Microvascular hematocrit and red cell flow in resting and contracting striated muscle

1979 ◽  
Vol 237 (4) ◽  
pp. H481-H490 ◽  
Author(s):  
B. Klitzman ◽  
B. R. Duling

Microvascular hematocrit and its possible relation to oxygen supply were systematically examined. We studied the red cell volume fraction (hematocrit) in arterial blood and in capillaries under a variety of circumstances. Control capillary hematocrit averaged 10.4 +/- 2.0% (SE) and arteriolar (14.2 micrometer ID) hematocrit averaged 13.9 +/- 1.2% in cremaster muscles of pentobarbital-anesthetized hamsters. Carotid artery hematocrit was 53.2 +/- 0.6%. The low microvessel hematocrit could not be entirely explained by a high red cell flux through arteriovenous channels other than capillaries (shunting). Hematocrit was not only low at rest, but varied with physiological stimuli. A 1-Hz muscle contraction increased capillary hematocrit to 18.5 +/- 2.4%, and maximal vasodilation induced a rise to 39.3 +/- 9.5%. The quantitative relations between capillary red cell flux, arterial hematocrit, and total blood flow could be explained by a two-element model of microvascular blood flow that incorporated a relatively slow-moving plasma layer (1.2 micrometer). Such a model would generate a low microvessel hematocrit and might reduce the diffusion capacity of individual capillaries, but would not reduce time-averaged red cell flux or alter steady-state vascular oxygen supply.

Author(s):  
Weiyu Li ◽  
Amy G. Tsai ◽  
Marcos Intaglietta ◽  
Daniel M. Tartakovsky

­­ ­Although some of the cardiovascular responses to changes in hematocrit (Hct) are not fully quantified experimentally, available information is sufficient to build a mathematical model of the consequences of treating anemia by introducing RBCs into the circulation via blood transfusion. We present such a model, which describes how the treatment of normovolemic anemia with blood transfusion impacts oxygen (O2) delivery (DO2, the product of blood O2 content and arterial blood flow) by the microcirculation. Our analysis accounts for the differential response of the endothelium to the wall shear stress (WSS) stimulus, changes in nitric oxide (NO) production due to modification of blood viscosity caused by alterations of both hematocrit (Hct) and cell free layer thickness, as well as for their combined effects on microvascular blood flow and DO2. Our model shows that transfusions of 1- and 2-unit of blood have a minimal effect on DO2 if the microcirculation is unresponsive to the WSS stimulus for NO production that causes vasodilatation increasing blood flow and DO2. Conversely, in a fully WSS responsive organism, blood transfusion significantly enhances blood flow and DO2, because increased viscosity stimulates endothelial NO production causing vasodilatation. This finding suggests that evaluation of a patients' pre-transfusion endothelial WSS responsiveness should be beneficial in determining the optimal transfusion requirements for treating anemic patients.


2003 ◽  
Vol 94 (6) ◽  
pp. 2323-2329 ◽  
Author(s):  
Sidharth Shah ◽  
Julie Allen ◽  
John G. Wood ◽  
Norberto C. Gonzalez

Systemic hypoxia (SHx) produces microvascular inflammation in mesenteric, cremasteric, and pial microcirculations. In anesthetized rats, SHx lowers arterial blood pressure (MABP), which may alter microvascular blood flow and microvascular Po2(PmO2) and influence SHx-induced leukocyte-endothelial adherence (LEA). These experiments attempted to determine the individual contributions of the decreases in PmO2, venular blood flow and shear rate, and MABP to the hypoxia-induced increase in LEA. Cremaster microcirculation of anesthetized rats was visualized by intravital microscopy. PmO2was measured by a phosphorescence-quenching method. SHx [inspired Po2of 70 Torr for 10 min, MABP of 65 ± 3 mmHg, arterial Po2(PaO2) of 33 ± 1 Torr] and cremaster ischemia (MABP of 111 ± 7 mmHg, PaO2of 86 ± 3 Torr) produced similar PmO2: 7 ± 2 and 6 ± 2 Torr, respectively. However, LEA increased only in SHx (1.9 ± 0.9 vs. 11.2 ± 1.1 leukocytes/100 μm, control vs. SHx, P < 0.05). Phentolamine-induced hypotension (MABP of 55 ± 4 mmHg) in normoxia lowered PmO2to 26 ± 6 Torr but did not increase LEA. Cremaster equilibration with 95% N2-5% CO2during air breathing (PaO2of 80 ± 1 Torr) lowered PmO2to 6 ± 1 Torr but did not increase LEA. On the other hand, when cremaster PmO2was maintained at 60–70 Torr during SHx (PaO2of 35 ± 1 Torr), LEA increased from 2.1 ± 1.1 to 11.1 ± 1.5 leukocytes/100 μm ( P < 0.05). The results show a dissociation between PmO2and LEA and support the idea that SHx results in the release of a mediator responsible for the inflammatory response.


1996 ◽  
Vol 271 (1) ◽  
pp. H203-H211 ◽  
Author(s):  
H. Bitterman ◽  
V. Brod ◽  
G. Weisz ◽  
D. Kushnir ◽  
N. Bitterman

This study investigated mechanisms of the hemodynamic effects of oxygen in hemorrhagic shock induced by bleeding 30% of the total blood volume in anesthetized rats. An ultrasonic flowmeter was used to monitor regional blood flow. Changes in tissue perfusion were assessed by the laser-Doppler technique. The inhalation of 100% oxygen induced a significant increase in mean arterial blood pressure (MABP) and vascular resistance in the hindquarters, with a concomitant decrease in blood flow in the distal aorta and biceps femoris muscle. In contrast, oxygen did not change vascular resistance in the superior mesenteric artery (SMA) and renal beds and induced a significant increase in blood flow to the renal artery, SMA, and small bowel in hemorrhaged rats. L-Arginine (100 mg/kg iv) but not D-arginine or the vehicle (0.9% NaCl) completely abolished the effects of oxygen on blood pressure and reversed its effects on blood flow and resistance in the hindquarters and biceps femoris muscle. Administration of the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (50 mg/kg iv) significantly increased MABP and the resistance in the three vascular beds. Pretreatment of hemorrhaged rats with a superoxide dismutase mimic, the NO-stable radical 2,2,6,6-tetramethylpiperidine-N-oxyl (5 mg/kg iv), resulted in significantly diminished effects of oxygen on hindquarter hemodynamics. These results demonstrate a differential effect of oxygen, which increases vascular resistance in the hindquarters without a significant effect in the splanchnic and renal beds, thus favoring an increase in splanchnic and renal perfusion. It is suggested that inactivation of NO by reactive oxygen species may underlie the effects of oxygen on hindquarter vascular tone during shock.


2019 ◽  
Vol 97 (8) ◽  
pp. 3337-3347 ◽  
Author(s):  
Victoria C Kennedy ◽  
James J Gaspers ◽  
Bethany R Mordhorst ◽  
Gerald L Stokka ◽  
Kendall C Swanson ◽  
...  

Abstract Objectives were to investigate the effects of supplementation with corn dried distiller’s grains plus solubles (DDGS) to late gestating beef cows on arterial blood flow to the mammary glands during late gestation and early lactation; colostrum and milk production; dystocia and immunity; and calf BW. Cows were fed a control (CON; n = 15; 5.1% CP; 36.2% ADF) diet consisting of 90% corn stover and 10% corn silage on a dry basis offered ad libitum or CON diet with supplementation of DDGS (0.30% of BW; SUP n = 12). Mammary gland blood flow was assessed on day 245 of gestation. At parturition, maternal and calving parameters were assessed; colostrum and jugular blood was sampled; and dams were weighed. Mammary gland blood flow and milk production was measured on day 44 of lactation. Calves were weighed fortnightly for 8 wk and at weaning. Colostrum production tended to be greater in SUP dams than in CON dams (837 vs. 614 ± 95 g, P = 0.10). Calves of SUP dams were heavier at birth and 24 h (0 h, 43.2 vs. 39.8 ± 1.0 kg, P = 0.02; 24 h, 44.0 vs. 40.4 ± 1.1 kg, P = 0.02). At birth and 24 h, blood pCO2 was greater in calves born to SUP dams (6.82 vs. 6.00 ± 0.41 kPa, P = 0.04). Serum IgG did not differ (P = 0.21) at 24 h. Ipsilateral mammary gland blood flow of SUP cows was greater than CON cows (2.76 vs. 1.76 ± 0.30 L/min; P = 0.03); however, when summed with contralateral, total blood flow was similar (P = 0.33). Hemodynamic measures on day 44 of lactation were similar (P ≥ 0.32). Milk production tended to be increased (13.5 vs. 10.2 ± 1.2 kg/d, P = 0.07) in SUP vs. CON cows. Despite similar BW through 56 d, calves from SUP cows were heavier (P = 0.04) at weaning (309.7 vs. 292.0 ± 6.0 kg). In conclusion, we accept our hypothesis that DDGS supplementation during gestation influenced mammary blood flow, milk production and calf weights. These findings implicate maternal nutrition’s leverage on both nutrient and passive immunity delivery to the calf early in life as well as potential advantages on long-term performance.


1974 ◽  
Vol 52 (3) ◽  
pp. 727-735 ◽  
Author(s):  
W. W. Lautt ◽  
G. L. Plaa

Blood flow in the intact liver of anesthetized cats did not change significantly over a period of 4 h following intraduodenal injection of CCl4 (1 ml/kg). Hepatocellular disruption was well underway by 2 h after the injection. Twenty-four hours following an oral dose of CCl4, the hepatic arterial resistance to blood flow was reduced and total blood flow to the liver was at least as high as in control animals. At this time, the hepatic artery appeared fully dilated and was less responsive to humoral (intra-arterial infusion of noradrenaline) and neural (reflex activation of the sympathetic nerves) constrictor influences. Thus, alterations in hepatic blood flow do not occur during the early phases of CCl4-induced hepatic injury. These data indicate that diminished blood flow is not a causative factor in the initial phases of CCl4-induced liver injury. By 24 h, hepatic blood flow is altered in such a manner that the damaged liver receives a higher proportion of arterial blood and a total blood flow that is not reduced in spite of a generally depressed cardiovascular system.


2005 ◽  
Vol 289 (1) ◽  
pp. H168-H173 ◽  
Author(s):  
H. Knotzer ◽  
W. Pajk ◽  
S. Maier ◽  
R. Ladurner ◽  
A. Kleinsasser ◽  
...  

We investigated intestinal oxygen supply and mucosal tissue Po2during administration of increasing dosages of continuously infused arginine vasopressin (AVP) in an autoperfused, innervated jejunal segments in anesthetized pigs. Mucosal tissue Po2was measured by employing two Clark-type surface oxygen electrodes. Oxygen saturation of jejunal microvascular hemoglobin was determined by tissue reflectance spectrophotometry. Microvascular blood flow was assessed by laser-Doppler velocimetry. Systemic hemodynamic variables, mesenteric venous and systemic acid-base and blood gas variables, and lactate measurements were recorded. Measurements were performed at baseline and at 20-min intervals during incremental AVP infusion ( n = 8; 0.007, 0.014, 0.029, 0.057, 0.114, and 0.229 IU·kg−1·h−1, respectively) or infusion of saline ( n = 8). AVP infusion led to a significant ( P < .05), dose-dependent decrease in cardiac index (from 121 ± 31 to 77 ± 27 ml·kg−1·min−1at 0.229 IU·kg−1·h−1) and systemic oxygen delivery (from 14 ± 3 to 9 ± 3 ml·kg−1·min−1at 0.229 IU·kg−1·h−1) concomitant with an increase in systemic oxygen extraction ratio (from 31 ± 4 to 48 ± 10%). AVP decreased microvascular blood flow (from 133 ± 47 to 82 ± 35 perfusion units at 0.114 IU·kg−1·h−1), mucosal tissue Po2(from 26 ± 7 to 7 ± 2 mmHg at 0.229 IU·kg−1·h−1), and microvascular hemoglobin oxygen saturation (from 51 ± 9 to 26 ± 12% at 0.229 IU·kg−1·h−1) without a significant increase in mesenteric venous lactate concentration (2.3 ± 0.8 vs. 3.4 ± 0.7 mmol/l). We conclude that continuously infused AVP decreases intestinal oxygen supply and mucosal tissue Po2due to a reduction in microvascular blood flow and due to the special vascular supply in the jejunal mucosa in a dose-dependent manner in pigs.


2013 ◽  
Vol 48 (2) ◽  
pp. 220-225 ◽  
Author(s):  
Robert Topp ◽  
Elizabeth R. Ledford ◽  
Dean E. Jacks

Context Injury management commonly includes decreasing arterial blood flow to the affected site in an attempt to reduce microvascular blood flow and edema and limit the induction of inflammation. Applied separately, ice and menthol gel decrease arterial blood flow, but the combined effects of ice and menthol gel on arterial blood flow are unknown. Objectives To compare radial artery blood flow, arterial diameter, and perceived discomfort before and after the application of 1 of 4 treatment conditions. Design Experimental crossover design. Setting Clinical laboratory. Participants or Other Participants Ten healthy men, 9 healthy women (mean age = 25.68 years, mean height = 1.73 m, mean weight = 76.73 kg). Intervention(s) Four treatment conditions were randomly applied for 20 minutes to the right forearm of participants on 4 different days separated by at least 24 hours: (1) 3.5 mL menthol gel, (2) 0.5 kg of crushed ice, (3) 3.5 mL of menthol gel and 0.5 kg of crushed ice, or (4) no treatment (control). Main Outcome Measure(s) Using high-resolution ultrasound, we measured right radial artery diameter (cm) and blood flow (mL/min) every 5 minutes for 20 minutes after the treatment was applied. Discomfort with the treatment was documented using a 1-to-10 intensity scale. Results Radial artery blood flow decreased (P &lt; .05) from baseline in the ice (−20% to −24%), menthol (−17% to −24%), and ice and menthol (−36% to −39%) treatments but not in the control (3% to 9%) at 5, 10, and 15 minutes. At 20 minutes after baseline, only the ice (−27%) and combined ice and menthol (−38%) treatments exhibited reductions in blood flow (P &lt; .05). Discomfort was less with menthol than with the ice treatment at 5, 10, and 20 minutes after application (P &lt; .05). Arterial diameter and heart rate did not change. Conclusions The application of 3.5 mL of menthol was similar to the application of 0.5 kg of crushed ice in reducing peripheral blood flood. Combining crushed ice with menthol appeared to have an additive effect on reducing blood flow.


1986 ◽  
Vol 108 (2) ◽  
pp. 161-167 ◽  
Author(s):  
G. Porenta ◽  
D. F. Young ◽  
T. R. Rogge

A nonlinear mathematical model of arterial blood flow, which can account for tapering, branching, and the presence of stenosed segments, is presented. With the finite-element method, the model equations are transformed into a system of algebraic equations that can be solved on a high-speed digital computer to yield values of pressure and volume rate of flow as functions of time and arterial position. A model of the human femoral artery is used to compare the effects of linear and nonlinear modeling. During periods of rapid alterations in pressure or flow, the nonlinear model shows significantly different results than the linear model. The effect of a stenosis on pressure and flow waveforms is also simulated, and the results indicate that these waveforms are significantly altered by moderate and severe stenoses.


2020 ◽  
Vol 318 (6) ◽  
pp. E1014-E1021 ◽  
Author(s):  
Lewan Parker ◽  
Dale J. Morrison ◽  
Andrew C. Betik ◽  
Katherine Roberts-Thomson ◽  
Gunveen Kaur ◽  
...  

Oral glucose ingestion leads to impaired muscle microvascular blood flow (MBF), which may contribute to acute hyperglycemia-induced insulin resistance. We investigated whether incorporating lipids and protein into a high-glucose load would prevent postprandial MBF dysfunction. Ten healthy young men (age, 27 yr [24, 30], mean with lower and upper bounds of the 95% confidence interval; height, 180 cm [174, 185]; weight, 77 kg [70, 84]) ingested a high-glucose (1.1 g/kg glucose) mixed-nutrient meal (10 kcal/kg; 45% carbohydrate, 20% protein, and 35% fat) in the morning after an overnight fast. Femoral arterial blood flow was measured via Doppler ultrasound, and thigh MBF was measured via contrast-enhanced ultrasound, before meal ingestion and 1 h and 2 h postprandially. Blood glucose and plasma insulin were measured at baseline and every 15 min throughout the 2-h postprandial period. Compared with baseline, thigh muscle microvascular blood volume, velocity, and flow were significantly impaired at 60 min postprandial (−25%, −27%, and −46%, respectively; all P < 0.05) and to a greater extent at 120 min postprandial (−37%, −46%, and −64%; all P < 0.01). Heart rate and femoral arterial diameter, blood velocity, and blood flow were significantly increased at 60 min and 120 min postprandial (all P < 0.05). Higher blood glucose area under the curve was correlated with greater MBF dysfunction ( R2 = 0.742; P < 0.001). Ingestion of a high-glucose mixed-nutrient meal impairs MBF in healthy individuals for up to 2 h postprandial.


Author(s):  
D. J. Newton ◽  
D. K. Harrison ◽  
G. B. Hanna ◽  
C. J. A. Thompson ◽  
J. J. F. Belch ◽  
...  

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