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ABSTRACT Hematocrit, hemoglobin concentration, and mean cell hemoglobin concentration (MCHC) were determined in the mangrove killifish, Kryptolebias marmoratus, a tropical fish that can undergo emersion for > 1 month when [...]

Hematocrit (Hct) of awake hamsters and CD-1 mice was acutely increased by isovolemic exchange transfusion of packed red blood cells (RBCs) to assess the relation between Hct and blood pressure. Increasing Hct 7-13% of baseline decreased mean arterial blood pressure (MAP) by 13 mmHg. Increasing Hct above 19% reversed this trend and caused MAP to rise above baseline. This relationship is described by a parabolic function ([R.sup.2] = 0.57 and P < 0.05). Hamsters pretreated with the nitric oxide (NO) synthase (NOS) inhibitor [N.sup.[omega]]-nitro-L-arginine methyl ester (L-NAME) and endothelial NOS-deficient mice showed no change in MAP when Hct was increased by < 19%. Nitrate/nitrite plasma levels of Hct-augmented hamsters increased relative to control and L-NAME treated animals. The blood pressure effect was stable 2 h after exchange transfusion. These findings suggest that increasing Hct increases blood viscosity, shear stress, and NO production, leading to vasodilation and mild hypotension. This was corroborated by measuring Al arteriolar diameters (55.0 [+ or -] 21.5 [micro]m) and blood flow in the hamster window chamber preparation, which showed statistically significant increased vessel diameter (1.04 [+ or -] 0.1 relative to baseline) and microcirculatory blood flow (1.39 [+ or -] 0.68 relative to baseline) after exchange transfusion with packed RBCs. Larger increases of Hct (>19% of baseline) led blood viscosity to increase >50%, overwhelming the NO effect through a significant viscosity-dependent increase in vascular resistance, causing MAP to rise above baseline values. nitric oxide; shear stress; vascular resistance; hypertension

Based on permittivity changes, a new method to measure hematocrit (HCT) in extracorporeal blood systems is presented. Human blood samples were tested at different HCT levels pairing the values of permittivity change, obtained by means of a commercial impedance analyzer, with traditional centrifugation measurements. Data were correlated using both linear and nonlinear regression. When using the lineal model, the comparison yielded a high correlation coefficient (r = 0.99). Theoretical simplifications suggest that the method is independent of changes in the conductivities of the intracellular and extracellular compartments. The influence of osmolarity and conductivity of the extracellular compartment was analyzed. It is shown that HCT can be predicted within an error lower than 5% when those parameters changed as much as 1 mS/cm and 50 mOsm/kg, respectively. Thus, the method appears as valid and viable showing good possibilities in applications such as renal dialysis. Index Terms--Blood, dielectrics, membrane, relaxation.

Saldivar, Enrique, Pedro Cabrales, Amy G. Tsai, and Marcos Intaglietta, Microcirculatory changes during chronic adaptation to hypoxia. Am J Physiol Heart Circ Physiol 285: H2064-H2071, 2003; 10.1152/ajpheart.00349.2003.--Microcirculatory changes in the window chamber preparation in Syrian golden hamsters, secondary to chronic hypoxia adaptation, are presented herein, Adaptation was attained by keeping animals in a 10% oxygen environment for 1 wk and 5% the following week. The following groups were studied: group 1, adapted to chronic hypoxia and kept in a 5% oxygen environment throughout the experiment; group 2, adapted to chronic hypoxia and kept in a 21% oxygen environment 24 h before and during the experiment; and group 3, control. Adaptation caused venule enlargement and hematocrit increase (68.6 [+ or -] 2.44 in group 1, 70 [+ or -] 2.66 in group 2, and 43.27 [+ or -] 2.30 in group 3; P < 0.05). Whereas heart rate decreased in adapted animals, blood pressure remained constant. Group 1 presented alkalosis, hypocapnia, and hypoxemia. The adapted groups had decreased blood flow velocity in arterioles and veins. We found no difference in microvasculature oxygen tension between groups 2 and 3; however, the number of capillaries with flow was markedly reduced in group 1 but significantly increased in group 2. Our findings suggest that, as an adaptation to hypoxia, erythropoiesis may prove beneficial by increasing blood viscosity and shear stress, leading to vasodilatation, in addition to the increase in oxygen-carrying capacity. Calculations show that oxygen extraction in the tissue of the window chamber model was significantly lowered in adapted animals breathing 5% oxygen, but was unchanged from the control when breathing 21% oxygen, even though blood hemoglobin content was increased from 14.5 [+ or -] 0.07 g/dl at control to 21.04 [+ or -] 1.24 g/dl in the adapted animals (P < 0.05). microcirculation; adaptation; hematocrit

Myoglobin and cytochrome c absortion were shown to peak with little apparent contribution of red blood cell hemoglobin using diffuse reflected light from the pig heart in vivo. To compare the effects of myoglobin and cytochromes with those of blood Hb on photon pathlengths and diffuse reflectance of visible wavelengths from the pig heart in vivo, Monte Carlo simulations of photon migration in tissue were performed. The results showed that diffuse reflected light in the 510- to 590-nm region will show spectral features uniquely associated with cytochrome c oxygenation and myoglobin states.

The effects of Doppler angle, hematocrit and fibrinogen concentration on ultrasonic Doppler power were investigated to elucidate its relationship with erythrocyte aggregation of whole blood under steady flow in a conduit. The possibility of plasma proteins other than fibrinogen affecting red cell aggregation was also investigated. Experimental results showed a minimal angular dependence at a mean shear rate of 102 s(super -1) and a weak angular dependence at a mean shear rate of 52 s(super -1) when the Doppler angle was altered from 40 degrees to 70 degrees. These results indicate that there is little or no alignment of the erythrocyte aggregates at high shear rates.

The shift of blood volume from microcirculation to macrocirculation, leading to a decrease in systemic hematocrit, is a counter response to haemorrhage. This shift of blood volume essentially maintains cardiovascular function through control of stroke volume, and compensates for hemorrhage. Blood density measurements and a compartmental assay of the circulation are conducted taking into account the Fahraeus effect, which depicts the low value of microvessel tube hematocrits and low blood density as compared to the systemic value. This yields an estimate of blood volume shift and microvascular-microvascular volume shift.

The effect of anemia on the coronary microcirculation was studied in young male rats. Chronic anemia resulted in increased left ventricular end-diastolic pressure and decreased functional reserve. Cardiac mass in anemic animals increased by 25%. Capillary and arteriolar densities in these hearts remained unchanged, indicating angiogenesis in this experimental situation (estimated aggregate capillary length in the left ventricle of anemic hearts was 3.06 km compared with 2.35 km in control hearts). Capillary hematocrit was decreased in chronic anemia less than systemic hematocrit: from 25 to 18% in anemia versus 45 to 28% in controls. Capillary hematocrit and red blood cell spacing were also studied after acute blood withdrawal. Here, capillary hematocrit was preserved even more: 22 versus 24% in systemic hematocrit. Finally, the same was studied in isolated hearts perfused with solutions of various hematocrits. After perfusion with low-hematocrit solution (14%), the capillary hematocrit (24%) was even higher than the perfusate hematocrit! In conclusion, we found evidence of angiogenesis in cardiomegaly induced by chronic anemia. Microvascular growth was accompanied by advantageous regulation of red blood cell spacing within these vessels. This was even more pronounced during acute hemodilution and in isolated perfused hearts. coronary microcirculation; hemodilution; arterioles; capillaries

Greenberg, Suzanne G., and Kenneth E. Clark. Hemodynamic effects of platelet-activating factor in nonpregnant and pregnant sheep. Am. J. Physiol. 277 (Regulatory Integrative Comp. Physiol. 46): R996-R1001, 1999.--The present study was designed to assess the dose-related effects of platelet-activating factor (PAF) on systemic, renal, and uterine hemodynamics in nonpregnant sheep and to evaluate how pregnancy might alter these responses. Nonpregnant and pregnant (110 [+ or -] 5 days gestation) ewes were instrumented for conscious measurements of maternal mean arterial pressure (MAP), renal blood flow (RBF), uterine blood flow (UBF), hematocrit, and urinary protein concentration. After recovery, dose-response curves to PAF were generated by systemic infusion at 10, 30, and 100 ng [multiplied by] [kg.sup.-1] [multiplied by] [min.sup.-1] (15 min/dose) into the maternal femoral vein. The above parameters were measured, and renal and uterine vascular resistances (RVR and UVR, respectively) were calculated. In pregnant sheep, PAF increased MAP, RVR, UVR, and urinary protein concentration. We also observed increases in hematocrit, indicative of reduced blood volume secondary to increased systemic microvascular protein permeability. These responses were similar in nonpregnant sheep, with the exception of UVR in nonpregnant ewes being decreased (and thus UBF was increased), whereas in pregnant sheep, UVR was increased, which resulted in decreased UBF. This suggests that pregnancy alters the mechanism of action of PAF within the uterine vasculature in a way that can reduce UBF and thereby potentially compromise placental perfusion. kidney; uterine vasculature; proteinuria; hematocrit

Teleost fishes are like most other vertebrates in that total plasma IGF-I and GH correlate positively and negatively with ration. We examined the relations between ration, growth, IGF-I and GH in salmon. Tanks of tagged fish were placed on high, medium, or low ration and sampled biweekly for eight weeks. Some fish received nonlethal blood draws, while others were killed. IGF-I increased in early September in all groups. GH peaked after the switch to low ration. Serial blood draws decreased hematocrit, growth, and IGF-I but did not affect GH. IGF-I changes over time in serially sampled fish suggested an approximately four week cycle in IGF-I. Possible cycles in length growth were also found. No relation was evident between growth and GH. In all fish, total plasma IGF-I was weakly positively correlated with length growth. Stronger correlations were obtained when repeated IGF-I measures in serial fish were averaged. Groups of fish showing IGF-I and length growth cycles had the strongest correlations between length growth and IGF-I.