Norepinephrine increases tolerance to acute anemia*

Meier, Jens; Pape, Andreas; Loniewska, D.; Lauscher, Patrick; Kertscho, H.; Zwißler, Bernhard; Häbler, O.

doi:10.1097/01.ccm.0000265740.62130.1c

Cited by 32 publications

(16 citation statements)

References 29 publications

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“…Consistently, the value of Hb crit in the Roc group (2.4 ± 0.5 g/dl) is comparable to that described in paralyzed animals [13,15,16,17,18,19], while the values of Hb crit obtained in nonparalyzed animals are similar to Hb crit observed in the Sal group [4,12]. …”

Section: Discussionsupporting

confidence: 73%

“…The anesthesia regimen applied in the present study (propofol, midazolam and fentanyl) has already been used in several of our previous investigations [13,14,17]. To the author’s experience, this anesthesia regimen has proven appropriate for pigs, as it provided sufficient anesthetic depth without severely compromising cardiovascular function.…”

Section: Discussionmentioning

confidence: 99%

“…In our previous experimental studies, critical normovolemic anemia was associated with 100% mortality if no further treatment (e.g. elevation of FiO 2 , transfusion of red blood cells, administration of catecholamines, infusion of artificial O 2 carriers) was instantaneously initiated at Hb crit [12,13,14,15]. …”

Section: Discussionmentioning

confidence: 99%

“…In several experimental studies, a decrease in Hb crit demonstrated that anemia tolerance is increased by (1) hypothermia (moderate reduction of body core temperature reduces total body O 2 demand [16]), (2) hyperoxic ventilation (bioavailability of physically dissolved O 2 is excellent in profound anemia [12,17,18]), (3) infusion of norepinephrine (stabilization of coronary perfusion pressure during hemodilution [13]), and (4) artificial O 2 carriers (maintenance of CaO 2 despite reduced hematocrit [19,20]). In contrast, anemia tolerance is decreased by (1) hypovolemia (reduction of microcirculatory O 2 supply), (2) profound anesthesia (pharmacologic reduction of the cardiac output response to hemodilution [21,22]) and (3) by coronary artery disease (reduced coronary flow reserve [23]).…”

Section: Discussionmentioning

confidence: 99%

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Neuromuscular Blockade with Rocuronium Bromide Increases the Tolerance of Acute Normovolemic Anemia in Anesthetized Pigs

et al. 2011

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Background: The patient’s individual anemia tolerance is pivotal when blood transfusions become necessary, but are not feasible for some reason. To date, the effects of neuromuscular blockade (NMB) on anemia tolerance have not been investigated. Methods: 14 anesthetized and mechanically ventilated pigs were randomly assigned to the Roc group (3.78 mg/kg rocuronium bromide followed by continuous infusion of 1 mg/kg/min, n = 7) or to the Sal group (administration of the corresponding volume of normal saline, n = 7). Subsequently, acute normovolemic anemia was induced by simultaneous exchange of whole blood for a 6% hydroxyethyl starch solution (130/0.4) until a sudden decrease of total body O₂ consumption (VO₂) indicated a critical limitation of O₂ transport capacity. The Hb concentration quantified at this time point (Hb_crit) was the primary endpoint of the protocol. Secondary endpoints were parameters of hemodynamics, O₂ transport and tissue oxygenation. Results: Hb_crit was significantly lower in the Roc group (2.4 ± 0.5 vs. 3.2 ± 0.7 g/dl) reflecting increased anemia tolerance. NMB with rocuronium bromide reduced skeletal muscular VO₂ and total body O₂ extraction rate. As the cardiac index increased simultaneously, total body VO₂ only decreased marginally in the Roc group (change of VO₂ relative to baseline –1.7 ± 0.8 vs. 3.2 ± 1.9% in the Sal group, p < 0.05). Conclusion: Deep NMB with rocuronium bromide increases the tolerance of acute normovolemic anemia. The underlying mechanism most likely involves a reduction of skeletal muscular VO₂. During acellular treatment of an acute blood loss, NMB might play an adjuvant role in situations where profound stages of normovolemic anemia have to be tolerated (e.g. bridging an unexpected blood loss until blood products become available for transfusion).

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Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Neuromuscular Blockade with Rocuronium Bromide Increases the Tolerance of Acute Normovolemic Anemia in Anesthetized Pigs

et al. 2011

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“…In particular, a reduction of Hb crit could be achieved by hypothermia (moderate reduction of body core temperature reduces total body O 2 demand [18]), infusion of norepinephrine (stabilization of CPP during hemodilution [19]), infusion of artificial O 2 carriers (maintenance of CaO 2 despite reduced hematocrit [20,21]) and continuous NMB (lowering skeletal muscular O 2 demand [22]). …”

Section: Discussionmentioning

confidence: 99%

The Limit of Anemia Tolerance during Hyperoxic Ventilation with Pure Oxygen in Anesthetized Domestic Pigs

et al. 2013

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Background: During acellular replacement of an acute blood loss, hyperoxic ventilation (HV) increases the amount of O₂ physically dissolved in the plasma and thereby improves O₂ supply to the tissues. While this effect could be demonstrated for HV with inspiratory O₂ fraction (FiO₂) 0.6, it was unclear whether HV with pure oxygen (FiO₂ 1.0) would have an additional effect on the physiological limit of acute normovolemic anemia. Methods: Seven anesthetized domestic pigs were ventilated with FiO₂ 1.0 and subjected to an isovolemic hemodilution protocol. Blood was drawn and replaced by a 6% hydroxyethyl starch (HES) solution (130/0.4) until a sudden decrease of total body O₂ consumption (VO₂) indicated the onset of O₂ supply dependency (primary endpoint). The corresponding hemoglobin (Hb) concentration was defined as ‘critical Hb' (Hb_crit). Secondary endpoints were parameters of myocardial function, central hemodynamics, O₂ transport and tissue oxygenation. Results: HV with FiO₂ 1.0 enabled a large blood-for-HES exchange (156 ± 28% of the circulating blood volume) until Hb_crit was met at 1.3 ± 0.3 g/dl. After termination of the hemodilution protocol, the contribution of O₂ physically dissolved in the plasma to O₂ delivery and VO₂ had significantly increased from 11.7 ± 2 to 44.2 ± 9.7% and from 29.1 ± 4.2 to 66.2 ± 11.7%, respectively. However, at Hb_crit, cardiovascular performance was found to have severely deteriorated. Conclusion: HV with FiO₂ 1.0 maintains O₂ supply to tissues during extensive blood-for-HES exchange. In acute situations, where profound anemia must be tolerated (e.g. bridging an acute blood loss until red blood cells become available for transfusion), O₂ physically dissolved in the plasma becomes an essential source of oxygen. However, compromised cardiovascular performance might require additional treatment.