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Early recovery of microvascular perfusion induced by t-PA in combination with abciximab or eptifibatide during postischemic reperfusion.

Bertuglia S, Giusti A - BMC Cardiovasc Disord (2002)

Bottom Line: GPIIb/IIIa inhibitors abciximab and eptifibatide have been shown to inhibit platelet aggregation in ischemic heart disease.We measured the microvessel diameter changes, the arteriolar red blood cell (RBC) velocity, the increase in permeability, the perfused capillary length (PCL), and the platelet and leukocyte adhesion on microvessels.Platelets are crucial in I/R injury, as shown by the treatment with abicixmab or eptifibatide, which decreased platelet aggregation in microvessels, and also decreased leukocyte adhesion in venules.

View Article: PubMed Central - HTML - PubMed

Affiliation: CNR Institute of Clinical Physiology, School of Medicine, University of Pisa, 56100 Pisa, Italy. sibert@ifc.cnr.it

ABSTRACT

Background: GPIIb/IIIa inhibitors abciximab and eptifibatide have been shown to inhibit platelet aggregation in ischemic heart disease. Our aim was to test the efficacy of abiciximab (Reo Pro) or eptifibatide (Integrilin) alone or in combination with plasminogen activator (t-PA) in an experimental model of ischemia reperfusion (I/R) in hamster cheek pouch microcirculation visualized by fluorescence microscopy. Hamsters were treated with saline, or abiciximab or eptifibatide or these drugs combined with t-PA infused intravenously 10 minutes before ischemia and through reperfusion. We measured the microvessel diameter changes, the arteriolar red blood cell (RBC) velocity, the increase in permeability, the perfused capillary length (PCL), and the platelet and leukocyte adhesion on microvessels.

Results: I/R elicited large increases in the platelet and leukocyte adhesion and a decrease in microvascular perfusion. These responses were significantly attenuated by abiciximab or eptifibatide (PCL:70 and 65% at 5-10 mins of reperfusion and 85 and 87% at 30 mins of reperfusion, respectively, p < 0.001) while t-PA combined with abiciximab or eptifibatide, was more effective and microvascular perfusion recovered immediately after postischemic reperfusion.

Conclusions: Platelets are crucial in I/R injury, as shown by the treatment with abicixmab or eptifibatide, which decreased platelet aggregation in microvessels, and also decreased leukocyte adhesion in venules. Arterial vasoconstriction, decreased arterial RBC velocity and alterations in the endothelial barrier with increased permeability delayed the complete restoration of blood flow, while t-PA combined with inhibition of platelet aggregation speeded up the capillary perfusion after reperfusion.

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Changes of arteriolar RBC velocity at baseline and during reperfusion in the group treated with saline (I/R) and those treated with abiciximab (AB), eptifibatide (EF), t-PA (tPA) and abiciximab plus t-PA (tAB) or eptifibatide plus t-PA (tEF), respectively. See text for details. Values are means ± SD, n = 20 experimental observations for each entry, *p < 0.05 I/R-tPA vs. baseline; °p < 0.05 AB, EF, tAB, and tEF vs. I/R and tPA; ** p < 0.05 tAB abd tEF vs.AB and EF.
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Figure 2: Changes of arteriolar RBC velocity at baseline and during reperfusion in the group treated with saline (I/R) and those treated with abiciximab (AB), eptifibatide (EF), t-PA (tPA) and abiciximab plus t-PA (tAB) or eptifibatide plus t-PA (tEF), respectively. See text for details. Values are means ± SD, n = 20 experimental observations for each entry, *p < 0.05 I/R-tPA vs. baseline; °p < 0.05 AB, EF, tAB, and tEF vs. I/R and tPA; ** p < 0.05 tAB abd tEF vs.AB and EF.

Mentions: There was not a significant difference in baseline RBC velocity in I/R and tPA groups. Just after the ischemic period a significant decrease in RBC velocity was observed in both groups and during the subsequent period of reperfusion (1.98 ± 0.35 mm/s at baseline, p < 0.05) (Fig. 2). In AB and EF groups RBC velocity increased significantly in arterioles during reperfusion in comparison with I/R (p < 0.05, Figs. 1,2) whereas it further increased in either groups treated with t-PA in combination with gpIIa/IIIb inhibitors (tAB: 42% and tEF: 46% vs. the AB and EF groups, respectively, p < 0.05).


Early recovery of microvascular perfusion induced by t-PA in combination with abciximab or eptifibatide during postischemic reperfusion.

Bertuglia S, Giusti A - BMC Cardiovasc Disord (2002)

Changes of arteriolar RBC velocity at baseline and during reperfusion in the group treated with saline (I/R) and those treated with abiciximab (AB), eptifibatide (EF), t-PA (tPA) and abiciximab plus t-PA (tAB) or eptifibatide plus t-PA (tEF), respectively. See text for details. Values are means ± SD, n = 20 experimental observations for each entry, *p < 0.05 I/R-tPA vs. baseline; °p < 0.05 AB, EF, tAB, and tEF vs. I/R and tPA; ** p < 0.05 tAB abd tEF vs.AB and EF.
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Related In: Results  -  Collection

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Figure 2: Changes of arteriolar RBC velocity at baseline and during reperfusion in the group treated with saline (I/R) and those treated with abiciximab (AB), eptifibatide (EF), t-PA (tPA) and abiciximab plus t-PA (tAB) or eptifibatide plus t-PA (tEF), respectively. See text for details. Values are means ± SD, n = 20 experimental observations for each entry, *p < 0.05 I/R-tPA vs. baseline; °p < 0.05 AB, EF, tAB, and tEF vs. I/R and tPA; ** p < 0.05 tAB abd tEF vs.AB and EF.
Mentions: There was not a significant difference in baseline RBC velocity in I/R and tPA groups. Just after the ischemic period a significant decrease in RBC velocity was observed in both groups and during the subsequent period of reperfusion (1.98 ± 0.35 mm/s at baseline, p < 0.05) (Fig. 2). In AB and EF groups RBC velocity increased significantly in arterioles during reperfusion in comparison with I/R (p < 0.05, Figs. 1,2) whereas it further increased in either groups treated with t-PA in combination with gpIIa/IIIb inhibitors (tAB: 42% and tEF: 46% vs. the AB and EF groups, respectively, p < 0.05).

Bottom Line: GPIIb/IIIa inhibitors abciximab and eptifibatide have been shown to inhibit platelet aggregation in ischemic heart disease.We measured the microvessel diameter changes, the arteriolar red blood cell (RBC) velocity, the increase in permeability, the perfused capillary length (PCL), and the platelet and leukocyte adhesion on microvessels.Platelets are crucial in I/R injury, as shown by the treatment with abicixmab or eptifibatide, which decreased platelet aggregation in microvessels, and also decreased leukocyte adhesion in venules.

View Article: PubMed Central - HTML - PubMed

Affiliation: CNR Institute of Clinical Physiology, School of Medicine, University of Pisa, 56100 Pisa, Italy. sibert@ifc.cnr.it

ABSTRACT

Background: GPIIb/IIIa inhibitors abciximab and eptifibatide have been shown to inhibit platelet aggregation in ischemic heart disease. Our aim was to test the efficacy of abiciximab (Reo Pro) or eptifibatide (Integrilin) alone or in combination with plasminogen activator (t-PA) in an experimental model of ischemia reperfusion (I/R) in hamster cheek pouch microcirculation visualized by fluorescence microscopy. Hamsters were treated with saline, or abiciximab or eptifibatide or these drugs combined with t-PA infused intravenously 10 minutes before ischemia and through reperfusion. We measured the microvessel diameter changes, the arteriolar red blood cell (RBC) velocity, the increase in permeability, the perfused capillary length (PCL), and the platelet and leukocyte adhesion on microvessels.

Results: I/R elicited large increases in the platelet and leukocyte adhesion and a decrease in microvascular perfusion. These responses were significantly attenuated by abiciximab or eptifibatide (PCL:70 and 65% at 5-10 mins of reperfusion and 85 and 87% at 30 mins of reperfusion, respectively, p < 0.001) while t-PA combined with abiciximab or eptifibatide, was more effective and microvascular perfusion recovered immediately after postischemic reperfusion.

Conclusions: Platelets are crucial in I/R injury, as shown by the treatment with abicixmab or eptifibatide, which decreased platelet aggregation in microvessels, and also decreased leukocyte adhesion in venules. Arterial vasoconstriction, decreased arterial RBC velocity and alterations in the endothelial barrier with increased permeability delayed the complete restoration of blood flow, while t-PA combined with inhibition of platelet aggregation speeded up the capillary perfusion after reperfusion.

Show MeSH
Related in: MedlinePlus