Effects of leukocyte and platelet depletion on ischemia-reperfusion injury to dog pancreas

Kuroda, Takai; Shiohara, Eiko; Homma, Tatsuji; Furukawa, Yasuyuki; Chiba, Shigetoshi

doi:10.1016/0016-5085(94)90238-0

Cited by 56 publications

(29 citation statements)

References 20 publications

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“…15,16 Platelets interact with activated endothelial cells and accumulate in the injured region. [17][18][19] In vivo studies have shown that platelets can roll on activated endothelium by means of P-selectin that is expressed on the endothelial cells in the course of their accumulation in the inflamed tissue.…”

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confidence: 99%

Argatroban Attenuates Leukocyte– and Platelet–Endothelial Cell Interactions After Transient Retinal Ischemia

Miyahara

Kiryu

Tsujikawa

et al. 2003

Stroke

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Background and Purpose-Argatroban, a direct thrombin inhibitor, has been shown to reduce neural injury after transient cerebral ischemia. It has also been reported that this neuroprotective effect results from an anticoagulant function. This study was designed to evaluate quantitatively the inhibitory effects of argatroban on leukocyte-and platelet-endothelial cell interactions after transient retinal ischemia. Methods-Retinal ischemia was induced for 60 minutes in male Long-Evans rats by temporary ligation of the optic sheath (nϭ342). Argatroban was administered just after induction of ischemia. Leukocyte and platelet behavior in the retinal microcirculation was then evaluated in vivo with scanning laser ophthalmoscopy. The expression of P-selectin and intracellular adhesion molecule-1 (ICAM-1) was evaluated by reverse transcription-polymerase chain reaction. After 10 days of reperfusion, ischemia-induced retinal damage was evaluated histologically. Results-Treatment with argatroban suppressed leukocyte-endothelial cell interactions; the maximum numbers of rolling and accumulated leukocytes were reduced by 90.1% (PϽ0.05) and 58.7% (PϽ0.05), respectively, at 12 hours after reperfusion. Treatment with argatroban also suppressed platelet-endothelial cell interactions; the maximum numbers of rolling and adhering platelets were reduced by 91.8% (PϽ0.01) and 78.9% (PϽ0.01), respectively, at 12 hours after reperfusion. The expression of P-selectin and ICAM-1 mRNA was suppressed significantly in the argatroban-treated retinas (PϽ0.01). Histologic examination demonstrated the protective effect of argatroban on ischemia-induced retinal damage (PϽ0.01). Conclusions-Argatroban treatment suppressed leukocyte-and platelet-endothelial cell interactions after transient retinal ischemia. This inhibitory effect on postischemic blood cell-endothelial cell interactions might partially contribute to its neuroprotective effects.

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confidence: 99%

Argatroban Attenuates Leukocyte– and Platelet–Endothelial Cell Interactions After Transient Retinal Ischemia

Miyahara

Kiryu

Tsujikawa

et al. 2003

Stroke

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“…Esta participação na fisiopatogenia da lesão de isquemia e reperfusão do coração (8) , pulmão (20) e pâncreas (15) (3):276-81. ABSTRACT -Background -Hepatic ischemia-reperfusion injury is responsible for a considerable morbidity and mortality.…”

Section: Discussionunclassified

“…Sabe-se que as plaquetas contribuem para lesão de isquemia e reperfusão no coração (8) , pulmão (20) e pâncreas (15) . No fígado, o bloqueio da agregação plaquetária também demonstrou efeito protetor na microcirculação (14) .…”

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Efeito protetor de antagonista das gliproteínas IIb/IIa nas alterações hepáticas e pulmonares secundárias à isquemia e reperfusão do fígado em ratos

Canedo

Machado

Coelho

et al. 2007

Arq. Gastroenterol.

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RESUMO -Racional -A lesão de isquemia e reperfusão hepática é um evento comum e responsável por considerável morbidade e mortalidade.Objetivo -Avaliar efeitos de inibidor da glicoproteína IIb/IIIa, cloridrato de tirofiban, nas alterações hepáticas e pulmonares da lesão de isquemia e reperfusão de fígado de ratos. Método -Vinte e três ratos Wistar divididos em três grupos: laparotomia (n = 6), isquemia e reperfusão que receberam solução fisiológica (n = 8), e submetidos a isquemia e reperfusão e tratados com o cloridrato de tirofiban (n = 9). Foram realizadas dosagens das aminotransferases e análise histológica hepática. Avaliação pulmonar foi realizada pelo teste do azul de Evans e pela dosagem tecidual da mieloperoxidase no parênquima pulmonar. A oxidação e fosforilação mitocondrial das células hepáticas também foram avaliadas. Resultados -O grupo tratado com cloridrato de tirofiban apresentou menores níveis de aminotransferases, assim como alterações histológicas menos intensas. Avaliação pulmonar demonstrou diminuição no teste de azul de Evans no grupo tratado com cloridrato de tirofiban. Grupo tratado com cloridrato de tirofiban apresentou aumento significativo do estado 3 da respiração mitocondrial e das relações adenosina difosfato utilizado para fosforilação sobre o oxigênio consumido na reação e de coeficiente respiratório. Conclusões -O uso do cloridrato de tirofiban exerceu papel protetor da lesão hepática de isquemia e reperfusão e impediu o aumento da permeabilidade vascular secundária à lesão de reperfusão hepática. DESCRITORES -Traumatismo por reperfusão. Fígado. Hepatectomia. Glicoproteínas da membrana de plaquetas. Ratos. INTRODUÇÃOA lesão de isquemia e reperfusão é a principal determinante da disfunção hepática após hepatectomias, e também, a causa mais importante da disfunção primária do enxerto hepático (2,3,23)

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“…This may be coupled with cardiac dysfunction as cardiac reoxygenation injury is also known to be partly mediated by platelets exposed to superoxide (30). The lung and pancreas may also be affected (31,32). It is therefore likely that circulating platelets can play a role in multiorgan failure in intact hypoxic newborn animals or infants.…”

Section: Discussionmentioning

confidence: 99%

Platelet Dysfunction in Asphyxiated Newborn Piglets Resuscitated with 21% and 100% Oxygen

et al. 2006

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Hemostatic disturbances are common in asphyxiated newborns after resuscitation. We compared platelet function in hypoxic newborn piglets reoxygenated with 21% or 100% oxygen. Piglets (1-3 d, 1.5-2.1 kg) were anesthetized and acutely instrumented for hemodynamic monitoring. After stabilization, normocapnic hypoxia was induced with an inspired oxygen concentration of 10 -15% for 2 h. Piglets were then resuscitated for 1 h with 21% or 100% oxygen, followed by 3 h with 21% oxygen. Platelet counts and collagen (2, 5, and 10 g/mL)-stimulated whole blood aggregation were studied before hypoxia and at 4 h of post-hypoxia/ reoxygenation. Platelet function was studied using transmission electron microscopy and by measuring plasma thromboxane B 2 (TxB 2 ) and matrix metalloproteinase (MMP)-2 and -9 levels. Control piglets were sham-operated without hypoxia/reoxygenation. The hypoxemic (PaO 2 33 mm Hg) piglets developed hypotension with metabolic acidosis (pH 7.02-7.05). Upon reoxygenation, piglets recovered and blood gases gradually normalized. At 4 h reoxygenation, platelet aggregation ex vivo was impaired as evidenced by a rightwarddownward shifting of the concentration-response curves. Electron microscopy showed features of platelet activation. Plasma MMP-9 but not MMP-2 activity significantly increased. Resuscitation with 100% but not 21% oxygen increased plasma TxB 2 levels. Platelet counts decreased after hypoxia/reoxygenation but were not different between groups during the experiment. Resuscitation of hypoxic newborn piglets caused platelet activation with significant deterioration of platelet aggregation ex vivo and increased plasma MMP-9 levels. High oxygen concentrations may aggravate the activation of prostaglandin-thromboxane mechanistic pathway. MMP-2 (constitutive isoform, 72 kD) and MMP-9 (inducible isoform, 92 kD) are zinc-dependent endopeptidases that play an important role in the regulation of platelet aggregation (6 -9). MMPs are activated by proteolysis and oxidants including the peroxynitrite anion (6,10). Increased plasma MMP-2 and -9 activity with platelet dysfunction was observed in an animal model of extracorporeal circulation with a high oxygen environment (11). Lemke et al. (12) recently reported a surge in plasma MMP-9 activity in the first day of postnatal life, which is consistent with a change from a low to a high oxygen environment. Interestingly, in neonatal models of asphyxia, resuscitation with 100% oxygen is associated with higher oxidative stress and MMP-2 activities in the heart and brain than those with 21% oxygen (13,14). However, there is little information on the activity of MMPs in plasma and its relationship to platelet aggregatory function in the reoxygenation of asphyxiated newborns.Asphyxiated infants are often resuscitated with 100% oxygen, and this is associated with increased oxidative stress up to 28 d after birth (15). In the midst of the debate between the use of 21% or 100% oxygen in the resuscitation of asphyxiated newborns, we designed this study to examin...

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Effects of leukocyte and platelet depletion on ischemia-reperfusion injury to dog pancreas

Cited by 56 publications

References 20 publications

Argatroban Attenuates Leukocyte– and Platelet–Endothelial Cell Interactions After Transient Retinal Ischemia

Argatroban Attenuates Leukocyte– and Platelet–Endothelial Cell Interactions After Transient Retinal Ischemia

Efeito protetor de antagonista das gliproteínas IIb/IIa nas alterações hepáticas e pulmonares secundárias à isquemia e reperfusão do fígado em ratos

Platelet Dysfunction in Asphyxiated Newborn Piglets Resuscitated with 21% and 100% Oxygen

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