Hemodilution with Oxyhemoglobin Mechanism of Oxygen Delivery and Its Superaugmentation with a Nitric Oxide Donor (Sodium Nitroprusside)

Rooney, Michael W.; Hirsch, Leroy J.; Mathru, M.

doi:10.1097/00000542-199307000-00011

Cited by 34 publications

(10 citation statements)

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“…In addition, new evidences against a major role for the decreased blood viscosity on the vasodilatory state associated to anemia, has arised from recent studies demonstrating that haemodilution with oxyhemoglobin does not produce the hyperdynamic circulation despite a marked reduction in blood viscosity (Anand and Chandrashekar 1993). This finding gives support to the hypothesis that low levels of hemoglobin in acute or chronic anemia results in reduced inhibition of basal NO activity leading to generalized vasodilation (Rooney et al 1993), which would be in keeping with the results of the current study. In these circumstances, the increased NO may act as a direct vasodilator activating soluble guanylate cyclase, or indirecty, by inhibiting endothelial production of the potent vasoconstrictors endothelin-1 and PGDF, as recently proposed (Kourembanas et al 1993).…”

Section: Discussionsupporting

confidence: 92%

Acute normovolaemic anaemia prevents ethanol-induced gastric damage in rats through a blood flow related mechanism

Casadevall

Piqué

Cirera

et al. 1994

Naunyn-Schmiedeberg's Arch Pharmacol

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The aim of the study was to assess whether changes in gastric mucosal blood flow induced by acute normovolaemic anaemia influence the susceptibility of the gastric mucosa to ethanol-induced damage, and the relationship of these changes with nitric oxide biosynthesis. Acute normovolaemic anaemia, promoted by exchanging 3 ml of blood by a plasma expander, induced a significant increase in gastric mucosal blood flow measured by hydrogen gas clearance, without changes in arterial blood pressure. After intragastric 60°7o ethanol administration, gastric blood flow was still significantly higher in anaemic than in control rats, and this was associated with a lower macroscopic and microscopic gastric damage. Following ethanol administration, anaemic rats pretreated with an inhibitor of nitric oxide biosynthesis (L-NMMA, 50 mg/kg, i.v.) had a lower gastric blood flow and a higher macroscopic gastric damage than anaemic rats without pretreatment. Anaemic rats pretreated with vasopressin also had after ethanol administration a lower gastric blood flow and a higher macroscopic gastric damage. It is concluded that acute normovolaemic anaemia protects the gastric mucosa against damage induced by intragastric ethanol. The inhibition of nitric oxide biosynthesis reverts in part this protective effect, and this seems to be related with the capability of nitric oxide to increase gastric mucosal blood flow, since vasoconstriction by a nitric oxide-independent mechanism causes a similar effect.

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Section: Discussionsupporting

confidence: 92%

Acute normovolaemic anaemia prevents ethanol-induced gastric damage in rats through a blood flow related mechanism

Casadevall

Piqué

Cirera

et al. 1994

Naunyn-Schmiedeberg's Arch Pharmacol

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“…On the other hand, no improvement in tissue O 2 delivery could be demonstrated in a swine resuscitation model with α,α-DBBF-cross-linked Hb ,,,,,, …”

Section: Traumamentioning

confidence: 95%

“…4-fold higher tissue O 2 extraction ratio that is seen with PFCs under normal conditions. In addition, when normovolemic hemodilution is performed, there is normally a substantial increase in cardiac output (the volume of blood ejected from the heart in a given period of time) as a result of increased fluidity of the diluted blood. ,, This increase in cardiac output is preserved when PFC emulsions are administered, which further enhances their O 2 delivery capacity, ,, while Hb products classically display an unchanged or reduced cardiac output that can negate or even outweigh the benefit of increased fluidity. ,− Further unfounded conclusions have sometimes been drawn on the basis of inadequate protocol design and even on the implicit expectation that the O 2 carrier should still have been active when it was no longer present in the circulation (see, for example, ref and the discussion that followed. , ).…”

Section: Oxygen Delivery To Tissuesmentioning

confidence: 99%

Oxygen Carriers (“Blood Substitutes”)Raison d'Etre, Chemistry, and Some PhysiologyBlut ist ein ganz besondrer Saft

2001

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Pharmaceutical Corporation in San Diego; however, the opinion expressed here are solely his and not necessarily those of the Corporation. Jean G. Riess received his chemical engineer and doctorat-e `s-sciences degrees (the latter with Professor Guy Ourisson in 1963) from the University of Strasbourg. He then spent two years with John Van Wazer at Monsanto in Saint-Louis, MO, learning some phosphorus and transitionmetal chemistry. In 1968 he became Professor at the University of Nice, France, where he founded, directed, and eventually became honorary director of the Unite ´de Chimie Mole ´culaire (associated with the Centre National de la Recherche Scientifique). His research successively involved phosphorus chemistry, transition-metal chemistry, organometallics, and eventually perfluorochemicals. His present interests are in fluorocarbons, fluorinated amphiphiles, and their colloid chemistry, including fluorocarbon emulsions for in vivo O 2 delivery, fluorinated self-assemblies, and drug delivery systems. Professor Riess has published about 360 papers and holds ca. 25 patents. He has served on numerous councils and committees and has chaired or co-chaired international conferences on phosphorus chemistry and blood substitutes. He has won awards from the French Academy of Sciences, French Chemical Society, Alexander von Humboldt Stifftung, City of Nice and Controlled Release Society, as well as Alliance's first Distinguished Contribution Award. He holds an honorary Research Associate position at the University of California at San Diego and sits on the Board of Directors of Alliance Pharmaceutical Corp.

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“…3,4 This side effect is now recognized to be caused by the fact that small Hb molecules extravasuate through the vascular endothelium and deplete the nitric oxide (NO), namely, the endothelial-derived relaxing factor, thus inducing the vasoconstriction. [5][6][7][8][9] It has been also shown that these pressor effects elicited by Hb are accompanied by a decrease in the heart rate (HR). 9,10 Although the precise mechanism of this bradycardia is still a source of controversy, the unfavorable hemodynamic alterations may limit the use of the Hb solutions as blood replacement compositions.…”

Section: Introductionmentioning

confidence: 99%

Human serum albumin incorporating synthetic heme: Red blood cell substitute without hypertension by nitric oxide scavenging

Tsuchida

Komatsu

Matsukawa

et al. 2002

J Biomedical Materials Res

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The administration of extracellular, hemoglobin-based oxygen carriers often elicits an acute increase in blood pressure by vasoconstriction. This side effect is now recognized to be due to the depletion of nitric oxide (endothelial-derived relaxing factor) by the extravasuated hemoglobins. We have recently found that the administration of a recombinant human serum albumin (rHSA)-based oxygen carrier involving synthetic tetraphenyporphinatoiron(II) derivative (FeP) (rHSA-FeP) does not induce such hypertensive action, because of its low permeability through the vascular endothelium. The heart rate responses after the rHSA-FeP injection were also negligibly small. Visualization of the intestinal microcirculatory changes clearly revealed the widths of the venule and arteriole to be fairly constant. The entirely synthetic rHSA-FeP becomes a promising material as a new type of red blood cell substitute.

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Hemodilution with Oxyhemoglobin Mechanism of Oxygen Delivery and Its Superaugmentation with a Nitric Oxide Donor (Sodium Nitroprusside)

Cited by 34 publications

References 0 publications

Acute normovolaemic anaemia prevents ethanol-induced gastric damage in rats through a blood flow related mechanism

Acute normovolaemic anaemia prevents ethanol-induced gastric damage in rats through a blood flow related mechanism

Oxygen Carriers (“Blood Substitutes”)Raison d'Etre, Chemistry, and Some PhysiologyBlut ist ein ganz besondrer Saft

Human serum albumin incorporating synthetic heme: Red blood cell substitute without hypertension by nitric oxide scavenging

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