Biomedical subjects

B R Duling

Publications and source records attributed to B R Duling.

At least 55 records · Page 3Linked to original sources

PubMed1993

A light-emitting diode light standard for photo- and videomicroscopy.

A light calibration system consisting of a compact light-emitting diode (LED) source with feedback control of intensity is described. The source is positioned in the focal plane of the microscope objective and produces flat-field illumination of up to 31 microW. The source can be easily used to determine the performance of microscope optics and camera response. It can also be used as a standard light source for calibration of experimental systems. Selectable light intensities are produced by controlling the LED input power via a feedback circuit consisting of a photodiode that detects output light intensity. Spectral coverage extends between 550 and 670 nm using green, yellow and red LEDs mounted side by side, which are selected individually. The LED chips are encapsulated in plastic diffusers which homogenize the light, and a flat field of illumination is obtained through a thin 1-mm-diameter aperture positioned directly over each chip. Provision is made for insertion of Ronchi rulings over the aperture to enable measurements of contrast modulation in a uniform field. The light may be pulse-modulated to assess camera response times and the device can be synchronized with video frames. Narrow bandpass interference filters can be placed between the objective lens and the LED source to produce monochromatic light without affecting the spacing of controlled light intensities since emission spectra do not shift appreciably over the range of LED powers chosen in this design. Results of tests using controlled light intensity and uniform illumination are presented.

Calibration↗

PubMed1993

Comparison of conduit vessel and resistance vessel reactivity: influence of intimal permeability.

Arterioles of hamster cheek pouches are less reactive to luminal application of small hydrophilic agents than to adventitial application. To explore possible longitudinal variations in response sidedness, we compared reactivity of isolated vessels from carotid arteries to first-order arterioles. Concentration-response curves for luminally or adventitially applied phenylephrine (PE) were constructed. Arterioles were 274-fold less responsive when PE was in luminal vs. adventitial responsiveness decreased as vessel diameters increased, from 24-fold in inferior saccular arteries to 18-fold in external maxillary arteries and, finally, to 3-fold in common carotid arteries. Differences in response to luminal or adventitial application of PE could be eliminated in arterioles by perfusion with 3-[(3-cholamidopropyl)-dimethylammonio]-1-propanesulfonate (CHAPS), which disrupts membrane integrity. Treatment with CHAPS also increased the transmural movement of sodium fluorescein across arteriolar vessel walls. We conclude that a diffusion barrier exists in arterial walls, that there is a longitudinal variation in this barrier as expressed by the differences in movement of small hydrophilic molecules from lumen to smooth muscle cell layers, and that the site of the barrier is likely to be at the endothelial cell membrane.

Animals↗

PubMed1993

Modification of vascular reactivity by alteration of intimal permeability: effect of TNF-alpha.

We investigated the effects of alterations in intimal permeability on microvascular reactivity to small hydrophilic agents in isolated, cannulated, perfused arterioles (65 +/- 6 microns ID) from hamster cheek pouches. Arterioles are 300-fold less responsive to the hydrophilic alpha 1-agonist, phenylephrine, applied to the lumen than when applied to the adventitia. Luminal treatment with tumor necrosis factor-alpha (TNF-alpha, 0.625 micrograms/ml, 1-2 h) potentiated reactivity to luminally applied phenylephrine, but the treatment did not change reactivity to adventitially applied phenylephrine. Similar results were obtained with a brief treatment with the detergent, 3-[(3-cholamidopropyl)dimethylammonio]-1- propanesulfonate (CHAPS; 0.3%, < 30 s). To confirm that a change in permeability had occurred, we measured the movement across the arteriolar wall of a low-molecular-weight hydrophilic fluorescent molecule, fluorescein, before and after luminal treatment with TNF-alpha or CHAPS. Either TNF-alpha or CHAPS significantly increased the rate of movement of fluorescein across the arteriolar wall. These data suggest that one element in the pathophysiology of TNF-alpha is an increase in arteriolar permeability to small, water-soluble agents, which may modify reactivity to circulating vasoactive substances.

Animals↗

PubMed1992

Arteriolar endothelial cell barrier separates two populations of muscarinic receptors.

The endothelium of arterioles can function as a barrier to diffusion of hydrophilic molecules when studied in vitro. Thus a substance applied to one side of the arteriole is relatively ineffective in reaching receptors on the opposite side of the vessel wall unless it is lipid soluble. To study the receptor populations on the two sides of the arteriolar endothelium, we used micropipettes to apply methacholine (MCh; 1.0 microM), either luminally or adventitially, for 5 s to the arterioles of the cheek pouch of pentobarbital-anesthetized hamsters. MCh equally dilated the arterioles regardless of the side of application. That different populations of receptors are located on either side of the arteriole was shown by the fact that adventitially applied hydrophilic methscopolamine was ineffective in blocking the effects of the luminally applied MCh but completely blocked the effects of abluminally applied MCh. In contrast, the luminal population of receptors was easily blocked by adventially applied scopolamine, which is lipophilic. Separate and independent populations of receptors in the vessel wall suggests the potential for differential control between humoral and adventitial sources of vasoactive metabolites.

Administration, Topical↗

PubMed1991

Ca2+ sensitivity of isolated arterioles from the hamster cheek pouch.

When isolated from the hamster cheek pouch, cannulated, and perfused, 60- to 90-microns arterioles spontaneously contracted to 67 +/- 4% of maximum diameter. Vessel sensitivity to variations in extracellular Ca2+ was then evaluated. Tone, regardless of its source, was highly dependent on the concentration of Ca2+ in the bathing solution. The magnitude of responses to changing Ca2+ depended upon which vessel surface (luminal or abluminal) the change was made. For K(+)-induced tone the Ca2+ concentration-response curve was right shifted 60-fold for luminal vs. abluminal changes. These results suggest that restricted diffusion of Ca2+ from lumen to smooth muscle dramatically reduces smooth muscle Ca2+ concentration and that under standard in vitro conditions the smooth muscle layer is effectively isolated from luminal contents. Both the cytosolic and stored Ca2+ in these microvessels were dependent on the Ca2+ concentration in the bathing solution. Abrupt removal of Ca2+ from bath produced a rapid maximal dilation with a mean time to half-maximal response (t1/2 max) of 14 +/- 4 s. Ca2+ replacement induced a return to the previous level of tone with a mean t1/2 max of 8 +/- 3 s. The magnitude of transient responses to caffeine (10 mM) was inversely related to the time of exposure to zero Ca2+ with a rapid decay in magnitude (t1/2 max = 2.7 +/- 0.8 min). These data suggest that the smooth muscle cells of arterioles have a particularly rapid transmembrane Ca2+ flux that is tightly controlled by an intracellular regulatory mechanism, which may explain the generally increased dependence of smaller vessels on extracellular Ca2+.

Animals↗

PubMed1991

Heterogeneity in conducted arteriolar vasomotor response is agonist dependent.

Microiontophoresis of acetylcholine onto cheek pouch arterioles of the pentobarbital-anesthetized hamster results in both a local response at the pipette tip and a conducted dilator response. The conducted response is not dependent on blood flow, and its magnitude decays with distance from the site of stimulation. In an attempt to define the mechanism responsible for activation of arteriolar conduction, vasoactive agonists directed toward different vascular wall cell types, receptor types, and second messengers were applied to arterioles by pressure-pulse microejection. As expected, microapplication caused a consistent arteriolar response at the site of application with each of the agonists tested (local response). However, a high degree of variability was observed among agonists in their ability to produce conducted responses. Acetylcholine, muscarine, and phenylephrine, invariably induced both local and conducted responses. In contrast, bradykinin, substance P, papaverine, isoproterenol, and adenosine, though consistently inducing local responses, displayed a highly variable ability to induce the conducted responses. When conduction was observed, the arteriolar response was similar regardless of the agonist used to induce the response. Microejection of sodium nitroprusside or arginine vasopressin produced local arteriolar responses with no evidence of a conducted response regardless of the dose. These studies reveal previously undetected heterogeneity among microvessel responses and may reflect variations in the coupling mechanisms linking the local vasomotor response to the conducted response.

Acetylcholine↗

PubMed1991

Microcirculatory dysfunction following perfusion with hyperkalemic, hypothermic, cardioplegic solutions and blood reperfusion. Effects of adenosine.

BACKGROUND: Cardioplegic solutions have been used to enhance myocardial preservation during cardiac surgery. The benefits derived from preventing myocardial ischemia with cardioplegic solutions may, however, be countered by tissue damage that occurs when the myocardium is reperfused with oxygenated blood. Furthermore, cardioplegia-induced endothelial dysfunction may contribute to depressed myocardial function postoperatively. The endothelium of coronary arteries and vein grafts is damaged by crystalloid cardioplegic solutions. There is less known about the effects of cardioplegic solutions on the microvasculature. METHODS AND RESULTS: The hypothesis that microvascular damage occurs following perfusion with hyperkalemic, crystalloid, cardioplegic solutions and blood reperfusion, leading to decreased blood flow and increased neutrophil accumulation, was tested in a model system. Intravital microscopic observations were performed during a 20-minute perfusion of the hamster cremaster muscle with cardioplegic solutions (10 degrees C) via the femoral artery with the iliac occluded and during a subsequent 2-hour blood reperfusion period (iliac open). Arteriolar vasoconstriction (27% decrease in diameter, p less than 0.05) and a 25% decrease in the density of perfused capillaries (p less than 0.05) occurred during reperfusion in hamsters receiving crystalloid cardioplegic solution (16 meq K+) compared to control hamsters (no cardioplegic solution given). Neutrophils accumulated on venular endothelium in treated animals (250% increase, p less than 0.05) and extravascularly (myeloperoxidase levels 2.0 +/- 0.4 U/g versus 1.3 +/- 0.3 U/g in control, p less than 0.05). The addition of adenosine (10(-4) M) and albumin (2 g%) to the cardioplegic perfusate, accompanied by the administration of adenosine (10(-4) M) during reperfusion, produced arteriolar vasodilation (34% diameter increase, p less than 0.05) and inhibited extravascular neutrophil accumulation (myeloperoxidase level of 1.5 +/- 0.2 U/g, p greater than 0.05 versus control). Capillary perfusion, however, was still significantly diminished (28% decrease, p less than 0.05.) CONCLUSIONS: We conclude that injury manifest by decreased microvascular blood flow and increased neutrophil accumulation in tissues occurs after perfusion with hypothermic, hyperkalemic, crystalloid cardioplegic solutions and blood reperfusion. Adenosine seems to partially attenuate this injury by dilating arterioles and decreasing extravascular neutrophil accumulation.

Adenosine↗

PubMed1990

Microcirculatory responses to exogenous endothelial cell-derived relaxing factor.

Endothelium-derived relaxing factor (EDRF) plays an important role in the vasodilatory responses of large blood vessels. However, such a role has yet to be conclusively shown for the microvasculature. In this study we tested the sensitivity of arterioles in the cheek pouch of pentobarbital-anesthetized hamsters to the EDRF-dependent agonists bradykinin and A23187, as well as to exogenous EDRF from cultured bovine aortic endothelial cells. The pouch superfusion fluid was arranged to first pass through a column containing endothelial cells and then on to the tissue. Bradykinin (10-30 nM) or A23187 (0.3 microM) was introduced either upstream or downstream to the endothelial cells, and the resultant responses were measured with video microscopy. Bradykinin and A23187 both caused a dose-dependent release of a microvessel dilator from cultured endothelial cells. We take this dilator to be EDRF based on the characteristics of the responses to the stimuli. Indomethacin (7.7 microM) was present in the superfusate to eliminate the production of cyclooxygenase products from the endothelial cells, and the magnitude of the response was diminished if the superfusate was first passed through a 3-min delay coil before arrival at the pouch. The arterioles dilated to the direct application of bradykinin in a dose-dependent fashion. They did not respond however to the direct application of A23187. These studies demonstrate that arteriolar smooth muscle is able to respond to exogenous EDRF and support the premise that EDRF may play an active role in the regulation of blood flow in the microcirculation.

Animals↗

PubMed1990

Heparinase treatment suggests a role for the endothelial cell glycocalyx in regulation of capillary hematocrit.

Physiological stimuli induce rapid and unexplained increases in the number of red blood cells within capillaries of skeletal muscle. We hypothesized that such alterations in intracapillary red cell numbers might be due to an undefined interaction between one or more components of blood and the luminal surface of the capillary. This proposition was tested by in situ microperfusion of capillaries with enzymes directed against macromolecules likely to be expressed on the surface of endothelial cells. The instantaneous fractional volume of red blood cells within a capillary (tube hematocrit) was used as an index of a capillary's response to enzyme microperfusion. Five to 8 min of perfusion with enzyme vehicle (0.25% albumin-Ringer solution) produced no significant alteration in capillary tube hematocrit. Perfusion with solutions containing heparinase raised the tube hematocrit at least twofold (P less than 0.05) without a significant change in red cell velocity. Heat-denatured heparinase and other enzymes such as neuraminidase, hyaluronidase, papain, pronase E, and clostripain had no detectable effect on the tube hematocrit (P greater than 0.05). After enzyme treatment, application of adenosine (10(-4) M) or oxygen caused brisk vasomotor responses in arterioles feeding perfused capillary units, but the usual changes in the tube hematocrit were not observed. Thus heparinase treatment results in a sustained elevation in the capillary tube hematocrit and a dissociation of the typical relationship between vasomotor changes and red cell distribution in capillaries. These findings suggest that physiological stimuli which alter the number of red blood cells within capillaries may operate by modifying interactions between plasma and one or more components on the luminal surface of capillaries.

Animals↗

PubMed1990

Arteriolar reactivity in vivo is influenced by an intramural diffusion barrier.

The endothelium of the hamster cheek pouch arteriole in vitro is able to greatly reduce the potency of luminally applied water-soluble drugs by acting as a barrier to diffusion from the lumen to the smooth muscle [Lew, Rivers, and Duling. Am. J. Physiol. 257 (Heart Circ. Physiol. 26): H10-H16, 1989]. Lipid-soluble drugs appear unaffected by the diffusion barrier, presumably because their ability to cross cell membranes allows them to freely cross the endothelium. We compared the effects of two alpha 1-adrenoceptor agonists, phenylephrine (water soluble) and SKF 89748A (lipid soluble), on systemic blood pressure and the arterioles of the hamster cheek pouch in vivo. Both agonists were able to activate the arterioles when applied topically to the outside of the arterioles (extraluminal application). The agonists were also injected as a brief bolus into the aortic arch at doses chosen to elicit similar peak pressor responses. At all levels of pressor response, the arteriolar responses to phenylephrine were smaller than those to SKF 89748A. In the cremasteric vasculature SKF 89748A was similarly found to be more effective in activating the arterioles after intravascular administration than was phenylephrine. We conclude that an intramural diffusion barrier exists in the arteriolar wall in vivo and that it can influence vascular reactivity.

Adrenergic alpha-Agonists↗

PubMed1989

Role of flow dispersion in the computation of microvascular flows by the dual-slit method.

Microvascular blood flow is commonly calculated from a "centerline" velocity derived from the dual-slit method. This is done by relating the computed centerline velocity to an average velocity through an empirically derived conversion factor. To determine the physical basis of the conversion factor, we utilized a Fourier transform and indicator dilution theory to model the parameters governing the conversion factor. We assumed Poiseuille flow from slit 1 to 2 and that the signals from the two slits were sinusoidal functions. Under these conditions, the conversion factor was found to depend primarily on a dimensionless time which is the product of the frequency of the sinusoidal signals and their time delay. Theory shows that if this dimensionless time is in the range of 3 to 7, the conversion factor lies within 1.5 to 1.7. Analysis of original dual-slit samples showed the conversion factor, obtained from the data of five arterioles and three venules, to be 1.58 +/- 0.03, and independent of the microvessel diameter.

Animals↗

PubMed1989

Propagation of vasomotor responses coordinates arteriolar resistances.

We tested the hypothesis that a conduction pathway intrinsic to the arteriolar wall possesses the properties necessary to coordinate vasomotor responses in the microcirculation. Acetylcholine (ACh) or norepinephrine (NE) was iontophoresed onto cheek pouch arterioles (15-35 microns diam) of pentobarbital-anesthetized hamsters, and diameter responses were observed using intravital video microscopy. ACh and NE induced vasodilation and vasoconstriction, respectively, that propagated both upstream and downstream from the site of application. Propagated vasomotor responses decayed with distance along the arterioles; this decay was characterized by mechanical length constants of 1.9 and 1.8 mm for ACh and NE, respectively. Vasodilations and vasoconstrictions initiated on daughter vessels of a branch propagated into parent arterioles that were approximately twice the diameter of the daughter vessels. Iontophoretic stimuli applied simultaneously to paired daughter vessels induced propagated responses that summed linearly in the parent vessel. We conclude that the arteriolar network functions as a highly coordinated syncytium and that diverse vasomotor stimuli can be summed and integrated within the peripheral microvasculature.

Acetylcholine↗

PubMed1989

Conduction of vasomotor responses in arterioles: a role for cell-to-cell coupling?

Vasomotor responses of arterioles triggered by the iontophoretic application of acetylcholine (ACh) or norepinephrine (NE) are conducted along the vessel wall. The present experiments focus on elucidating the mechanism of conduction in arterioles of the superfused cheek pouch preparation in pentobarbital-anesthetized hamsters. Localized muscarinic or adrenergic receptor blockade on an arteriolar segment produced by atropine or phentolamine, respectively, did not affect propagation through the region of blockade but did block vasomotor responses to ACh or NE applied to the segment. Thus muscarinic and alpha-adrenergic receptors can trigger the propagation of vasomotor responses, but these receptors are not involved in their conduction. Tetrodotoxin did not affect either local or propagated responses to ACh or NE. Treatment of arteriolar segments with calcium antagonists (verapamil, diltiazem, nifedipine, or manganese) caused maximal dilation locally but did not affect propagation through the dilated region. The preceding findings argue against a neural pathway for propagation. A depolarizing solution (137 mM KCl) applied by micropipette to arteriolar segments caused both local and propagated vasoconstriction and significantly attenuated propagated vasodilation induced with ACh (P less than 0.05). Putative antagonists of gap-junctional communication (hypertonic sucrose solution, octanol, CO2) reversibly attenuated or abolished propagated responses. We hypothesize that propagation of vasomotor responses along arterioles is initiated via a local change in membrane potential secondary to receptor occupation and that changes in potential spread electrotonically through gap junctions coupling smooth muscle cells, endothelial cells, or both.

Animals↗

PubMed1989

Arteriolar smooth muscle responses are modulated by an intramural diffusion barrier.

Arterioles (40-80 micron diameter) were isolated from the hamster cheek pouch, cannulated at both ends, and perfused with 3-(N-morpholino)propanesulfonic acid (MOPS)-buffered physiological salt solution (PSS). The vessels were observed with an inverted microscope and video system, and arteriolar diameter was measured. Arterioles were found to be 100 times more responsive to the alpha 1-adrenoceptor agonist phenylephrine when applied to the adventitial surface than when applied to the luminal surface. In contrast, SKF 89748-A, also an alpha 1-adrenoceptor selective agonist, but with a much greater lipid solubility than phenylephrine, was equipotent from either surface of the arteriole. We hypothesized that the difference between the two drugs was due to the ability of SKF 89748-A to permeate a diffusion barrier in the arteriolar wall because of its lipid-solubility. To test this hypothesis, a spectrum of antagonists with different sites of action and lipid solubilities was tested. The alpha-adrenoceptor antagonists phentolamine and benextramine and the muscarinic receptor antagonists atropine, scopolamine, and methscopolamine were all found to be more potent at blocking the action of appropriate agonists when applied to the same surface of the arteriole as the agonist than when applied to the opposite surface. Octanol-water partition coefficients were measured for each of the compounds, and these were found to be highly correlated with the ratio of luminal potency to adventitial potency for each of the drugs tested. These data support the hypothesis that the endothelial cell layer in these arterioles forms a barrier to the diffusion of small, water-soluble molecules from the lumen to the smooth muscle cell layer. Such a barrier may have a significant effect on arteriolar reactivity.

Acetylcholine↗

PubMed1989

Myogenic response and wall mechanics of arterioles.

The magnitude of the arteriolar response to altered intraluminal pressure was assessed in isolated, cannulated vessels of the hamster cheek pouch. Microvessels were studied during various levels of smooth muscle activation, either occurring spontaneously, or resulting from the application of exogenous agonists including potassium (35 or 70 mM) and phenylephrine (1.25 or 2.50 x 10(-6) M). Diameter-pressure curves were obtained by lowering intraluminal pressure from 60 to 0 mmHg in seven steps at 3-min intervals. At an intraluminal pressure of 40 mmHg, spontaneous tone produced an average constriction to 34 +/- 2% of the maximum diameter. Step reductions in pressure typically led to reductions in the level of activation of the muscle, which resulted in a net dilation over a significant pressure range. This "myogenic response" was more effective in modifying spontaneous tone than in modifying exogenous tone. In fact, the data suggest that reduction of the intraluminal pressure to zero can result in complete inactivation of spontaneous tone. Complete inactivation was not observed when contractions were induced by exogenous agonists, however. The magnitude of the myogenic response in arterioles was consistent with a role in autoregulation, which is 2.5-fold greater than that previously reported for small arteries. The data demonstrate that in the analysis of the mechanics of submaximally activated blood vessels one must include considerations of two phenomenon: the classical stress-length behavior as determined under conditions of maximal activation, and a superimposed modification of the activation level induced by stress- or length-dependent processes. Furthermore, the findings indicate substantial differences in response when tone is spontaneous compared with the case when tone is induced by exogenous agonists.

Animals↗

PubMed1988

A study of the functional elements regulating capillary perfusion in striated muscle.

The microcirculatory anatomy of the hamster tibialis anterior muscle is based on modules (units) consisting of groups of 12-20 capillaries which run parallel to muscle fibers. The units are supplied by a common terminal arteriole and drained by a common terminal venule; a single terminal arteriole commonly supplies two microvascular units or a "unit pair." Regulation of the tibialis muscle microcirculation was investigated in pentobarbital-anesthetized hamsters using epifluorescence microscopy. We examined the patterns of capillary control in response to physiological and pharmacological stimuli including elevation of superfusate oxygen content, direct muscle stimulation, and topical application of phenylephrine. Changes in capillary perfusion were rarely manifested as responses of individual capillaries. The predominant response consisted of a coordinated change in virtually all the capillaries of a unit pair. For example, gradual elevation of superfusate PO2 resulted in simultaneous arrest or "derecruitment" of capillary flow in all capillaries of a unit pair in 37 of 43 such elements studied. In the 6 unit pairs showing atypical behavior, no more than four individual capillaries showed atypical behavior. Capillaries in 28 of 29 unit pairs were also recruited during muscle stimulation as members of a unit pair. In 18 of 21 unit pairs, exposure to topical phenylephrine resulted in simultaneous arrest of capillary flow in all capillaries of a unit pair. These data suggest that in this striated muscle, regulation of capillary perfusion is accomplished by control of capillary unit pairs. Accordingly, the patterns of interdigitation of units will ultimately determine the precision of control of tissue diffusion distance as well as oxygenation.

Animals↗

PubMed1988

Red cell velocity during functional hyperemia: implications for rheology and oxygen transport.

Muscle blood flow increases during work. Any associated change in blood velocity that occurs during functional hyperemia can have profound effects on wall shear rate and arteriolar hemoglobin saturations. We measured arteriolar red cell velocity and cross-sectional area during muscle contraction to determine the physiological significance of any of these changes in calculations of wall shear rate and the in situ spectrophotometric measurement of hemoglobin oxygen saturation. Calculated cremaster muscle blood flow increased 64-236% during twitch and tetanic stimulation, respectively, which was due entirely to an increase in cross-sectional area, with muscle work producing little change in either the red cell velocity or the calculated wall shear rate. Small changes ranging from a 3% increase to a 4% decrease in hemoglobin saturation were evident in second- and third-order arterioles, which apparently reflects offsetting effects of the increase in metabolic rate and the increase in arteriolar blood volume. A simple model explaining the microcirculatory adjustments made during muscle work requires dilation of both feed arteries and arterioles if red cell velocity is to remain constant during hyperemia.

Animals↗

PubMed1987

Microvessel hematocrit: measurement and implications for capillary oxygen transport.

Microvascular preparations of the hamster cheek pouch and cremaster muscle were used to establish the relationship among three measures of red cell distribution: 1) the systemic hematocrit defined as the volume percentage of red cells sampled from a toe clip; 2) the tube hematocrit defined as the instantaneous volume fraction of red cells in a microvessel segment of measured length and diameter; and 3) the discharge hematocrit defined as the volume percentage of red cells that flowed into micropipettes inserted into microvessels. The results show the tube hematocrit is low and highly variable in the presence of a nearly constant systemic hematocrit. The discharge hematocrit, in contrast, consistently approximated systemic values in blood taken from arterioles or venules with diameters of 6-98 micron. Indeed, the mean ratio of the discharge to the systemic hematocrit did not differ from unity (P greater than 0.25). The observed similarity between the discharge and systemic hematocrit indicates that red cells are distributed uniformly across capillary networks. Differences between the absolute value and variance of the tube hematocrit compared with the discharge hematocrit imply that the anatomical volume of a microvessel can differ from the volume available to cells and plasma within a microvessel. Thus moment-to-moment variation in the tube hematocrit or capillary red cell spacing may be indicative of a change in the effective capillary flow cross section and not solely on the inflow hematocrit.

Animals↗