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: Intravenous thrombolysis is the preferred treatment for acute ischemic stroke; however, it remains unestablished in the area of cardiac catheterization. We report three patients with acute ischemic stroke after cardiac catheterization. After reversing the anticoagulant effect of unfractionated heparin with protamine, all of the patients were successfully off-label thrombolyzed with reduced doses of intravenous recombinant tissue plasminogen activator (0.6 mg/kg). This dose was preferred to reduce the risk of symptomatic cerebral or systemic bleeding. The sequential pathway of protamine recombinant tissue plasminogen activator at reduced doses may be safer for reducing intracranial or systemic bleeding events, whereas remaining efficacious for the treatment of acute ischemic stroke after cardiac catheterization.

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In this case report, we describe a child with biliary atresia who underwent a living LDLT and developed severe coagulopathy after reperfusion of the graft. The ROTEM analysis strongly suggested the presence of either a heparin effect or severe deficiency of coagulation factors. The former diagnosis was supported by a subsequent in-vitro HEPTEM. A small dose of protamine sulphate was then administered, which promptly restored hemostasis. The remainder of the procedure was uneventful.

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PURPOSE: We reproduced a non-bacterial experimental model to assess bladder inflammation and urinary glycosaminoglycans (GAG) excretion and examined the effect of dimethyl sulfoxide (DMSO). MATERIALS AND METHODS: Female rats were instilled with either protamine sulfate (PS groups) or sterile saline (control groups). At different days after the procedure, 24 h urine and bladder samples were obtained. Urinary levels of hyaluronic acid (HA) and sulfated glycosaminoglycans (S-GAG) were determined. Also to evaluate the effect of DMSO animals were instilled with either 50% DMSO or saline 6 hours after PS instillation. To evaluate the effect of DMSO in healthy bladders, rats were instilled with 50% DMSO and controls with saline. RESULTS: In the PS groups, bladder inflammation was observed, with polymorphonuclear cells during the first days and lymphomononuclear in the last days. HA and S-GAG had 2 peaks of urinary excretion, at the 1st and 7th day after PS injection. DMSO significantly reduced bladder inflammation. In contrast, in healthy bladders, DMSO produced mild inflammation and an increase in urinary HA levels after 1 and 7 days and an increase of S-GAG level in 7 days. Animals instilled with PS and treated with DMSO had significantly reduced levels of urinary HA only at the 1st day. Urinary S-GAG/Cr levels were similar in all groups. CONCLUSIONS: Increased urinary levels of GAG were associated with bladder inflammation in a PS-induced cystitis model. DMSO significantly reduced the inflammatory process after urothelial injury. Conversely, this drug provoked mild inflammation in normal mucosa. DMSO treatment was shown to influence urinary HA excretion.

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PURPOSE: We reproduced a non-bacterial experimental model to assess bladder inflammation and urinary glycosaminoglycans (GAG) excretion and examined the effect of dimethyl sulfoxide (DMSO). MATERIALS AND METHODS: Female rats were instilled with either protamine sulfate (PS groups) or sterile saline (control groups). At different days after the procedure, 24 h urine and bladder samples were obtained. Urinary levels of hyaluronic acid (HA) and sulfated glycosaminoglycans (S-GAG) were determined. Also to evaluate the effect of DMSO animals were instilled with either 50 percent DMSO or saline 6 hours after PS instillation. To evaluate the effect of DMSO in healthy bladders, rats were instilled with 50 percent DMSO and controls with saline. RESULTS: In the PS groups, bladder inflammation was observed, with polymorphonuclear cells during the first days and lymphomononuclear in the last days. HA and S-GAG had 2 peaks of urinary excretion, at the 1st and 7th day after PS injection. DMSO significantly reduced bladder inflammation. In contrast, in healthy bladders, DMSO produced mild inflammation and an increase in urinary HA levels after 1 and 7 days and an increase of S-GAG level in 7 days. Animals instilled with PS and treated with DMSO had significantly reduced levels of urinary HA only at the 1st day. Urinary S-GAG/Cr levels were similar in all groups. CONCLUSIONS: Increased urinary levels of GAG were associated with bladder inflammation in a PS-induced cystitis model. DMSO significantly reduced the inflammatory process after urothelial injury. Conversely, this drug provoked mild inflammation in normal mucosa. DMSO treatment was shown to influence urinary HA excretion.

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Protamine inhibits angiogenesis and blocks endothelial, fibroblast and platelet growth factors. Human and experimental gliomas spread and grow in response to both paracrine and autocrine release of these factors. Our objective was to study the effect of protamine administration on cell proliferation, angiogenesis and tumoral growth of C6 glioma. Additionally, we compared the antitumoral effect of protamine with that of another inhibitor of angiogenesis, suramin, and investigated a potential synergistic antitumoral action of low doses of protamine combined with the antineoplastic carmustine. C6 glioma cells were implanted subcutaneously in Wistar rats. A highly malignant glioma developed in 80% of animals; when the tumour reached a diameter of 1.5 cm, either protamine, suramin, carmustine or protamine plus carmustine were administered in various doses. Tumour parameters were measured and compared between groups. In a dose-dependent manner, protamine reduced tumour volume (P < 0.001), mitotic index (P < 0.05), vascular density (P < 0.05) and cell viability (P < 0.005) of C6 glioma. An ultrastructural study demonstrated membranous inclusions in the cytoplasm of 28% of tumoral and endothelial cells of tumours from animals treated with protamine. The inhibition of tumoral growth produced by moderate doses of protamine was similar to that produced by toxic doses of suramin. The combination of protamine and carmustine had a synergistic curtailing effect on tumoral growth (P < 0.001). Our results indicate that protamine is an effective agent against glioblastoma; in non-toxic doses it could potentiate the antineoplastic effect of nitrosoureas for the treatment of glial tumours.

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It was previously shown that topical application of heparin produces enhanced bleeding from small vessels and capillaries. Adenosine triphosphate at low concentrations is able to dislodge heparin bound to a receptor, counteracting its antihemostatic activity. These results led us to measure the amounts of heparin remaining in the blood after protamine neutralization of the patients subjected to cardiopulmonary bypass operation and to test the topical application of the nucleotide. Adenosine triphosphate at a concentration of 10(-4) mol/L significantly reduces the blood volume (p < 0.005) oozed from the thoracic cavity of the patients (mean, 288 +/- 188 mL) when compared with controls (mean, 564 +/- 288 mL). Adenosine triphosphate at 5 x 10(-5) mol/L reduces the blood loss to a mean of 370 +/- 155 mL in the patients tested (p < 0.08). About 10% of heparin of low molecular weight (< or = 6.0 Kda), which is also found in the oozed blood, is not neutralized by protamine. We suggest that the excessive blood loss of the patients is probably produced by low molecular weight heparins in the commercial preparations that are not neutralized by protamine.

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The possible antiherpetic effect of three polyanions (heparin, chondroitin sulfate and dextran sulfate), as well as one polycation (protamine sulfate) was tested in vitro and in vivo against pseudorabies virus (Suid herpesvirus 1). The in vitro experiments revealed that heparin, dextran sulfate and protamine sulfate significantly reduced the number of lytic plaques. Chondroitin sulfate only caused a decrease in mean plaque size. Experiments in vivo disclosed that heparin injected subcutaneously before the experimental infection, was the only polyanion that protected mice against pseudorabies virus. Protamine sulfate had a paradoxic effect: whereas in vitro it reduced the number of lytic plaques, in vivo it increased the lethality of pseudorabies virus. Chondroitin sulfate and dextran sulfate did not modify the virulence of the virus in mice.

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El objetivo de este trabajo es demostrar la utilidad del cálculo del tiempo de coagulación activado para la dosificación y neutralización de heparina durante cirugía con circulación extracorpórea. Se midieron en forma prospectiva los volúmenes de sangrado en ml, en 30 pacienes sometidos a esta cirugía, sus parámetros fueron: 861, 33 ñ 87,4419 (X ñ ES). La comparación se realizó con un grupo histórico de 30 individuos cuyos datos fueron: 1286,66 ñ 127,2939 (X ñ ES). Se demostró diferencia altamente significativa utilizando análisis de varianza (F = 7,58; F0,01 = 7,10 para 1 y 58 grados de libertad) entre ambos métodos a favor del cálculo del tiempo de coagulación activado

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El objetivo de este trabajo es demostrar la utilidad del cálculo del tiempo de coagulación activado para la dosificación y neutralización de heparina durante cirugía con circulación extracorpórea. Se midieron en forma prospectiva los volúmenes de sangrado en ml, en 30 pacienes sometidos a esta cirugía, sus parámetros fueron: 861, 33 ñ 87,4419 (X ñ ES). La comparación se realizó con un grupo histórico de 30 individuos cuyos datos fueron: 1286,66 ñ 127,2939 (X ñ ES). Se demostró diferencia altamente significativa utilizando análisis de varianza (F = 7,58; F0,01 = 7,10 para 1 y 58 grados de libertad) entre ambos métodos a favor del cálculo del tiempo de coagulación activado (AU)

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