Microvascular benefits of increasing plasma viscosity and maintaining blood viscosity: Counterintuitive experimental findings

Vázquez, Beatriz Y. Salazar; Martini, Judith; Negrete, Adolfo Chávez; Cabrales, Pedro; Tsai, Amy G.; Intaglietta, Marcos

doi:10.3233/bir-2009-0539

Cited by 54 publications

(13 citation statements)

References 30 publications

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“…The first is that changes in blood viscosity influence the viscoelastic TEG method, resulting in a mechanical bias of the TEG tracing. The second possibility is that the ALG itself exerts a direct effect on clot kinetics and strength and is not as biologically inert as has been previously proposed . While autologous RBCs or plasma proteins could have been used to alter whole blood viscosity, we would not have been able to separate the effect of these native components on coagulation from the effect of viscosity.…”

Section: Discussionmentioning

confidence: 91%

Effects of hematocrit and red blood cell–independent viscosity on canine thromboelastographic tracings

et al. 2013

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Section: Discussionmentioning

confidence: 91%

Effects of hematocrit and red blood cell–independent viscosity on canine thromboelastographic tracings

et al. 2013

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“…NO is a neurotransmitter, a macrophage-derived host-defense molecule, an inhibitor of platelet aggregation and endothelium adhesion molecule expression, an antioxidant, cardiac chronotropic, and a potent vasodilator. 7 Our hypotheses to explain the hemorrhagic shock induced cardiovascular collapse are that the production of NO is impaired by 1) drastic reduction on endothelial shear stress (due to low blood pressure, cardiac output, circulating volume and blood viscosity) 8 ; 2) free radical formation/accumulation, uncoupling the endothelial NO synthase (NOS) 9 ; and 3) hypoxia, as oxygen is a substrate for NO production 10 . Thus, restoration of NO bioavailability impaired during hemorrhagic shock will reduce many hemorrhagic shock induced complications.…”

Section: Introductionmentioning

confidence: 99%

Exogenous nitric oxide prevents cardiovascular collapse during hemorrhagic shock

Nachuraju

Friedman

et al. 2011

Resuscitation

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This study investigated the systemic and microvascular hemodynamic changes related to increased nitric oxide (NO) availability following significant hemorrhage, made available by administration of NO releasing nanoparticles (NO-nps). Hemodynamic responses to hemorrhagic shock were studied in the hamster window chamber. Acute hemorrhage was induced by arterial controlled bleeding of 50% of blood volume, and the resulting hemodynamic parameters were followed over 90 min. Exogenous NO was administered in the form of NO-nps (5 mg/kg. suspended in 50 µl saline) 10 min following induced hemorrhage. Control groups received equal dose of NO free nanoparticles (Control-nps) and Vehicle solution. Animals treated with NO-nps partially maintained systemic and microvascular function during hypovolemic shock compared to animals treated with Control-nps or the Vehicle (50 µl saline). The continuous NO released by the NO-nps reverted arteriolar vasoconstriction, partially recovered both functional capillary density and microvascular blood flows. Additionally, NO supplementation post hemorrhage prevented cardiac decompensation, and thereby maintained and stabilized the heart rate. Paradoxically, the peripheral vasodilation induced by the NO-nps did not decrease blood pressure, and combined with NO’s effects on vascular resistance, NO-nps promoted intravascular pressure redistribution and blood flow, avoiding tissue ischemia. Therefore, by increasing NO availability with NO-nps during hypovolemic shock, it is possible that cardiac stability and microvascular perfusion can be preserved, ultimately increasing survivability and local tissue viability, and reducing hemorrhagic shock sequelae. The relevance, stability, and efficacy of exogenous NO therapy in the form of NO-nps will potentially facilitate the intended use in battlefield and trauma situations.

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“…Rapid increases in Hct and blood viscosity increase vessel wall shear stress and the production of NO by the endothelium . Because FMD is evaluated by shear stress‐induced vasodilation, it is possible that upregulation of Hb or Hct by ESAs can increase FMD independently of improving endothelial function.…”

Section: Discussionmentioning

confidence: 99%

“…Erythropoiesis‐stimulating agents are able to directly prevent endothelial dysfunction via endothelial nitric oxide synthase (eNOS) activation and their antioxidative effects, and it is thought that ESAs can also indirectly influence FMD via the stimulated hematopoiesis. Increased hematocrit (Hct) can augment fluid viscosity and, consequently, wall shear stress, leading to increasing NO production by the endothelium . Because FMD is evaluated by shear stress‐induced vasodilation, it is possible that upregulation of hemoglobin (Hb) or Hct by ESAs can increase FMD independently of improving endothelial function.…”

Section: Introductionmentioning

confidence: 99%

Epoetin beta pegol ameliorates flow‐mediated dilation with improving endothelial nitric oxide synthase coupling state in nonobese diabetic rats

Serizawa¹,

Tashiro²,

Kawasaki³

et al. 2017

Cardiovascular Therapeutics

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SummaryBackground/AimsPatients with diabetic nephropathy have a high cardiovascular mortality. Epoetin beta pegol (continuous erythropoietin receptor activator, C.E.R.A.) is a drug for the treatment of renal anemia. In this study, we investigated the effect of C.E.R.A. on vascular endothelial function as evaluated by flow‐mediated dilation (FMD) and the relationship between hematopoiesis and FMD in diabetic nephropathy rats.MethodsMale Spontaneously Diabetic Torii rats (SDT, 22 weeks old) were used. C.E.R.A. (0.6, 1.2 μg/kg) was administered subcutaneously once every 2 weeks for 8 weeks. At 1 week after last administration (31 weeks old), we assessed FMD in the femoral arteries of anesthetized rats using a high‐resolution ultrasound system. FMD was also measured 1 week after single C.E.R.A. treatment (5.0 μg/kg) to examine the influence of hematopoiesis.ResultsFlow‐mediated dilation was significantly decreased in SDT rats before the start of C.E.R.A. treatment (22 weeks old). Repeated administration of C.E.R.A. dose‐dependently improved FMD in SDT rats (31 weeks old) without changing blood glucose, nitroglycerin‐induced vasodilation, or kidney function. Long‐term administration of C.E.R.A. improved the state of endothelial nitric oxide synthase uncoupling in the femoral arteries of SDT rats, which showed a positive correlation with FMD. On the other hand, there was no correlation between FMD and Hb or Hct in SDT rats. Furthermore, at 1 week after single administration of C.E.R.A., FMD was not significantly improved although hemoglobin levels were comparable with levels following long‐term C.E.R.A. treatment.ConclusionLong‐term treatment with C.E.R.A. improved FMD in SDT rats even after onset of endothelial dysfunction.

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Microvascular benefits of increasing plasma viscosity and maintaining blood viscosity: Counterintuitive experimental findings

Cited by 54 publications

References 30 publications

Effects of hematocrit and red blood cell–independent viscosity on canine thromboelastographic tracings

Effects of hematocrit and red blood cell–independent viscosity on canine thromboelastographic tracings

Exogenous nitric oxide prevents cardiovascular collapse during hemorrhagic shock

Epoetin beta pegol ameliorates flow‐mediated dilation with improving endothelial nitric oxide synthase coupling state in nonobese diabetic rats

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