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PubMed1996

Endothelin-1 constricts fetoplacental microcirculation and decreases fetal O2 consumption in sheep.

Endothelin-1 produced by umbilicoplacental tissues may regulate fetal placental perfusion. To investigate its site of action, we measured segmental resistance in this bed in unanesthetized fetal sheep near term during fetal endothelin-1 infusion. A 15-min intravenous infusion of endothelin-1 at 1 micrograms/min significantly increased fetal blood pressure in the aorta (+33%), cotyledon artery and vein, and inferior vena cava, and endothelin-1 decreased fetal heart rate (-40%). Vascular resistance in the placental microcirculation increased significantly (+332%), but smaller increases in resistance of the umbilical artery and vein were not significant. Nevertheless, the stiffness of the umbilical arterial wall appeared to increase because vascular input impedance increased significantly both at the heart rate frequency (+85%) and when averaged > 2 Hz (characteristic impedance; +138%). Mean blood flow in the umbilical artery decreased by 64%, and the flow pulsatility index increased 137% (P < 0.05 for both). Despite the large decrease in placental perfusion, there was no significant change in descending aortic oxygen tension or oxygen content, because fetal oxygen consumption was reduced by 40%. We conclude that endothelin-1 is a potent constrictor of the placental microcirculation in sheep. Endothelin-1 also decreases fetal oxygen consumption by an unknown mechanism.

Animals↗

PubMed1997

Role of nitric oxide in vasodilator response induced by salbutamol in rat diaphragmatic microcirculation.

To determine the contribution of nitric oxide (NO) to the vasodilator response induced by salbutamol in diaphragmatic microcirculation, we studied a diaphragmatic preparation in anesthetized rats. With bicarbonate-buffered Ringer solution continuously suffusing the diaphragm, laser-Doppler flowmetry was used to record microvascular blood flow (QLDF). The drugs were applied to the surface of the diaphragm. Salbutamol (3.2 x 10(-7)-10(-4) M), isoproterenol (3.2 x 10(-8)-3.2 x 10(-6) M), and forskolin (3.2 x 10(-7)-10(-5) M) each elicited a concentration-dependent increase in QLDF. The vasodilator response induced by salbutamol (3.2 x 10(-7), 10(-6), and 3.2 x 10(-6) M) was attenuated by a 15-min suffusion of N omega-nitro-L-arginine (L-NNA, 10(-4) M), and pretreatment with L-arginine (10(-2) M) could restore salbutamol-induced vasodilator responses. Salbutamol-induced vasodilation was also abolished by propranolol (10(-5) M). Similarly, the vasodilator response elicited by isoproterenol (3.2 x 10(-8), 10(-7), and 3.2 x 10(-7) M) and forskolin (3.2 x 10(-7), 10(-6), and 3.2 x 10(-6) M) was inhibited by L-NNA (10(-4) M). In contrast, the vasodilator response induced by adenosine (10(-6), 10(-5), and 10(-4) M) was not affected by L-NNA (10(-4) M). These data indicate that in rat diaphragmatic microcirculation salbutamol-induced vasodilation may be partly mediated by beta-adrenoceptors on the endothelium. Moreover, these data suggest that an elevation of cyclic AMP in the endothelium may cause release of NO.

Adenosine↗

PubMed1997

Anesthetics alter relative contributions of NO and EDHF in rat cremaster muscle microcirculation.

The contributions of the vasodilators nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) were investigated in the rat cremaster muscle microcirculation during halothane, isoflurane, or ketamine anesthesia. After inhibition of prostaglandin synthesis with indomethacin, changes in diameter of fourth-order arterioles to acetylcholine (ACh) or bradykinin (BK) were studied in the presence or absence of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthase, and/or 20 mM K+, an inhibitor of EDHF action. L-NMMA inhibited ACh- and BK-induced vasodilation during isoflurane but not halothane or ketamine anesthesia. Superfusion of the muscle with buffer containing 20 mM K+ dilated arterioles. EDHF was responsible for most of the NO-independent response to ACh, because 20 mM K+ unmasked ACh-stimulated, NO-dependent relaxation during halothane or ketamine anesthesia. However, 20 mM K+ did not inhibit BK-induced vasodilation during halothane or ketamine anesthesia. Our data suggest that anesthetics can alter the balance between NO and EDHF vasodilation in the microcirculation and that NO-dependent mechanisms are enhanced and EDHF action inhibited during isoflurane anesthesia.

Abdominal Muscles↗

PubMed2000

Evidence for involvement of the PKC-alpha isoform in myogenic contractions of the coronary microcirculation.

The role of protein kinase C (PKC) isoforms in myogenic tone of the ferret coronary microcirculation was investigated by measuring fura 2 Ca(2+) signals, PKC immunoblots, contractile responses, and confocal microscopy of PKC translocation. Phorbol ester-evoked contractions were completely abolished in the absence of extracellular Ca(2+) but involved a Ca(2+) sensitization relative to KCl contractions. Immunoblotting using isoform-specific antibodies showed the presence of PKC-alpha and -iota and traces of PKC-epsilon and -mu in the ferret coronary microcirculation. PKC-beta was not detectable. When intraluminal pressure (40 to 60 and 80 mmHg) was increased, ferret coronary arterioles showed a transient increase in fura 2 Ca(2+) signals, whereas the myogenic tone remained sustained. The increase in Ca(2+) and tone was sustained at 100 mmHg. Isolated ferret coronary arterioles were fixed and immunostained for PKC-alpha at 40 and 100 mmHg intraluminal pressure. PKC translocation was determined by confocal microscopy. Increased PKC translocation was observed when vessels were exposed to 100 mmHg relative to that at resting pressure (40 mmHg). These results suggest a link between the Ca(2+) sensitization that occurs during the myogenic contraction and activation of the alpha-isoform of PKC.

Animals↗

PubMed2000

Mechanism of adenosine-induced vasodilation in rat diaphragm microcirculation.

The mechanism of adenosine-induced vasodilation in rat diaphragm microcirculation was investigated using laser Doppler flowmetry. Adenosine (10(-5), 3.2 x 10(-5), and 10(-4) M), the nonselective adenosine agonist 5'-N-ethylcarboxamido-adenosine (NECA) (10(-8)-10(-7) M), the specific A(2A) agonist 2-p-(2-carboxyethyl)phenyl-amino-5'-N-ethyl carboxamidoadenosine (CGS-21680) (10(-8)-10(-7) M), and the adenosine agonist with higher A(1)-receptor affinity, R-N(6)-phenylisopropyladenosine (R-PIA) (10(-7), 3.2 x 10(-7), and 10(-6) M) elicited a similar degree of incremental increase of microcirculatory flow in a dose-dependent manner. The ATP-dependent potassium (K(ATP)) channel blocker glibenclamide (3.2 x 10(-6) M) significantly attenuated the vasodilation effects of these agonists. Adenosine-induced vasodilation could be significantly attenuated by the nonselective adenosine antagonist 8-(p-sulfophenyl)-theophylline (3 x 10(-5) M) or the selective A(2A) antagonist 4-(2-[7-amino-2-(2-furyl)[1,2, 4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl) phenol (ZM-241385, 10(-6) M), but not by the selective A(1) antagonist 8-cyclopentyl-1, 3-dipropylxanthine (5 x 10(-8) M). Adenylate cyclase inhibitor N-(cis-2-phenyl-cyclopentyl) azacyclotridecan-2-imine-hydrochloride (MDL-12330A, 10(-5)M) effectively suppressed the vasodilator response of adenosine and forskolin. These results suggest that adenosine-induced vasodilation in rat diaphragm microcirculation is mediated through the stimulation of A(2A) receptors, which are coupled to adenylate cyclase activation and opening of the K(ATP) channel.

Adenosine↗

PubMed2001

12-lipoxygenase in porcine coronary microcirculation: implications for coronary vasoregulation.

Noncyclooxygenase metabolites of arachidonic acid (AA) have been proposed to mediate endothelium-dependent vasodilation in the coronary microcirculation. Therefore, we examined the formation and bioactivity of AA metabolites in porcine coronary (PC) microvascular endothelial cells and microvessels, respectively. The major noncyclooxygenase metabolite produced by microvascular endothelial cells was 12(S)-hydroxyeicosatetraenoic acid (HETE), a lipoxygenase product. 12(S)-HETE release was markedly increased by pretreatment with 13(S)-hydroperoxyoctadecadienoic acid but not by the reduced congener 13(S)-hydroxyoctadecadienoic acid, suggesting oxidative upregulation of 12(S)-HETE output. 12(S)-HETE produced potent relaxation and hyperpolarization of PC microvessels (EC(50), expressed as -log[M] = 13.5 +/- 0.5). Moreover, 12(S)-HETE potently activated large-conductance Ca(2+)-activated K(+) currents in PC microvascular smooth muscle cells. In contrast, 12(S)-HETE was not a major product of conduit PC endothelial AA metabolism and did not exhibit potent bioactivity in conduit PC arteries. We suggest that, in the coronary microcirculation, 12(S)-HETE can function as a potent hyperpolarizing vasodilator that may contribute to endothelium-dependent relaxation, particularly in the setting of oxidative stress.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMed2001

Endothelium-derived hyperpolarizing factor in coronary microcirculation: responses to arachidonic acid.

In coronary resistance vessels, endothelium-derived hyperpolarizing factor (EDHF) plays an important role in endothelium-dependent vasodilation. EDHF has been proposed to be formed through cytochrome P-450 monooxygenase metabolism of arachidonic acid (AA). Our hypothesis was that AA-induced coronary microvascular dilation is mediated in part through a cytochrome P-450 pathway. The canine coronary microcirculation was studied in vivo (beating heart preparation) and in vitro (isolated microvessels). Nitric oxide synthase (NOS) (N(omega)-nitro-L-arginine, 100 microM) and cyclooxygenase (indomethacin, 10 microM) or cytochrome P-450 (clotrimazole, 2 microM) inhibition did not alter AA-induced dilation. However, when a Ca(2+)-activated K(+) channel channel or cytochrome P-450 antagonist was used in combination with NOS and cyclooxygenase inhibitors, AA-induced dilation was attenuated. We also show a negative feedback by NO on NOS-cyclooxygenase-resistant AA-induced dilation. We conclude that AA-induced dilation is attenuated by cytochrome P-450 inhibitors, but only when combined with inhibitors of cyclooxygenase and NOS. Therefore, redundant pathways appear to mediate the AA response in the canine coronary microcirculation.

Animals↗

PubMed1991

Effects of acute nitric oxide inhibition on rat glomerular microcirculation.

Endothelium-derived relaxing factor (EDRF), recently identified as nitric oxide (NO), has been shown to be released by glomerular endothelial cells and might influence the glomerular microcirculation. To examine this hypothesis, we studied in rats the renal effect of acute administration of NG-monomethyl-L-arginine (L-NMMA), a specific inhibitor of NO synthesis. Adult male Munich-Wistar rats were studied before and after intravenous administration of either pure saline or a bolus injection of L-NMMA (20 mg) followed by a continuous infusion of the inhibitor (0.4 mg/min). Although saline alone had no effect on systemic or glomerular hemodynamics, L-NMMA promoted marked systemic hypertension, glomerular arteriolar vasoconstriction, and glomerular hypoperfusion. Since efferent resistance was disproportionately increased, glomerular hydraulic pressure was also markedly elevated. The glomerular ultrafiltration coefficient (Kf) fell to 42% of control. Single-nephron glomerular filtration rate was unaffected. Striking polyuria was also observed. These findings suggest that EDRF exerts a basal relaxing effect on the glomerular microcirculation.

Animals↗

PubMed1997

Facilitated transport in vasa recta: theoretical effects on solute exchange in the medullary microcirculation.

A new theoretical model describing the exchange of water and solutes between the renal medullary interstitium and the microcirculation was developed to account for the presence of water channels and urea transporters, both of which were recently identified in the descending vasa recta (DVR) of the renal medulla. Small solutes, which are excluded from the water channels, are freely exchanged through a parallel pathway shared with water. The transcapillary concentration gradients of sodium and urea across the water channels induce water efflux from DVR, whereas classic Starling forces across the shared pathway favor volume uptake by DVR. Because small solute concentration gradients are large in the inner medulla, the model predicts net water removal from DVR, in agreement with experimental observations. The descending and ascending vasa recta (AVR) function as a countercurrent exchanger, the efficiency of which is inversely related to the net amount of solute taken up by the medullary microcirculation. Our results indicate that net solute removal from the medulla is governed by convective uptake into AVR and thus depends predominantly on the parameters affecting AVR transcapillary volume flux. The simulations also suggest that the urea transporter significantly enhances the exchange of both sodium and urea and might serve to abrogate a reduction in exchanger efficiency imparted by water channels.

Animals↗

PubMed1987

Effects of prostaglandin F2 alpha and prostacyclin on pulmonary microcirculation in the cat.

In pulmonary microcirculation, using a new X-ray television system, we measured the effects of prostaglandin F2 alpha (PGF2 alpha) and prostacyclin on the internal diameter (ID), flow velocity, volume flow, and transit times of a contrast medium in small arteries (Ta) and veins (Tv) in anesthetized cats. The ID of the arteries and veins ranged from 100 to 500 micron. PGF2 alpha, 0.3, 1, and 3 micrograms/kg, predominantly decreased ID on the arterial side in a dose-dependent manner but increased flow velocity 27-62%. Consequently, volume flow was kept relatively constant. With PGF2 alpha, Ta and Tv were decreased 18-41% and 4-15%, respectively. Prostacyclin, 2 and 4 micrograms/kg, uniformly dilated the ID of small arteries 9-16% but did not change small veins. With prostacyclin, flow velocity was unchanged or decreased, whereas volume flow was increased significantly, 27-32%. No significant changes of Ta and Tv were observed in response to prostacyclin. When both prostaglandins, PGF2 alpha and prostacyclin, were administered, they canceled each other with respect to the ID of small pulmonary arteries. Prostacyclin also prevented the PGF2 alpha-induced vasoconstriction of the pulmonary venous microcirculation.

Animals↗

PubMed1993

Role of nitric oxide in effects of tumor necrosis factor-alpha on microcirculation in rat.

The involvement of nitric oxide (NO) in the effects of tumor necrosis factor-alpha (TNF-alpha) on the microcirculation was studied by in vivo microscopy in rat cremaster muscle. We examined second-, third-, and fourth-order arterioles with mean diameters under control conditions of 62.2, 37.4, and 16.9 microns, respectively. The vasodilation observed after topical administration of 100 ng/ml recombinant TNF-alpha (rTNF-alpha) was partly but significantly inhibited when NO synthesis was inhibited by 2 x 10(-4) M N omega-nitro-L-arginine (L-NNA). Almost complete inhibition of the acute vasodilatory effect of rTNF-alpha was found when both NO and prostaglandin synthesis were blocked by simultaneous administration of L-NNA and mefanamic acid. The effect of rTNF-alpha on vasoconstriction in response to norepinephrine (NE) was a dramatic reduction after 2 h of exposure to 1 ng/ml rTNF-alpha. Concomitant administration of 2 x 10(-4) M L-NNA prevented this hyporeactivity for second- and third-order, but not for fourth-order, arterioles. However, at 2 x 10(-3) M, L-NNA totally prevented the hyporeactivity to NE for all arteriolar orders. No changes in vasoconstriction to 70 mM KCl were observed either immediately after rTNF-alpha administration or after 2 h of exposure. We conclude that 1) the direct acute vasodilatory effect of rTNF-alpha on the microcirculation is mediated by both prostaglandins and NO, 2) long exposure to rTNF-alpha diminishes the response of the arterioles to NE but not to KCl, and 3) this effect is mediated by NO.

Animals↗

PubMed2001

Comparison of OPS imaging and conventional capillary microscopy to study the human microcirculation.

Orthogonal polarization spectral (OPS) imaging is a new clinical technique for observation of the microcirculation of organ surfaces. For validation purposes, we compared OPS images of the nailfold skin with those obtained from conventional capillary microscopy at rest and during venous occlusion in 10 male volunteers. These images were computer analyzed to provide red blood cell velocity and capillary diameters of the same nailfold capillaries at rest and during venous occlusion. Results showed that OPS images provided similar values for red blood cell velocity and capillary diameter as those obtained from capillary microscopy images. OPS imaging, however, provided significantly better image quality, as shown by comparison of image contrast between OPS imaging and capillary microscopy. This made image analysis better and easier to perform. It is anticipated, therefore, that OPS imaging will become a new and powerful technique in the study of the human microcirculation in vivo because it can be used on human internal organs.

Adult↗

PubMed2002

Vascular and neural mechanisms of ACh-mediated vasodilation in the forearm cutaneous microcirculation.

The relative contribution of endothelial vasodilating factors to acetylcholine (ACh)-mediated vasodilation in the forearm cutaneous microcirculation is unclear. The aims of this study were to investigate the contributions of prostanoids and cutaneous C fibers to basal cutaneous blood flow (CuBF) and ACh-mediated vasodilation. ACh was iontophoresed into the forearm, and cutaneous perfusion was measured by laser-Doppler flowmetry. To inhibit the production of prostanoids, four doses of acetylsalicylic acid (ASA; 81, 648, 972, and 1,944 mg) were administered orally. Cutaneous nerve fibers were blocked with topical anesthesia. Cyclooxygenase inhibition did not change basal CuBF or endothelium-mediated vasodilation to ACh. In contrast, ASA (972 and 1,944 mg) significantly reduced the C-fiber-mediated axon reflex in a dose-dependent fashion. Blockade of C-fiber function significantly reduced axon reflex-mediated vasodilation but did not affect basal CuBF or endothelium-dependent vasodilation. The findings suggest that prostanoids do not contribute significantly to basal CuBF or endothelium-dependent vasodilation in the forearm microcirculation. In contrast, prostanoids are mediators of the ACh-provoked axon reflex.

Acetylcholine↗

PubMed2000

Impact of gastrin-releasing peptide on intestinal microcirculation after ischemia-reperfusion in rats.

We investigated the effect of gastrin-releasing peptide (GRP) and its antagonist RC-3095 on intestinal microcirculation after ischemia-reperfusion. Intestinal ischemia was induced in female Wistar rats by occlusion of the superior mesenteric artery for 40 min. Ten minutes prior to reperfusion, infusion of GRP or RC-3095 was started. A jejunal segment was exteriorized and the microhemodynamics of the mucosa and submucosa were examined by intravital microscopy and compared both with normal and ischemic controls (without application of the regulatory peptide). Ischemia-reperfusion significantly decreased functional capillary density from 891.2 +/- 14.1 to 398.3 +/- 11.4 cm(-1). Capillary red blood cell velocity was reduced from 0.46 +/- 0.01 to 0.37 +/- 0.01 mm/s (p < 0.05). Furthermore, both sticking and rolling of leukocytes were enhanced. 3.4 +/- 1.1% of the villi were not perfused at all. GRP infusion reversed the microcirculatory ischemia-reperfusion injury by increasing functional capillary density to 669.8 +/- 8.3 cm(-1) and red blood cell velocity to 0.62 +/- 0.01 mm/s (p < 0.05). In addition, application of GRP resulted in a complete absence of stasis (0%) in the villi. Leukocyte-endothelium adherence remained unchanged when compared to the ischemic controls. In contrast, application of RC-3095 caused an aggravation of microcirculatory disturbances demonstrated by a markedly increased number of non-perfused villi (42.5 +/- 4.2%; p < 0.05 vs. ischemic controls) and a significantly reduced functional capillary density (346.2 +/- 8.4 cm(-1), p < 0.05 vs. ischemic controls). In addition, RC-3095 led to an increased permanent leukocyte adherence in postcapillary venules whereas rolling was significantly reduced when compared to normal controls. We conclude that GRP in pharmacological doses has a protective effect on intestinal microcirculation during reperfusion. Furthermore, these data suggest that endogenous GRP may play a decisive role in the maintenance of microvascular integrity during reperfusion.

Analysis of Variance↗

PubMedDate not supplied

Effects of NO synthase inhibitors on the synovial microcirculation in the mouse knee joint.

Production of nitric oxide by the inducible NO synthase (iNOS) is known to be enhanced in chronic joint inflammation and osteoarthritis as well as aseptic loosening of joint prostheses. Initial studies yielded promising results after inhibition of the nitric oxide synthase (NOS). However, the effect of NOS inhibition has not been studied at the site of the primary function of NO, the microcirculation of the synovium in vivo. Using our recently developed model for the in vivo study of synovial microcirculation in the mouse knee joint, the effects of selective versus nonselective inhibition of iNOS were investigated by means of intravital fluorescence microscopy. After resection of the patella tendon, the synovial fatty tissue was exposed for intravital microscopy. Diameter of arterioles, functional capillary density (FCD), diameter of venules, venular red blood cell velocity and leukocyte-endothelial cell interaction were quantitatively analyzed before, and 10 and 60 min after intravenous injection of NOS inhibitors [selective iNOS inhibitor N-iminoethyl-L-lysine (L-NIL), and nonselective NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME)]. Our results demonstrate that L-NAME causes a significant decrease in the arteriolar diameter and FCD associated with an increase in the leukocyte accumulation in the synovium in vivo. In contrast, L-NIL neither altered the microhemodynamics nor the leukocyte-endothelial cell interaction in the synovium, indicating its potential use for selective inhibition of iNOS in joint inflammation. Using our method, further studies will provide new insights into the unknown effect of NOS inhibition on the synovial microvasculature in inflammatory joint disease in vivo.

Animals↗

PubMedDate not supplied

EEMCO guidance for the measurement of skin microcirculation.

The blood supply to the skin is provided by a network of arterioles, capillaries and venules organized into a superficial and a deep plexus. The assessment of skin microcirculation is of valuable interest in cosmetology in the quantification of the sun protection factor, skin irritation and efficacy of antiredness treatments. Skin microcirculation can be measured by means of different techniques, based mainly on the quantification of optical and thermal properties of the skin which are modified by the amount of blood perfusion. Relevant and reproducible data can be obtained only through the understanding of the biophysical background of the technique(s) utilized. Standardization of measuring conditions and procedures is particularly required for blood flow assessment. In this paper, the advantages and disadvantages of the main techniques in use are discussed, and optimization of measurements for laser Doppler techniques is described.

Animals↗

PubMed2005

Protective effects of insulin during ischemia-reperfusion injury in hamster cheek pouch microcirculation.

OBJECTIVE: The effects of insulin (0.18 nM-0.18 microM) on reduced capillary perfusion, microvascular permeability increase and leukocyte adhesion induced by ischemia-reperfusion injury were investigated in the hamster cheek pouch microcirculation. To gain insight into the insulin's mechanism of action, the effects of its higher concentration (0.18 microM) were investigated after inhibition of tyrosine kinase (TK), nitric oxide synthase (NOS), protein kinase C (PKC), phosphatidylinositol 3-kinase and K+(ATP) channels, alone or in combination. Two concentrations for each inhibitor were used. METHODS: Microcirculation was visualized by fluorescence microscopy. Perfused capillary length, microvascular permeability, leukocyte adhesion to venular walls, vessel diameter and capillary red blood cell velocity were assessed by computer-assisted methods. Measurements were made at baseline (B), after 30 min of ischemia (I), and after 30 min of reperfusion (R). RESULTS: In control animals, perfused capillary length decreased by 63 +/- 5% of baseline at R. Microvascular permeability increased at I and R, while leukocyte adhesion was most pronounced in V1 postcapillary venules at R. Insulin dose-dependently preserved capillary perfusion at R (-28 +/- 6 and -15 +/- 6% of baseline), but was unable to prevent the increase in permeability at I (0.25 +/- 0.05 and 0.29 +/- 0.06 Normalized Grey Levels, NGL) and R (0.49 +/- 0.10 and 0.53 +/- 0.09 NGL), according to the concentrations. Adhesion of leukocytes was observed mostly in V3 venules at R (9 +/- 2 and 10 +/- 2/100 microm venular length, with the lower and higher concentration, respectively). Nitric oxide synthase inhibition by N(G)-nitro-L-arginine-methyl ester prior to insulin did not affect capillary perfusion at R (-18 +/- 3% of baseline with higher concentration), but prevented permeability increase (0.20 +/- 0.04 NGL, according to higher concentration) and reduced leukocyte adhesion in V3 venules at R (1.5 +/- 1.0/100 microm of venular length, with higher concentration). Blockade of K+(ATP) channels by glibenclamide prior to insulin decreased perfused capillary length at R (-58 +/- 6% of baseline with higher concentration), attenuated leakage at R (0.30 +/- 0.04 NGL, according to higher concentration) and caused leukocyte adhesion mainly in V1 venules at R (9.0 +/- 1.5/100 microm of venular length, with higher concentration). Inhibition of either TK, PKC or phosphatidylinositol 3-kinase did not affect microvascular responses to insulin. Simultaneous inhibition of TK and NOS did not increase protection. CONCLUSIONS: Insulin prevents ischemia-reperfusion injury by promoting capillary perfusion through an apparent activation of K+(ATP) channels and increase in nitric oxide release.

Alkaloids↗

PubMed2006

Age-related changes of the cutaneous microcirculation in vivo.

BACKGROUND: The architectural frameworks of the skin microcirculation are rather complex and change continuously with aging. But these changes are yet poorly documented in vivo. OBJECTIVES: Using non-invasive methods belonging to the field of biometrology, the study aimed to investigate quantitatively the changes of the cutaneous microvasculature in different anatomic sites with age. METHODS: Measurements were performed on crow's feet, forehead, volar forearm and dorsum of hand in 50 women (aged 20-74 years who consisted of 10 probands in each live decades). The superficial vascular plexus was scanned by videocapillaroscopy and assessed with the software Capilab Toolbox. The subpapillary vascular plexus was explored with laser Doppler flowmetry. The skin color a* was analyzed by chromametry. RESULTS: A marked site and age effect on the skin microcirculation has been demonstrated. The density of capillary loops in the eldest group decreased by about 40-70% compared with the youngest group whereas the vascular length increased by 35-156%. The capillary density in the back of the hand was 4 times higher than in the crow's feet. The vascular length in the crow's feet was 3 times longer than in the back of the hand. Both blood flow and skin redness (a*) increased also with age. CONCLUSION: Both morphology and quantification of the cutaneous microvasculature showed changes with site and age. Videocapillaroscopy associated to an image processing and laser Doppler flowmetry revealed different vascular layers. So the combination of both instruments offers an easy way to observe the architectural frameworks in vivo.

Adult↗