Figure 7.
Figure 7. Acute intravenous tPA promotes bradykinin generation in patients with ischemic stroke. (A-B) Time-course of plasma samples collection in patients with ischemic stroke who received thrombolytic therapy. Blood samples were obtained at 0 (before), 1, 2, 12, and 24 hours after tPA infusion. (C-D) Representative western blots of plasmatic HMWK levels (120 KDa) in patients with stroke before and after tPA infusion, showing that plasmin generation promotes HMWK cleavage. Both high (B) and low (C) profiles of HMWK cleavage were found in the small cohort of patients with stroke. Recombinant HMWK was used as a reference. (E) Mean percentage of plasmatic HMWK levels in patients with stroke over time. Baseline levels were used to normalize samples (100%) (n = 8). (F) Quantification of bradykinin (BK) levels in those patients at the baseline level (before) and at the end of thrombolysis (+1 hour), showing that HMWK cleavage promotes bradykinin generation. *P < .05 vs control.

Acute intravenous tPA promotes bradykinin generation in patients with ischemic stroke. (A-B) Time-course of plasma samples collection in patients with ischemic stroke who received thrombolytic therapy. Blood samples were obtained at 0 (before), 1, 2, 12, and 24 hours after tPA infusion. (C-D) Representative western blots of plasmatic HMWK levels (120 KDa) in patients with stroke before and after tPA infusion, showing that plasmin generation promotes HMWK cleavage. Both high (B) and low (C) profiles of HMWK cleavage were found in the small cohort of patients with stroke. Recombinant HMWK was used as a reference. (E) Mean percentage of plasmatic HMWK levels in patients with stroke over time. Baseline levels were used to normalize samples (100%) (n = 8). (F) Quantification of bradykinin (BK) levels in those patients at the baseline level (before) and at the end of thrombolysis (+1 hour), showing that HMWK cleavage promotes bradykinin generation. *P < .05 vs control.

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