Increased cardiac output and microvascular blood flow during mild hemoconcentration in hamster window model

Martini, Judith; Tsai, Amy G.; Cabrales, Pedro; Johnson, Paul C.; Intaglietta, Marcos

doi:10.1152/ajpheart.01218.2005

Cited by 28 publications

(31 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this study we characterize the changes of MAP following small changes in Hct due to isovolemic hemodilution. We compare our findings with those from previous studies with small increases in Hct (13,14) with the objective of presenting the continuum of acute cardiovascular responses due to small changes in blood viscosity within the range of variability of Hct present in the normal population. We monitored MAP and Hct after small acute isovolumic changes in Hct 2 h after the induced change in awake animals, which was a period in which the animals were hemodynamically stable.…”

mentioning

confidence: 72%

“…By contrast, the normal population presents a significantly smaller variability of Hct and corresponding variability of blood viscosity (11) that does not appear to influence mean arterial blood pressure (MAP) (19). However, small acute elevations of Hct (ϳ10%) in awake hamsters and mice performed by Martini et al (13,14) cause a significant lowering of MAP and elevation in cardiac output (CO) but not in endothelial nitric oxide (NO) synthase knockout mice, which do not produce NO via endothelial NO synthase. These studies and those of Salazar Vázquez et al (20) with non-oxygen-carrying, non-NO-scavenging red blood cells (RBCs) suggested that the effect due to small changes in Hct is related to the management of NO bioavailability.…”

mentioning

confidence: 99%

See 1 more Smart Citation

The variability of blood pressure due to small changes of hematocrit

Vázquez

Martini

Tsai

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

View full text Add to dashboard Cite

Vázquez BY, Martini J, Tsai AG, Johnson PC, Cabrales P, Intaglietta M. The variability of blood pressure due to small changes of hematocrit. Am J Physiol Heart Circ Physiol 299: H863-H867, 2010. First published July 2, 2010; doi:10.1152/ajpheart.00496.2010.-The hematocrit (Hct) of awake hamsters was lowered to 90% of baseline by isovolemic hemodilution using hamster plasma to determine the acute effect of small changes in Hct and blood viscosity on systemic hemodynamics. Mean arterial blood pressure increased, reaching a maximum of about 10% above baseline (8.6 Ϯ 5.5 mmHg) when Hct decreased 8.4 Ϯ 1.9% (P Ͻ 0.005). Cardiac output increased continuously with hemodilution. These conditions were reached at ϳ60 min after exchange transfusion and remained stationary for 1 h. Peripheral vascular resistance was approximately constant up to a decrease of Hct of about 10% and then fell continuously with lowering Hct. Vascular hindrance or vascular resistance independent of blood viscosity increased by about 20% and remained at this level up to an Hct decrease of 20%, indicating that the vasculature constricted with the lowered Hct. The results for the initial 2-h period are opposite but continuous with previous findings with small increases in Hct. In conclusion, limited acute anemic conditions increase mean arterial blood pressure during the initial period of 2 h, an effect that is quantitatively similar but opposite to the acute increase of Hct during the same period. hemodilution; acute anemia; blood viscosity; nitric oxide HEMATOCRIT (Hct) in the healthy population varies primarily as function of age and sex. Environmental factors, genetics, nutrition, level of hydration, time in the daily cycle, and seasonal variations (9) cause an additional variability, yielding a dispersion of values that, although not well documented, may be of the order of Ϯ10% of the average for the population grouped according to age and sex.Hct determines blood viscosity, regulating peripheral vascular resistance (PVR) and therefore, in principle, blood pressure. Increasing the viscosity of a fluid flowing in rigid tubes increases flow resistance and tube wall shear stress. However, this does not necessarily occur in blood vessels where the vessel wall shear stress due to flowing blood modulates the production of vasodilators by mechanotransduction (15,22). Thus, in the circulation, increasing blood viscosity can produce two opposing effects on PVR: a direct effect related to hemodynamic hindrance and an opposite effect due to changes in vessel diameter.Changes in Hct cause hemoconcentration or hemodilution, factors that affect blood viscosity and therefore vascular resistance (VR). Our understanding of these phenomena is based on the work of Richardson and Guyton (18) and Messmer et al. (16), showing how the heart and the circulation respond to changes of Hct and therefore blood viscosity. A common denominator of these studies (12) is that the induced changes of Hct were comparatively large, similar to the Hct perturbations found in hemorrh...

show abstract

mentioning

confidence: 72%

mentioning

confidence: 99%

The variability of blood pressure due to small changes of hematocrit

Vázquez

Martini

Tsai

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…Measurements were performed at baseline and after an increase in Hct of 20% using functional RBCs. This value was chosen because this increase in Hct corresponded to levels at which MAP, CI, and VR return to baseline values (4,5). Therefore, this could be defined as a situation in which the presumed NO bioavailability increases due to augmented shear stress and is balanced by NO scavenging and the increased blood viscosity.…”

Section: Discussionmentioning

confidence: 99%

“…However, a recent study by Martini and coworkers (4) showed that mean arterial pressure (MAP) increases only when Hct is increased 20% above baseline using functional RBCs, and that MAP decreased when the change in Hct were less than 20%. In this range, cardiac output (CO) also increased and peripheral vascular resistance (VR) decreased (4,5).…”

mentioning

confidence: 99%

Lowering of Blood Pressure by Increasing Hematocrit with Non–Nitric Oxide–Scavenging Red Blood Cells

Vázquez¹,

Cabrales²,

Tsai³

et al. 2008

Am J Respir Cell Mol Biol

Self Cite

View full text Add to dashboard Cite

Isovolemic exchange transfusion of 40% of the blood volume in awake hamsters was used to replace native red blood cells (RBCs) with RBCs whose hemoglobin (Hb) was oxidized to methemoglobin (MetHb), MetRBCs. The exchange maintained constant blood volume and produced different final hematocrits (Hcts), varying from 48 to 62% Hct. Mean arterial pressure (MAP) did not change after exchange transfusion, in which 40% of the native RBCs were replaced with MetRBCs, without increasing Hct. Increasing Hct with MetRBCs lowered MAP by 12 mm Hg when Hct was increased 12% above baseline. Further increases of Hct with MetRBCs progressively returned MAP to baseline, which occurred at 62% Hct, a 30% increase in Hct from baseline. These observations show a parabolic ''U'' shaped distribution of MAP against the change in Hct. Cardiac index, cardiac output divided by body weight, increased between 2 and 17% above baseline for the range of Hcts tested. Peripheral vascular resistance (VR) was decreased 18% from baseline when Hct was increased 12% from baseline. VR and MAP were above baseline for increases in Hct higher than 30%. However, vascular hindrance, VR normalized by blood viscosity (which reflects the contribution of vascular geometry), was lower than baseline for all the increases in Hct tested with MetRBC, indicating prevalence of vasodilation. These suggest that acute increases in Hct with MetRBCs increase endothelium shear stress and stimulate the production of vasoactive factors (e.g., nitric oxide [NO]). When MetRBCs were compared with functional RBCs, vasodilation was augmented for MetRBCs probably due to the lower NO scavenging of MetHb. Consequently, MetRBCs increased the viscosity related hypotension range compared with functional RBCs as NO shear stress vasodilation mediated responses are greater.Keywords: blood pressure; shear stress; NO bioavailability; hematocrit; plasma layer Increased hematocrit (Hct) above baseline is usually associated with elevation of systemic blood pressure due to the increase in blood viscosity. These effects were found in studies in which Hct was increased 40% or more above baseline (1-3). However, a recent study by Martini and coworkers (4) showed that mean arterial pressure (MAP) increases only when Hct is increased 20% above baseline using functional RBCs, and that MAP decreased when the change in Hct were less than 20%. In this range, cardiac output (CO) also increased and peripheral vascular resistance (VR) decreased (4, 5).According to Martini and colleagues (4), the cause of this paradoxical effect is that acute augmentation in Hct directly increases shear stress on the endothelium. This phenomenon may be due, in part, to the increase in viscosity and the decrease in cell-free layer (plasma layer) width, affecting blood properties and the endothelium interface, where shear signals are produced.Increased endothelial shear stress promotes production of endothelium vasoactive and nonvasoactive factors (6). Knockout mice deficient in endothelial nitric oxide (NO) synthases, and ham...

show abstract

“…Martine et al revealed that in a hamster model mild hemoconcentration and increased viscosity of blood augmented cardiac output and microvascular blood flow in the myocardium, and improved oxygen delivery. 21 Other potential mechanisms include optimization of preload and improved oxygen delivery to peripheral tissues, as shown by increased hematocrit, as well as reduction of systemic edema, which might favorably alter systemic vascular resistance and afterload.…”

Section: Mechanism Of Muf-induced Improvement In Ventricular Functionmentioning

confidence: 99%

Diagnosis-Based Differences in Response of Global Ventricular Performance to Modified Ultrafiltration in Children

Honjo

Osaki

Kotani

et al. 2010

Circ J

View full text Add to dashboard Cite

Background: To determine diagnosis-based differences in the response of global ventricular performance to modified ultrafiltration (MUF) using transesophageal echocardiography during congenital heart surgery. Methods and Results:The study included 38 children with atrial septal defect (n=10), ventricular septal defect (VSD) (n=8), tetralogy of Fallot (TOF) (n=9), or a single ventricle (n=11). Arteriovenous MUF was performed for 10-15 min after cardiopulmonary bypass (CPB). The myocardial performance index (MPI) of the systemic ventricles and the % change in MPI before and after MUF were assessed. Impairment of MPI was noted at termination of CPB compared with baseline values in the VSD and TOF groups (P<0.05). MUF resulted in an improvement in MPI in all groups (P<0.01). There was a weak correlation between aortic cross-clamping or CPB time, and the degree of improvement in MPI (r=−0.385, P=0.019; r=−0.348, P=0.037, respectively). MUF improved fractional shortening in all groups (P<0.05) and reversed abnormal relaxation in the VSD and TOF groups. Conclusions:Modified ultrafiltration ameliorated MPI in all groups, indicating improved systemic ventricular function with MUF. The MPI recovery rate differed among the groups. MUF may be particularly useful for restoring the global ventricular performance of patients undergoing longer CPB and may have minimal advantages for simple open-heart surgery. (Circ J 2010; 74: 86 - 92)

show abstract

Increased cardiac output and microvascular blood flow during mild hemoconcentration in hamster window model

Cited by 28 publications

References 46 publications

The variability of blood pressure due to small changes of hematocrit

The variability of blood pressure due to small changes of hematocrit

Lowering of Blood Pressure by Increasing Hematocrit with Non–Nitric Oxide–Scavenging Red Blood Cells

Diagnosis-Based Differences in Response of Global Ventricular Performance to Modified Ultrafiltration in Children

Contact Info

Product

Resources

About