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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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Related in: MedlinePlus

The permeability (normalized to baseline) 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. *p < 0.05 AB, EF, tAB and tEF vs. I/R and t-PA; ° p < 0.05 tAB and tEF vs.AB and EF.
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Figure 3: The permeability (normalized to baseline) 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. *p < 0.05 AB, EF, tAB and tEF vs. I/R and t-PA; ° p < 0.05 tAB and tEF vs.AB and EF.

Mentions: Before ischemia no detectable fluorescent dextran leakage was observed in all the groups. In the I/R and tPA groups a significant increase in permeability was observed in postcapillary and collecting venules during reperfusion (baseline: 0.09 ± 0.01 normalized grey levels, p < 0.05, Fig. 3). The treatment with abiciximab and eptifibatide significantly attenuated the I/R-induced increase in permeability from venules 30 min after reperfusion. In AB and EF groups a slight increase in permeability was observed from 20–30 min after reperfusion when compared with tEF and tAB groups (tAB -25% and tEF: -57% vs. the ABI 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)

The permeability (normalized to baseline) 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. *p < 0.05 AB, EF, tAB and tEF vs. I/R and t-PA; ° p < 0.05 tAB and tEF vs.AB and EF.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC117121&req=5

Figure 3: The permeability (normalized to baseline) 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. *p < 0.05 AB, EF, tAB and tEF vs. I/R and t-PA; ° p < 0.05 tAB and tEF vs.AB and EF.
Mentions: Before ischemia no detectable fluorescent dextran leakage was observed in all the groups. In the I/R and tPA groups a significant increase in permeability was observed in postcapillary and collecting venules during reperfusion (baseline: 0.09 ± 0.01 normalized grey levels, p < 0.05, Fig. 3). The treatment with abiciximab and eptifibatide significantly attenuated the I/R-induced increase in permeability from venules 30 min after reperfusion. In AB and EF groups a slight increase in permeability was observed from 20–30 min after reperfusion when compared with tEF and tAB groups (tAB -25% and tEF: -57% vs. the ABI 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