Granulocytes and No-Reflow Phenomenon in Irreversible Hemorrhagic Shock
Recent evidence shows that circulating granulocytes play an important role in capillary stasis and tissue injury. We investigated two aspects of the problem in a Wiggers hemorrhagic shock model of the ratthe survival rate and the microvascular no-reflow phenomenon. A conventional group of rats with...
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Published in | Circulation research Vol. 63; no. 2; pp. 437 - 447 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
American Heart Association, Inc
01.08.1988
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Subjects | |
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Abstract | Recent evidence shows that circulating granulocytes play an important role in capillary stasis and tissue injury. We investigated two aspects of the problem in a Wiggers hemorrhagic shock model of the ratthe survival rate and the microvascular no-reflow phenomenon. A conventional group of rats with normal blood cells and a neutropenic group of rats pretreated with intraperitoneal antigranulocyte antibody were used to evaluate the effects of granulocytes. Two hemorrhagic shock protocols (HSP) were carried out. In HSP-1, the rats were subjected to 40 mm Hg mean arterial pressure for 3 hours. The conventional group (n = 11) showed a 36% survival rate compared with 100% in the neutropenic group (n = 6). In HSP-2, the hypotension was more severe, 30 mm Hg mean arterial pressure for 7 hours. There were no survivors in the conventional group (n = 8), compared with a 100% survival rate in the neutropenic group (n = 6). The extent, location, and mechanism of the no-reflow phenomenon was investigated by examining histological sections from several organs after infusion of a contrast medium to mark vessels with flow in a control group without shock and in the HSP-2 model 2 hours after blood replacement. The arterioles and venules uniformly contained contrast medium in all three groups; only capillaries showed no-reflow. A significantly higher percentage of no-reflow was observed in the capillaries of the conventional shock group than in the neutropenic shock group. We concluded that the obstruction of capillaries was largely due to trapped granulocytes, suggesting that these leukocytes play a key role in the capillary no-reflow phenomenon and survival from hemorrhagic shock. |
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AbstractList | Recent evidence shows that circulating granulocytes play an important role in capillary stasis and tissue injury. We investigated two aspects of the problem in a Wiggers hemorrhagic shock model of the rat: the survival rate and the microvascular no-reflow phenomenon. A conventional group of rats with normal blood cells and a neutropenic group of rats pretreated with intraperitoneal antigranulocyte antibody were used to evaluate the effects of granulocytes. Two hemorrhagic shock protocols (HSP) were carried out. In HSP-1, the rats were subjected to 40 mm Hg mean arterial pressure for 3 hours. The conventional group (n = 11) showed a 36% survival rate compared with 100% in the neutropenic group (n = 6). In HSP-2, the hypotension was more severe, 30 mm Hg mean arterial pressure for 7 hours. There were no survivors in the conventional group (n = 8), compared with a 100% survival rate in the neutropenic group (n = 6). The extent, location, and mechanism of the no-reflow phenomenon was investigated by examining histological sections from several organs after infusion of a contrast medium to mark vessels with flow in a control group without shock and in the HSP-2 model 2 hours after blood replacement. The arterioles and venules uniformly contained contrast medium in all three groups; only capillaries showed no-reflow. A significantly higher percentage of no-reflow was observed in the capillaries of the conventional shock group than in the neutropenic shock group. We concluded that the obstruction of capillaries was largely due to trapped granulocytes, suggesting that these leukocytes play a key role in the capillary no-reflow phenomenon and survival from hemorrhagic shock. Recent evidence shows that circulating granulocytes play an important role in capillary stasis and tissue injury. We investigated two aspects of the problem in a Wiggers hemorrhagic shock model of the ratthe survival rate and the microvascular no-reflow phenomenon. A conventional group of rats with normal blood cells and a neutropenic group of rats pretreated with intraperitoneal antigranulocyte antibody were used to evaluate the effects of granulocytes. Two hemorrhagic shock protocols (HSP) were carried out. In HSP-1, the rats were subjected to 40 mm Hg mean arterial pressure for 3 hours. The conventional group (n = 11) showed a 36% survival rate compared with 100% in the neutropenic group (n = 6). In HSP-2, the hypotension was more severe, 30 mm Hg mean arterial pressure for 7 hours. There were no survivors in the conventional group (n = 8), compared with a 100% survival rate in the neutropenic group (n = 6). The extent, location, and mechanism of the no-reflow phenomenon was investigated by examining histological sections from several organs after infusion of a contrast medium to mark vessels with flow in a control group without shock and in the HSP-2 model 2 hours after blood replacement. The arterioles and venules uniformly contained contrast medium in all three groups; only capillaries showed no-reflow. A significantly higher percentage of no-reflow was observed in the capillaries of the conventional shock group than in the neutropenic shock group. We concluded that the obstruction of capillaries was largely due to trapped granulocytes, suggesting that these leukocytes play a key role in the capillary no-reflow phenomenon and survival from hemorrhagic shock. |
Author | Schmid-Schönbein, Geert W Zweifach, Benjamin W Barroso-Aranda, Jorge Engler, Robert L |
AuthorAffiliation | From the AMES-Bioengineering, University of California, San Diego, La Jolla, California, the Department of Medicine, University of California, San Diego, and VA Medical Center, San Diego, California |
AuthorAffiliation_xml | – name: From the AMES-Bioengineering, University of California, San Diego, La Jolla, California, the Department of Medicine, University of California, San Diego, and VA Medical Center, San Diego, California |
Author_xml | – sequence: 1 givenname: Jorge surname: Barroso-Aranda fullname: Barroso-Aranda, Jorge organization: From the AMES-Bioengineering, University of California, San Diego, La Jolla, California, the Department of Medicine, University of California, San Diego, and VA Medical Center, San Diego, California – sequence: 2 givenname: Geert surname: Schmid-Schönbein middlename: W fullname: Schmid-Schönbein, Geert W – sequence: 3 givenname: Benjamin surname: Zweifach middlename: W fullname: Zweifach, Benjamin W – sequence: 4 givenname: Robert surname: Engler middlename: L fullname: Engler, Robert L |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/3396160$$D View this record in MEDLINE/PubMed |
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SubjectTerms | Animals Blood Cell Count Blood Pressure Blood Vessels - pathology Blood Volume Granulocytes - physiology Heart Rate Microcirculation Regional Blood Flow Shock, Hemorrhagic - pathology Shock, Hemorrhagic - physiopathology |
Title | Granulocytes and No-Reflow Phenomenon in Irreversible Hemorrhagic Shock |
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