Acetylsalicylic Acid Stimulates Murine Megakaryocyte Precursor Cells

Sullivan, Patrick S.; McDonald, T. P.

doi:10.3181/00379727-194-43081

Cited by 9 publications

(6 citation statements)

References 11 publications

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“…Mice given injections of aspirin showed a reduced maximum percentage of aggregation (58.7%), as compared with untreated control mice (69.1%). This finding agrees with the data of Sullivan and McDonald (6), which showed a significant reduction in aggregation of platelets at 8 hr after injections of aspirin and a reduced, but not significant, level of aggregation after 24 hr.…”

supporting

confidence: 93%

“…Box 1071, Knoxville, TN 37901-1071 of megakaryocyte precursor cells. the small acetylcholinesterase-positive (SAChE+) cells (6). In this work, poor platelet function was linked to increases in blood platelet production.…”

mentioning

confidence: 93%

“…Donor Mice Treatment. Donor mice were given a single intraperitoneal injection of 5 mg of ASA (Sigma Chemical Co., St. Louis, MO) in a 0.086 M NaOH buffer (pH 7.4), as described previously (6). After anesthesia with sodium pentobarbital, the mice were bled by cardiac puncture into heparin-coated syringes at 22 hr after ASA injection.…”

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confidence: 99%

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Thrombopoietin Production in Mice Treated with Acetylsalicylic Acid

Clift

Cottrell

McDonald

1991

Experimental Biology and Medicine

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Recent work revealed that mice in which platelet function was inhibited by acetylsalicylic acid (ASA) treatment showed evidence of increased platelet production. It was proposed that poorly functioning platelets gave rise to elevated thrombocytopoiesis by causing the release and action of thrombopoietin. However, direct evidence is lacking. Therefore, in the work reported here, plasma from mice treated with ASA was injected into normal recipient mice in an attempt to document the existence of the humoral factor. Compared with control mice given normal plasma, the injection of mice with plasma from ASA-treated mice resulted in increased thrombocytopoiesis, as evidenced by significant increases in the percentage of 35S incorporation into platelets, larger platelet size, and elevated megakaryocyte precursor cells (the small acetylcholinesterase-positive cell). For a positive control, additional mice were treated with plasma from animals made thrombocytopenic by an injection of antiplatelet serum. These mice also showed significant increases in thrombocytopoiesis. The results support the hypothesis that platelet production in ASA-treated mice is elevated by release and action of thrombopoietin.

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Thrombopoietin Production in Mice Treated with Acetylsalicylic Acid

Clift

Cottrell

McDonald

1991

Experimental Biology and Medicine

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“…Because circulating platelet counts were also decreased in some CRF patients [5, 6], decreased thrombopoiesis has been associated with the pathogenesis of uremic bleeding. However, Sullivan and McDonald [7]found that platelet dysfunction is one of the stimulators of reactive thrombopoiesis, and later reports have actually demonstrated elevated serum thrombopoietin (TPO) levels in CRF patients [6, 8], suggesting increased thrombopoiesis in CRF, although it has not directly been examined in megakaryocytes, the site of thrombopoiesis.…”

Section: Introductionmentioning

confidence: 99%

Compensatory Thrombopoietin Production from the Liver and Bone Marrow Stimulates Thrombopoiesis of Living Rat Megakaryocytes in Chronic Renal Failure

Kazama

Endo²,

Toyama³

et al. 2011

Nephron Extra

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Background/Aims: Decreased thrombopoiesis has been ascribed a role in the pathogenesis of uremic bleeding in chronic renal failure (CRF). However, serum thrombopoietin (TPO) levels are usually elevated in CRF patients, suggesting increased thrombopoiesis. The aim of this study was to determine the thrombopoietic activity in CRF. Methods: Male Sprague-Dawley rats that underwent 5/6 nephrectomy were used as the model of CRF. Age-matched sham-operated rats were used as controls. Single megakaryocytes were isolated from the rat bone marrow, and their size distribution was examined. Megakaryocyte membrane invaginations were monitored by confocal imaging of di-8-ANEPPS staining, and patch clamp whole-cell recordings of membrane capacitance. TPO gene expression was assessed in various tissues. Results: Circulating platelet counts and the number of large megakaryocytes were increased in the bone marrow of CRF rats. Massive di-8-ANEPPS staining and increased membrane capacitance in large megakaryocytes demonstrated increased membrane invaginations. Unaffected Kv1.3-channel currents per cell surface area demonstrated unaltered channel densities. TPO transcription was decreased in the renal cortex but increased in the liver and bone marrow of CRF rats. Conclusion: Increased thrombopoiesis in CRF was thought to be a reactive mechanism to platelet dysfunction. Increased TPO production from the liver and bone marrow compensated for decreased production from damaged kidneys.

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“…Moreover, the inhibition of human megakaryocyte cyclooxygenase with low doses of aspirin is incomplete, and megakaryocyte cyclooxygenase seems to recover within 12 hours after aspirin ingestion 29,30 . Second, interruption of the platelet function by aspirin results in the production of new platelets, presumably through the action of a feedback system controlling thrombocytopoiesis 31 . With the newly formed platelets from the bone marrow in the absence of aspirin, these mechanisms may affect the platelet activity recovery time faster than the life span of the mature platelets.…”

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confidence: 99%

Recovery Time of Platelet Function After Aspirin Withdrawal

Lee

Kim

et al. 2014

Current Therapeutic Research

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IntroductionInappropriate antiplatelet therapy discontinuation increases the risk of thrombotic complications and bleeding after dental procedures. To determine the platelet reactivity recovery time after aspirin withdrawal in vivo, our study was conducted in patients with low-risk cardiovascular disease who can stop aspirin administration following the guidelines stipulated by the American College of Chest Physicians. The time it takes for platelet activity to normalize and the diagnostic accuracy of testing methods were assessed for a residual antiplatelet activity with multiple electrode aggregometry. Our study included patients with clinically indicated hypertension preparing for a dental extraction procedure.Materials and methodsA total of 212 patients not taking aspirin (control group) and 248 patients with hypertension receiving long-time aspirin treatment at a 100-mg daily dose were prospectively included in the study, which involved stopping aspirin intake before dental extraction. The residual platelet activity and dental bleeding in patients who stopped aspirin intake were analyzed and compared with those of the control group. In addition, platelet reactivity recovery time and bleeding risk in patients who stopped taking aspirin every 24 hours for 0 to 5 days (0–143 hours) before dental extraction was also assessed.ResultsPlatelet reactivity normalized 96 hours after aspirin withdrawal. The cut-off value of 49 arbitrary units in the arachidonic acid platelet aggregation test excluded the effect of aspirin with 91% sensitivity and 66% specificity. AUC showed 0.86 (P < 0.001) diagnostic accuracy. The immediate bleeding complications in all treatment groups were similar to those seen in the control group and were successfully managed with local hemostatic measures.ConclusionsThe antiplatelet effects of aspirin disappeared 96 hours after aspirin withdrawal in our study, and dental extractions may be safely performed in this period when appropriate local hemostatic measures are taken. Based on these results, a shorter aspirin intake cessation period may be allowable in complex dental procedures and surgery for which a longer aspirin intake cessation period (7–10 days) is recommended based on the American College of Chest Physicians guidelines.

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Acetylsalicylic Acid Stimulates Murine Megakaryocyte Precursor Cells

Cited by 9 publications

References 11 publications

Thrombopoietin Production in Mice Treated with Acetylsalicylic Acid

Thrombopoietin Production in Mice Treated with Acetylsalicylic Acid

Compensatory Thrombopoietin Production from the Liver and Bone Marrow Stimulates Thrombopoiesis of Living Rat Megakaryocytes in Chronic Renal Failure

Recovery Time of Platelet Function After Aspirin Withdrawal

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