Possible role of substance P in the ischemia-reperfusion injury in the isolated rabbit lung
The origin of the endothelial damage leading to the ischemia-reperfusion injury after lung transplantation has not been elucidated. We postulated that neurotransmitters released during the preservation of the donor lung might explain this vascular derangement. Thus, in isolated rabbit lungs preserve...
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| Veröffentlicht in: | Transplantation 2004-07, Vol.78 (2), p.296-299 |
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| creator | ARREOLA, José L VARGAS, Mario H SEGURA, Patricia CHAVEZ, Jaime SOMMER, Bettina CARVAJAL, Veronica MONTANO, Luis M |
| description | The origin of the endothelial damage leading to the ischemia-reperfusion injury after lung transplantation has not been elucidated. We postulated that neurotransmitters released during the preservation of the donor lung might explain this vascular derangement. Thus, in isolated rabbit lungs preserved over 24 hours, we evaluated the release of acetylcholine (ACh) and substance P (SP), the activity of their major degrading enzymes, acetylcholinesterase (AChE) and neutral endopeptidase (NEP), and changes in the capillary permeability. Both neurotransmitters showed the highest release rate in the first 15 minutes, followed by a sharp exponential decrement at 1, 6, 12 and 24 hours. AChE and NEP activities showed no variation at these time intervals. Basal capillary permeability significantly increased (P |
| doi_str_mv | 10.1097/01.TP.0000128192.84765.72 |
| format | Article |
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We postulated that neurotransmitters released during the preservation of the donor lung might explain this vascular derangement. Thus, in isolated rabbit lungs preserved over 24 hours, we evaluated the release of acetylcholine (ACh) and substance P (SP), the activity of their major degrading enzymes, acetylcholinesterase (AChE) and neutral endopeptidase (NEP), and changes in the capillary permeability. Both neurotransmitters showed the highest release rate in the first 15 minutes, followed by a sharp exponential decrement at 1, 6, 12 and 24 hours. AChE and NEP activities showed no variation at these time intervals. Basal capillary permeability significantly increased (P<0.01) after 24 hours preservation with saline. This increased permeability was avoided (P<0.01) by the SP fragment 4-11 (an SP receptors antagonist), but not by atropine. These results suggest for the first time a pathogenic role of SP in the ischemia-reperfusion injury, and thus the potential usefulness of SP antagonists as additives in the lung preservation solutions should be explored.</description><identifier>ISSN: 0041-1337</identifier><identifier>EISSN: 1534-6080</identifier><identifier>DOI: 10.1097/01.TP.0000128192.84765.72</identifier><identifier>PMID: 15280694</identifier><identifier>CODEN: TRPLAU</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott</publisher><subject>Animals ; Atropine - pharmacology ; Biological and medical sciences ; Combined surgery. Multiple transplantations ; In Vitro Techniques ; Lung - drug effects ; Lung - physiology ; Lung - physiopathology ; Male ; Medical sciences ; Models, Animal ; Organ Preservation - methods ; Rabbits ; Reperfusion Injury - physiopathology ; Substance P - physiology ; Surgery (general aspects). Transplantations, organ and tissue grafts. 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We postulated that neurotransmitters released during the preservation of the donor lung might explain this vascular derangement. Thus, in isolated rabbit lungs preserved over 24 hours, we evaluated the release of acetylcholine (ACh) and substance P (SP), the activity of their major degrading enzymes, acetylcholinesterase (AChE) and neutral endopeptidase (NEP), and changes in the capillary permeability. Both neurotransmitters showed the highest release rate in the first 15 minutes, followed by a sharp exponential decrement at 1, 6, 12 and 24 hours. AChE and NEP activities showed no variation at these time intervals. Basal capillary permeability significantly increased (P<0.01) after 24 hours preservation with saline. This increased permeability was avoided (P<0.01) by the SP fragment 4-11 (an SP receptors antagonist), but not by atropine. These results suggest for the first time a pathogenic role of SP in the ischemia-reperfusion injury, and thus the potential usefulness of SP antagonists as additives in the lung preservation solutions should be explored.</description><subject>Animals</subject><subject>Atropine - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Combined surgery. Multiple transplantations</subject><subject>In Vitro Techniques</subject><subject>Lung - drug effects</subject><subject>Lung - physiology</subject><subject>Lung - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Models, Animal</subject><subject>Organ Preservation - methods</subject><subject>Rabbits</subject><subject>Reperfusion Injury - physiopathology</subject><subject>Substance P - physiology</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. 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Multiple transplantations</topic><topic>In Vitro Techniques</topic><topic>Lung - drug effects</topic><topic>Lung - physiology</topic><topic>Lung - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Models, Animal</topic><topic>Organ Preservation - methods</topic><topic>Rabbits</topic><topic>Reperfusion Injury - physiopathology</topic><topic>Substance P - physiology</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. 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We postulated that neurotransmitters released during the preservation of the donor lung might explain this vascular derangement. Thus, in isolated rabbit lungs preserved over 24 hours, we evaluated the release of acetylcholine (ACh) and substance P (SP), the activity of their major degrading enzymes, acetylcholinesterase (AChE) and neutral endopeptidase (NEP), and changes in the capillary permeability. Both neurotransmitters showed the highest release rate in the first 15 minutes, followed by a sharp exponential decrement at 1, 6, 12 and 24 hours. AChE and NEP activities showed no variation at these time intervals. Basal capillary permeability significantly increased (P<0.01) after 24 hours preservation with saline. This increased permeability was avoided (P<0.01) by the SP fragment 4-11 (an SP receptors antagonist), but not by atropine. These results suggest for the first time a pathogenic role of SP in the ischemia-reperfusion injury, and thus the potential usefulness of SP antagonists as additives in the lung preservation solutions should be explored.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott</pub><pmid>15280694</pmid><doi>10.1097/01.TP.0000128192.84765.72</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Atropine - pharmacology Biological and medical sciences Combined surgery. Multiple transplantations In Vitro Techniques Lung - drug effects Lung - physiology Lung - physiopathology Male Medical sciences Models, Animal Organ Preservation - methods Rabbits Reperfusion Injury - physiopathology Substance P - physiology Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases |
| title | Possible role of substance P in the ischemia-reperfusion injury in the isolated rabbit lung |
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