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PubMed1992

Microvascular oxygen transport: impact of a left-shifted dissociation curve.

The impact of an increased hemoglobin oxygen affinity (decreased P50) on oxygen transport was evaluated in capillaries of the retractor muscle under nonhypoxic (FIo2 = 0.30 and 0.21) and hypoxic (FIo2 = 0.10) conditions in hamsters with normal oxygen affinity [control; P50 = 26.1 +/- 1.0 (SD) mmHg, n = 12] and in hamsters with an increased oxygen affinity [treated; P50 = 16.2 +/- 1.6 (SD) mmHg, n = 7] induced by chronic short-term administration of sodium cyanate. Using in vivo video microscopy and computer-aided image analysis, we determined oxygen saturation (SO2) and associated hemodynamic parameters in both arteriolar (n = 30 control, 18 treated) and venular (n = 25 control, 17 treated) capillaries. In response to hypoxia, systemic arterial PO2 decreased to 29.6 +/- 6.0 (SD) mmHg in control animals and 24.7 +/- 3.8 (SD) mmHg in treated animals associated with abrupt decreases in systemic arterial blood pressure and increases in respiratory rate. The decrease in SO2 across the capillary network during nonhypoxic ventilation was 13.3% SO2 for control animals and 11.0% SO2 for treated animals. During hypoxic ventilation, the decrease in SO2 was 9.1% SO2 in control animals and 8.7% SO2 in treated animals. Hemodynamic parameters were not significantly different in the two groups during hypoxia. Estimated end-capillary PO2 was significantly lower in the treated animals. These data indicate that an increased oxygen affinity does not provide an obvious advantage for oxygen transport during hypoxia at the level of the capillary network in resting striated muscle; however, such an advantage might become apparent in the presence of an increased metabolic rate or a more severe hypoxic challenge.

Animals↗
PubMed1992

Concentration profile of blood platelets differs in arterioles and venules.

Platelet distribution was investigated in 21 venules (V) and 10 arterioles (A) of the rabbit mesentery (vessel diam 15-33 microns). Circulating platelets were labeled in vivo with the dye acridine red and observed with fluorescence video microscopy. Only platelets flowing in a thin (5-7 microns) optical section located about the median plane of the vessel were used. The relative position of each platelet, i.e., the distance of its centroid to the left vessel wall divided by the local vessel diameter, was determined. In addition, in 10 venules leukocyte margination was inhibited by intravenous injection of dextran sulfate (500,000 mol wt; 30 mg/kg body wt). The number of platelets per unit volume (i.e., platelet density) relative to the mean density was significantly higher in the vessel center of V (1.04) than of A (0.55; P less than 0.005). In contrast, near the wall this density was significantly higher in A compared with V. Mean values were as follows: at radial position (R) = 0.9-1.0, 0.30 in A and 0.11 in V (P greater than 0.05); at R = 0.8-0.9, 1.63 in A and 0.84 in V (P less than 0.002); at R = 0.7-0.8, 1.60 in A and 1.36 in V (P greater than 0.05); at R = 0.6-0.7, 1.16 in A and 1.60 in V (P less than 0.02); and at R = 0.5-0.6, 0.92 in A and 1.36 in V (P less than 0.02). These differences in platelet distribution between arterioles and venules are not caused by the presence of leukocyte margination in venules.

Animals↗
PubMed1993

Factors affecting renal microvascular blood flow in rat hyperdynamic bacteremia.

To determine whether angiotensin II and alpha-adrenergic activity contribute to the mechanism of impaired renal microvascular blood flow during hyperdynamic live Escherichia coli (E. coli) bacteremia, we used in vivo video microscopy in the chronic unilateral hydronephrotic kidney of decerebrate male Sprague-Dawley rats. Intravenous infusion of E. coli caused arteriolar constriction to 83 +/- 4% of baseline (BL) in cortical radial arteries (CRA), 82 +/- 3% of BL in afferent (AFF) arterioles, and decreased flow to 54 +/- 9% of BL. Subsequent local inhibition of renal prostaglandin synthesis with mefenamate increased preglomerular arteriolar constriction to 55 +/- 6% of BL in CRA and 51 +/- 6% of BL in AFF arterioles and decreased renal microvascular blood flow to 26 +/- 8% of BL values in E. coli animals but had no effect on control animals. Subsequent local renal angiotensin II receptor blockade with saralasin acetate increased renal microvascular blood flow in E. coli animals to 64 +/- 9% of BL by dilating CRA to 78 +/- 5% of BL and AFF arterioles to 89 +/- 5% of BL. Phentolamine caused further dilation of CRA to 104 +/- 7% BL and AFF arterioles to 116 +/- 109% and increased flow to 99 +/- 8% of BL. Acetylcholine increased diameters further to 110 +/- 3% of BL in CRA and 136 +/- 12% of BL in AFF arterioles. These data indicate that in our chronic hydronephrotic kidney model during E. coli bacteremia, renal microvascular tone is due to increased angiotensin II and alpha-adrenergic activity and some other, as yet, undefined factor.

Acetylcholine↗
PubMed1993

Relationship between capillary and systemic venous PO2 during nonhypoxic and hypoxic ventilation.

We evaluated the relationship between end-capillary and systemic venous PO2 values in the retractor muscle of 14 anesthetized hamsters during both nonhypoxic and hypoxic ventilation to ascertain whether the level of tissue oxygenation could be reliably estimated from the systemic parameter. End-capillary PO2 was estimated from measurements of oxygen saturation in capillaries at the venular end of the network obtained using in vivo video microscopy and computer-aided image-analysis techniques at three different levels of inspired oxygen (0.3, 0.21, and 0.1). Measurements of systemic arterial and venous blood gases were made in conjunction with these capillary determinations. In addition, in a portion of the study we utilized an oxygen microelectrode to determine the PO2 in the first-order venule draining the portion of the muscle containing the capillaries under study. We found that only when the animals were made acutely hypoxic was there any correspondence between the systemic venous and end-capillary PO2 values. In addition, these data provide support for the presence of arteriovenous shunting of oxygen during nonhypoxic ventilation.

Animals↗
PubMed1993

Arteriolar dilation mediated by capsaicin and calcitonin gene-related peptide in rats.

In addition to altering vascular tone by stimulating primary afferent nerves and acting through reflex pathways, capsaicin acts locally. We examined effects of topically applied capsaicin on arteriolar diameter in striated muscle and tested the hypothesis that capsaicin can alter microvascular tone by releasing substance P (SP) or calcitonin gene-related peptide (CGRP). In anesthetized rats, the right cremaster muscle was exposed and suspended in a tissue bath filled with a physiological salt solution. Diameters of third-order arterioles were displayed and measured using in vivo video microscopy. In 17 of 20 rats, addition of capsaicin (3 x 10(-7) M) to the bath dilated arterioles (85 +/- 14% above control). Failure of a second administration of capsaicin to produce a sustained dilation in 6 of 7 arterioles that had previously dilated to capsaicin is consistent with the hypothesis that this agent causes depletion of an endogenous vasodilator. Pretreatment with an SP inhibitor did not alter capsaicin-induced dilation. CGRP (1 x 10(-10) to 2 x 10(-8) M) caused dilation similar to that caused by capsaicin. Pretreatment with a CGRP inhibitor to the bath prevented capsaicin-induced dilation, but not constriction. These results suggest that capsaicin can dilate microvessels by releasing CGRP, which can modulate tone.

Animals↗
PubMed1994

Basic FGF enhances endothelium-dependent relaxation of the collateral-perfused coronary microcirculation.

The effect of chronic, periadventitial administration of basic (b) fibroblast growth factor (FGF) on endothelial dysfunction in the collateral-dependent and normally perfused coronary microcirculation was examined. Ameroid constrictors were placed on the proximal left circumflex coronary artery (LCX) in 23 pigs. In 11 pigs, bFGF was released from calcium alginate microcapsules into the perivascular space of the proximal left anterior descending coronary artery (LAD) and LCX. After 5-8 wk, coronary arterial microvessels (80-170 microns) were studied in a pressurized (40 mmHg) no-flow state with video microscopy. Receptor-mediated endothelium-dependent relaxations to ADP and serotonin were reduced while contraction to acetylcholine was enhanced in the collateral-dependent LCX microvessels of non-bFGF-treated control hearts. Relaxation of vessels to the non-receptor-mediated, endothelium-dependent agent A-23187; endothelium-independent relaxation to nitroprusside; and contraction to KCl were similar in all groups. Chronic treatment with bFGF normalized responses to ADP, serotonin, and acetylcholine in the collateral-dependent LCX region but had no effect on the responses of vessels in the normally perfused LAD region. Arteriolar density in the collateral-perfused LCX region of bFGF-treated hearts was markedly increased (4-fold compared with that in untreated hearts, suggesting a link between the angiogenic effect of bFGF and its action on endothelial preservation. Thus the periadventitial, sustained delivery of bFGF preserves receptor-mediated, endothelium-dependent responses in the collateral-dependent LCX region but has no effect on responses of microvessels in the normally perfused LAD region or on non-receptor-mediated endothelium-dependent relaxation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1994

Adrenergic regulation of coronary microcirculation after extracorporeal circulation and crystalloid cardioplegia.

The purpose of the present study was to examine whether adrenoceptor-mediated responses of porcine coronary resistance arteries are affected by cardioplegic arrest under conditions of extracorporeal circulation (cardiopulmonary bypass; CPB). Pigs were placed on CPB. The hearts were arrested with a cold hyperkalemic crystalloid cardioplegic solution for 1 h, then were reperfused for 1 h. In vivo and in vitro beta-adrenoceptor-mediated responses were compared before CPB and 2 min and 1 h after initiation of reperfusion. In vitro responses were studied in a pressurized no-flow state with video microscopy. Isoproterenol (0.02 micrograms.kg-1.min-1, intracoronary) increased coronary blood flow by 100 +/- 32% (P < 0.001) before CPB and cardioplegic arrest, 17 +/- 7% 2 min postcardioplegia (P < 0.01), and 71 +/- 9 (P < 0.001) after 1 h of reperfusion. Relaxation of precontracted microvessels (90-180 micron) to isoproterenol, NaF, forskolin, and adenosine was reduced after cardioplegic arrest (all P < 0.001). After 1 h of postcardiolegia-reperfusion, relaxation responses to forskolin and adenosine were completely restored, whereas the responses to isoproterenol (P < 0.05) and NaF (P < 0.10) were only partially recovered. Cardioplegic arrest and postcardioplegia-reperfusion blunted the alpha 2-adrenoceptor-mediated endothelium-dependent relaxation to clonidine (P < 0.001) but did not affect the minimal (< 4%) contractile response to the alpha 1-adrenoceptor agonist phenylephrine or the relaxation to nitroprusside. These results show that hyperkalemic cardioplegia results in the generalized defect in the beta-adrenoceptor-GS protein-adenylate cyclase pathway, which is significantly restored after reperfusion.

Adenosine↗
PubMed1995

In vivo differentiation of leukocytes rolling in mesenteric postcapillary venules.

A method is presented to assess in vivo in transparent tissues the leukocyte subtypes that roll in microvessels. In nine rabbits anesthetized with ketamine-xylazine, leukocyte nuclei were stained in situ with acridine yellow (3 mg/kg i.v. for 5 min). Intravital fluorescence video microscopy in 24 mesenteric venules (17-29 microns, median 21) indicated labeling of all rolling leukocytes. On the basis of the shape of their nucleus, 67-100% (median 89) could be classified unequivocally (13-366 cells analyzed, median 77) as polymorphonuclear (PMN, i.e., granulocytes) or monomorphonuclear (lymphocytes and monocytes). Of these classified cells, 94-100% were PMNs (median 100, including 1 stray value of 69%). This PMN percentage was independent of the level of leukocyte rolling (2-36/min, median 14), vessel diameter, flow velocity (0.5-2.5 mm/s), or duration of the experiment (< 6 h). The dye had no significant influence on hemodynamic parameters, systemic leukocyte counts (1.5-7.8 x 10(9)/l), or in vitro differentiation pattern (27-38% granulocytes, 0-2% monocytes, 61-71% lymphocytes). In conclusion, our method demonstrated that the leukocytes that roll in postcapillary venules of the exteriorized rabbit mesentery are almost exclusively granulocytes.

Aminoacridines↗
PubMed1995

Effects of Hoe-140 and ramiprilat on arteriolar tone and dilation to bradykinin in skeletal muscle of rats.

In skeletal muscle of pentobarbital sodium-anesthetized rats, the mechanism of action and possible role of the potent vasodilator bradykinin (BK) in regulation of arteriolar tone were investigated. Changes in diameter of third-order arterioles of cremaster muscle in response to topical administration of BK and other vasoactive agents were measured with an image-shearing monitor and recorded with video microscopy. All agonists were administered topically on the exteriorized muscle. With use of Hoe-140, a B2-receptor antagonist, the presence of kinin receptors in arterioles was studied. In control preparations, 10(-5) M arachidonic acid (AA), 0.5 x 10(-6) M acetylcholine (ACh), and 10(-5) M adenosine (ADO) evoked dilation of arterioles of up to 70% of resting diameter. BK (10(-9), 10(-8), 10(-7), and 10(-6) M) elicited dose-dependent arteriolar dilations (1.3 +/- 1.3, 4.1 +/- 0.5, 10.3 +/- 1.6, and 13.3 +/- 1.3 microns, respectively). In the presence of 10(-7) M Hoe-140, dilations to AA, ACh, and ADO were not affected, but those to 10(-9)-10(-7) M BK were eliminated or significantly inhibited (10(-6) M BK: to 2.9 +/- 1.8 microns). Also, whereas Hoe-140 significantly reduced basal arteriolar diameters (from 16.7 +/- 0.9 to 13.8 +/- 1.1 microns, P < 0.05), it did not affect constrictions to norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Visualization of oxygen level inside a single cardiac myocyte.

The present paper describes theoretical and experimental bases for quantitation of the oxygen level inside a single isolated ventricular rat myocyte. We applied three-wavelength microspectrophotometry to a single cardiomyocyte, where the sensitivity of the spectrophotometry was augmented by a digital image processing technique known as video-enhanced microscopy. Oxygen-dependent changes in light absorption of the intracellular pigments were detected and represented with the use of a newly defined variable, Z, where one pixel of the reconstructed cell image corresponded to 0.2 microns. Theoretically, Z is a single-valued function of the fractional oxygen saturation of the intracellular pigment. We demonstrated in quiescent cardiomyocytes that Z changed according to extracellular PO2, where the relationship was sigmoidal with the extracellular PO2 for a half-maximal Z of 3.2 Torr. In the aerobic cell, conversion of cytochromes to the reduced forms by NaCN did not affect Z value. Therefore, we conclude that Z mainly represents the fractional oxygen saturation of myoglobin, thus reporting cytosolic PO2. We also demonstrated that for extracellular PO2 of 1.3 Torr, abolition of mitochondrial oxygen consumption by NaCN significantly elevated the intracellular oxygen level, suggesting existence of oxygen pressure gradients in a quiescent single cardiomyocyte that were proportional to oxygen flux.

Animals↗
PubMed1995

Adhesion of flowing neutrophils to cultured endothelial cells after hypoxia and reoxygenation in vitro.

Using a novel in-line deoxygenating system linked to an in vitro flow-based adhesion assay and video microscopy, we have studied neutrophil recruitment and migration after hypoxia and reoxygenation of cultured human umbilical vein endothelial cells (HUVEC). Unstimulated purified neutrophils were perfused over reoxygenating HUVEC immediately after various periods of endothelial hypoxia. Adhesion to HUVEC was dependent on the duration of hypoxia, with 30, 60, and 100 min of exposure causing graded increments in neutrophil recruitment. The degree of hypoxia also markedly influenced the endothelial response. Severe hypoxia (O2 < 2.5%) induced stationary attachment and then migration of neutrophils, in contrast to rolling adhesion alone under a less intense regime (O2 = 2.5-4.0%). Judged from studies with monoclonal antibodies, P-selectin was essential for adhesion after severe hypoxia, and neutrophil immobilization was attributable to the activation of neutrophil beta 2-integrin. Perfusion of neutrophils with an antibody against interleukin-8 or a platelet-activating factor antagonist reduced levels of adhesion. However, IL-8 appeared to be the dominant agent involved in the immobilization from flow, whereas platelet-activating factor was the more potent agent involved in initiating subendothelial migration. Thus endothelial cells alone can initiate all stages of adhesion and migration of flowing neutrophils after hypoxia and reperfusion.

Cell Adhesion↗
PubMed1996

Endotoxin pretreatment enhances portal venous contractile response to endothelin-1.

To test whether endotoxin pretreatment modulates the portal hemodynamic response to endothelin (ET)-1 and phenylephrine (PE), two potent vasoconstrictors in the portal circulation of the normal liver, rats received intraperitoneal injections of Escherichia coli lipopolysaccharide (LPS; 1 mg/kg body wt) or saline. Livers were isolated after 6 or 24 h and perfused with Krebs buffer containing 5% autologous erythrocytes. Analyses of portal pressure-flow (P-Q) relationships and epifluorescence video microscopy were performed before and after ET-1 (10(-9) M) or PE (10(-5) M) administration. LPS pretreatment increased total portal resistances (Rt), zero-flow pressures (PQ = 0), and linear regression slopes of P-Q relationships, and decreased the sinusoidal diameters (Ds) and sinusoidal volumetric flow (Qv). The response to ET-1 was enhanced 6 and 24 h after LPS administration, leading to greater increases in Rt, PQ = 0, and slope and more pronounced decreases in Dx, red blood cell velocity (VRBC), and Qv. In contrast, PE effects were similar (PQ = 0, slope, Ds) or even attenuated (Rt, VRBC, Qv) in livers from LPS-treated compared with control animals. Thus endotoxin pretreatment increased the portal contractile response to ET-1 but not to PE. This enhanced ET-1 response appeared to occur at sinusoidal and presinusoidal levels and may contribute to endotoxin-induced hepatic microcirculatory failure.

Animals↗
PubMed1996

Angiotensin II and contraction of isolated myocytes from human, guinea pig, and infarcted rat hearts.

The effects of angiotensin II on myocardial contractility were assessed in isolated cardiac myocyte preparations, using video microscopy with a computerized edge-detection system. Angiotensin II (1 nM-10 microM) did not affect the contraction of rat (n = 10), guinea pig (n = 11), or human ventricular myocytes (n = 8) or of human atrial myocytes (n = 12). Isoproterenol or raised extracellular calcium increased the contraction amplitude of the cardiac myocytes to a maximum of between 150 and 560% above basal, and there were corresponding increases in the velocities of contraction and relaxation. In rat and guinea pig ventricular myocytes 1 microM angiotensin II did not affect the inotropic response to isoproterenol. Seven days after left coronary artery ligation in seven rats, the basal contraction amplitude was reduced in myocytes from the infarcted region (4.0 +/- 1.9%) compared with the noninfarcted region (5.0 +/- 2.8%, P = 0.03) and with myocytes from six sham-operated hearts (5.0 +/- 2.8%, P = 0.03). There was a switch in myosin isoform expression from the V1 to the V3 isoform in myocytes from both the infarcted and noninfarcted regions. Angiotensin II (1 nM-10 microM) had no significant effect on the contraction characteristics of myocytes from the infarcted rat hearts. In conclusion, angiotensin II had no significant inotropic effect on isolated cardiac myocyte preparations from guinea pig ventricle, normal and infarcted rat ventricle, human ventricle, and human atrium.

Adult↗
PubMed1997

Developmental changes in flow-wave propagation velocity in embryonic chick vascular system.

We analyzed flow-wave propagation velocity in the early embryonic vascular system and its responses to acute alterations in circulating blood volume. Two 20-MHz pulsed Doppler velocimeters were positioned along the arterial system in stage 18 (n = 12), 21 (n = 10), and 24 (n = 11) chick embryos. Distance between the two measurement sites was measured by video-microscopy. Phase velocity was calculated using Fourier transform up to the fourth harmonics. Wave-front velocity was also calculated by threshold technique. In a subset of embryos at stage 24 (n = 10), circulating blood volume was acutely altered to change stroke volume. Mean phase velocity increased from 42.9 +/- 3.3 to 95.8 +/- 7.5 cm/s from stage 18 to 24 (P < 0.05 by analysis of variance), whereas wave-front velocity increased from 52.8 +/- 2.4 to 72.2 +/- 5.2 cm/s. Stroke volume and mean aortic pressure paralleled the changes in mean phase velocity and wave-front velocity in normal development and in response to changes in circulating blood volume. Thus developmental changes in wave-propagation velocity were consistent with changes in the size of the vascular system, pressure range, and elastic properties of the arterial wall during systemic vasculogenesis in the embryo.

Animals↗
PubMed1997

Ventricular-vascular uncoupling by acute conotruncal occlusion in the stage 21 chick embryo.

Embryonic ventricular diastolic and systolic function was evaluated during normal ejection (coupled) and during acute ventricular outflow tract occlusion (uncoupled) in the stage 21 chick embryo. We simultaneously measured ventricular pressure with a servo-null system and ventricular dimensions using video microscopy. Experimental protocols included 1) baseline recording followed by acute conotruncal (CT) ligation (n = 15) and 2) baseline recording, preload increase using Krebs-Henseleit buffer (3 microliters), preload reduction via venous hemorrhage, and then CT occlusion (n = 20). Ventricular epicardial cross-sectional area was converted to internal volume using wall volume measures and assuming an ellipsoid geometry to produce pressure-volume loops. We calculated the time constant of ventricular pressure decline using a monoexponential decay function with a pressure asymptote. As previously noted, heart rate was unaffected by acutely altered preload or afterload. CT ligation increased end-systolic pressure, maximal +dP/dt, and the time constant of ventricular pressure decline and decreased stroke volume indexed for end-diastolic volume. Thus the embryonic ventricle has significant contractile reserve masked in vivo by the dynamic coupling between the ventricle and arterial circulation.

Animals↗
PubMed1999

Ischemia-reperfusion induced microvascular responses in LDL-receptor -/- mice.

The objective of this study was to determine whether the microvascular responses to ischemia and reperfusion (I/R) are altered in an animal model of atherosclerosis, the low-density lipoprotein-receptor knockout (LDLr -/-) mouse. Intravital video microscopy was used to monitor venular wall shear rate, leukocytes rolling velocity, the number of rolling, adherent and emigrated leukocytes, and albumin leakage in cremasteric postcapillary venules of wild-type (B6129) and LDLr -/- mice exposed to 60 min of ischemia and 60 min of reperfusion. The postcapillary venules of LDLr -/- mice exhibited two- to threefold larger increments in the number of adherent leukocytes and a more profound albumin leakage response to I/R than venules in wild-type mice. The exaggerated inflammatory responses noted in LDLr -/- mice placed on a normal diet were not exacerbated by a high-cholesterol diet. Treatment of LDLr -/- mice with either a platelet-activating factor (PAF) receptor antagonist (WEB-2086) or a monoclonal antibody (YN-1) against the endothelial cell adhesion molecule, intercellular adhesion molecule 1 (ICAM-1), markedly attenuated the I/R-induced leukocyte adherence and albumin leakage. These findings indicate that atherogenic mice are more vulnerable to the deleterious microvascular effects of I/R and that PAF-mediated, ICAM-1-dependent leukocyte adhesion contributes to this exaggerated response to I/R.

Animals↗
PubMed1999

Cotransmission from sympathetic vasoconstrictor neurons to small cutaneous arteries in vivo.

This study has characterized constrictions of small cutaneous arteries in the guinea pig ear in response to electrical stimulation of the cervical sympathetic nerve (SNS) in vivo. Video microscopy and on-line image analysis were used to examine diameter changes of ear arteries (80-140 micrometers resting diameter) in anesthetized guinea pigs. Trains of 50-300 impulses, but not single pulses or short trains, produced frequency-dependent (2-20 Hz) constrictions. The purinoceptor antagonist suramin (30 microM) greatly reduced constrictions produced by exogenous ATP but did not affect constrictions produced by SNS at 10 Hz or exogenous norepinephrine. The alpha(2)-adrenoceptor antagonist yohimbine (1 microM) enhanced the peak amplitude of sympathetic constrictions at lower stimulation frequencies (1-5 Hz). The amplitude of constrictions to SNS at 10 Hz was reduced, and the latency of constrictions was increased by the alpha(1)-adrenoceptor antagonist prazosin (1 microM). Constrictions to SNS at 10 Hz remaining after prazosin treatment were reduced in amplitude by dihydroergotamine (2 microM) and were attenuated further by the neuropeptide Y Y(1)-receptor antagonist 1229U91 (0.3 microM). Thus norepinephrine and neuropeptide Y act as cotransmitters to mediate sympathetic constriction of small ear arteries at higher stimulation frequencies (10 Hz), but ATP does not seem to contribute directly to these constrictions.

Adenosine Triphosphate↗
PubMed1999

Permeation of the luminal capillary glycocalyx is determined by hyaluronan.

The endothelial cell glycocalyx influences blood flow and presents a selective barrier to movement of macromolecules from plasma to the endothelial surface. In the hamster cremaster microcirculation, FITC-labeled Dextran 70 and larger molecules are excluded from a region extending almost 0.5 micrometer from the endothelial surface into the lumen. Red blood cells under normal flow conditions are excluded from a region extending even farther into the lumen. Examination of cultured endothelial cells has shown that the glycocalyx contains hyaluronan, a glycosaminoglycan which is known to create matrices with molecular sieving properties. To test the hypothesis that hyaluronan might be involved in establishing the permeation properties of the apical surface glycocalyx in vivo, hamster microvessels in the cremaster muscle were visualized using video microscopy. After infusion of one of several FITC-dextrans (70, 145, 580, and 2,000 kDa) via a femoral cannula, microvessels were observed with bright-field and fluorescence microscopy to obtain estimates of the anatomic diameters and the widths of fluorescent dextran columns and of red blood cell columns (means +/- SE). The widths of the red blood cell and dextran exclusion zones were calculated as one-half the difference between the bright-field anatomic diameter and the width of the red blood cell column or dextran column. After 1 h of treatment with active Streptomyces hyaluronidase, there was a significant increase in access of 70- and 145-kDa FITC-dextrans to the space bounded by the apical glycocalyx, but no increase in access of the red blood cells or in the anatomic diameter in capillaries, arterioles, and venules. Hyaluronidase had no effect on access of FITC-Dextrans 580 and 2,000. Infusion of a mixture of hyaluronan and chondroitin sulfate after enzyme treatment reconstituted the glycocalyx, although treatment with either molecule separately had no effect. These results suggest that cell surface hyaluronan plays a role in regulating or establishing permeation of the apical glycocalyx to macromolecules. This finding and our prior observations suggest that hyaluronan and other glycoconjugates are required for assembly of the matrix on the endothelial surface. We hypothesize that hyaluronidase creates a more open matrix, enabling smaller dextran molecules to penetrate deeper into the glycocalyx.

Animals↗