaked 3 h after reperfusion in the 30-min ischemia group, at which time it decreased. In the 2-h ischemia group, iNOS mRNA increased 3 h after reperfusion, peaked 24 h after reperfusion, and then decreased.
CONCLUSION
These results indicated the occurrence of delayed apoptosis in transient cerebral ischemia. Increased expression of iNOS is closely associated with this apoptosis, and oxygen free radical-producing materials, such as nitric oxide, may play an important role in the induction of this apoptosis.
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