Sodium nitroprusside ameliorates systemic but not pulmonary HBOC-201-induced vasoconstriction: An exploratory study in a swine controlled haemorrhage model

Arnaud, Françoise; Scultetus, Anke; Haque, Ashraful; Saha, Banani; Kim, Bobby; Auker, Charles R.; Moon-Massat, Paula F.; McCarron, Richard M.; Freilich, Daniel

doi:10.1016/j.resuscitation.2012.01.018

Cited by 8 publications

(6 citation statements)

References 24 publications

(45 reference statements)

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“…The higher calcium concentration in serum may help maintain an optimal binding between the hemoglobin molecule and its membrane receptors. Sugar metabolism is not affected in the experiments described here; glycaemia remained constant, as also noted in other experiments, performed under different conditions[ 27 , 28 ].…”

Section: Discussionsupporting

confidence: 86%

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Comparative In Vivo Effects of Hemoglobin-Based Oxygen Carriers (HBOC) with Varying Prooxidant and Physiological Reactivity

et al. 2016

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Section: Discussionsupporting

confidence: 86%

“…However, the variations compared to the healthy control animals do not suggest pathophysiological relevance. Comparatively, a study on controlled hemorrhagic model on pigs also revealed slightly abnormal values for clotting parameters (fibrinogen, PT, aPTT)[ 27 , 28 ].…”

Section: Discussionmentioning

confidence: 99%

Comparative In Vivo Effects of Hemoglobin-Based Oxygen Carriers (HBOC) with Varying Prooxidant and Physiological Reactivity

et al. 2016

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“…As there was no difference between the two fluid types, these results simply suggest that an acute cumulative 8% (Dose 3) to 30% (Dose 4) increase in blood volume in a healthy animal will produce a corresponding increase in MAP when either colloidal fluid, with their long intravascular retention times, is infused. This result is contradictory to some earlier studies, which showed that the MAP after HBOC-201 was higher than the MAP of the volume control (Philbin et al, 2007; Katz et al, 2010; Arnaud et al, 2012). An explanation could be that these earlier studies did not use an iso-oncotic colloid or because these studies also included the influences of hypovolemia, anemia or tissue trauma.…”

Section: Discussioncontrasting

confidence: 99%

Effects of a hemoglobin-based oxygen carrier (HBOC-201) and derivatives with altered oxygen affinity and viscosity on systemic and microcirculatory variables in a top-load rat model

Song

Nugent

Moon-Massat

et al. 2014

Microvascular Research

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The effects of a polymerized bovine hemoglobin-based oxygen carrier (HBOC) and two derivatives on arteriolar vasoactivity and tissue oxygen tension were explored by administering HBOC in a dose-response fashion to normovolemic rats. The effect of oxygen affinity (P50) and viscosity were also explored, where the P50 and viscosity of the parent compound (HBOC-201) and its modifications (MP50 and LP50A) were as follows: 40 mmHg and 3.0 cP (HBOC-20l); 18 mmHg and 4.4 cP (MP50); and 17 mmHg and 12.1 cP (LP50A). Anesthetized male Sprague-Dawley rats (N = 32) were randomized to receive one of the HBOC solutions, and were administered four infusions that increased in concentration for each dose (2, 22, 230 and 780 mg/kg, IV). Data were compared to rats receiving an equivalent volume for each of the four infusions (0.4, 0.4, 3.8, 13.1 ml/kg, IV) of iso-oncotic 5.9% human serum albumin (HSA). Increasing doses of either HBOC solutions or HSA were associated with increasing MAP. Doses 3 and 4 of HBOC-201, MP50 and HSA produced significant increases in MAP, whereas similar increases began at a lower dose (Dose 2) with LP50A. There were no significant changes in arteriolar diameters at any dose for any group. Interstitial partial pressure of oxygen (ISF PO2) remained unchanged for HBOC-201, MP50 and HSA, but LP50A caused a significant decrease in ISF PO2 compared to baseline after Doses 3 and 4. In conclusion, there was no evidence that HBOC-201 would perform better with increased oxygen affinity (40 to 18 mmHg) or viscosity (3.0 to 4.4 cP).

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“…Notably, the administration of 0.325 g/kg OC99 did not produce clinically relevant increases in PAP (i.e., >25 mm Hg) while 0.65 g/kg OC99 resulted in a pulmonary vasopressor effect by the end of the dosing period (26% increase from prehemorrhage values). Experimental studies in hemorrhaged swine and newborn lambs suggest that the pulmonary vasopressor effect is caused by cell free Hb p and NO dysregulation and that breathing low levels (30–80 ppm) of NO or administration of various NO donors (nitroglycerin, sodium nitroprusside, and sodium nitrite) is palliative [33, 34]. Dissimilarities between systemic and pulmonary vasoconstrictive responses to cell-free Hb are attributed to phenotypic differences and a greater dependency of the muscularized pulmonary circulation to the vasoregulatory effects of NO [35].…”

Section: Discussionmentioning

confidence: 99%

Dose-Dependent Hemodynamic, Biochemical, and Tissue Oxygen Effects of OC99 following Severe Oxygen Debt Produced by Hemorrhagic Shock in Dogs

Muir

Río

Ueyama

et al. 2014

Critical Care Research and Practice

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We determined the dose-dependent effects of OC99, a novel, stabilized hemoglobin-based oxygen-carrier, on hemodynamics, systemic and pulmonary artery pressures, surrogates of tissue oxygen debt (arterial lactate 7.2 ± 0.1 mM/L and arterial base excess −17.9 ± 0.5 mM/L), and tissue oxygen tension (tPO2) in a dog model of controlled severe oxygen-debt from hemorrhagic shock. The dose/rate for OC99 was established from a pilot study conducted in six bled dogs. Subsequently twenty-four dogs were randomly assigned to one of four groups (n = 6 per group) and administered: 0.0, 0.065, 0.325, or 0.65 g/kg of OC99 combined with 10 mL/kg lactated Ringers solution administered in conjunction with 20 mL/kg Hextend IV over 60 minutes. The administration of 0.325 g/kg and 0.65 g/kg OC99 produced plasma hemoglobin concentrations of 0.63 ± 0.01 and 1.11 ± 0.02 g/dL, respectively, improved systemic hemodynamics, enhanced tPO2, and restored lactate and base excess values compared to 0.0 and 0.065 g/kg OC99. The administration of 0.65 g/kg OC99 significantly elevated pulmonary artery pressure. Plasma hemoglobin concentrations of OC99 ranging from 0.3 to 1.1 g/dL, in conjunction with colloid based fluid resuscitation, normalized clinical surrogates of tissue oxygen debt, improved tPO2, and avoided clinically relevant increases in pulmonary artery pressure.

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Sodium nitroprusside ameliorates systemic but not pulmonary HBOC-201-induced vasoconstriction: An exploratory study in a swine controlled haemorrhage model

Cited by 8 publications

References 24 publications

Comparative In Vivo Effects of Hemoglobin-Based Oxygen Carriers (HBOC) with Varying Prooxidant and Physiological Reactivity

Comparative In Vivo Effects of Hemoglobin-Based Oxygen Carriers (HBOC) with Varying Prooxidant and Physiological Reactivity

Effects of a hemoglobin-based oxygen carrier (HBOC-201) and derivatives with altered oxygen affinity and viscosity on systemic and microcirculatory variables in a top-load rat model

Dose-Dependent Hemodynamic, Biochemical, and Tissue Oxygen Effects of OC99 following Severe Oxygen Debt Produced by Hemorrhagic Shock in Dogs

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