scholarly journals Endothelial function is impaired in the cutaneous microcirculation of adults with psoriasis through reductions in nitric oxide-dependent vasodilation

2018 ◽  
Vol 314 (2) ◽  
pp. H343-H349 ◽  
Author(s):  
Billie K. Alba ◽  
Jody L. Greaney ◽  
Sara B. Ferguson ◽  
Lacy M. Alexander
Keyword(s):  
Nitric Oxide ◽  
Endothelial Function ◽  
Local Heating ◽  
Microvascular Dysfunction ◽  
Ringer Solution ◽  
Healthy Individuals ◽  
Doppler Flowmetry ◽  
Control Subjects ◽  
Underlying Mechanisms ◽  
Synthase Inhibitor

Psoriasis is an independent risk factor for cardiovascular disease; however, the underlying mechanisms are not fully understood. Deficits in conduit arterial function are evident in patients with psoriasis, but potential impairments in microcirculatory endothelial function remain unclear. We hypothesized that cutaneous microvascular dysfunction would be detectable in otherwise healthy individuals with psoriasis. Two intradermal microdialysis fibers were placed in (nonlesional) forearm skin of nine patients (3 men and 6 women, 39 ± 5 yr) with moderate (16 ± 2% of body surface area) plaque psoriasis and nine healthy (nonpsoriatic) control subjects (3 men and 6 women, 38 ± 5 yr) for local delivery of 1) lactated Ringer solution (control) and 2) 10 mM l-ascorbate (a nonspecific antioxidant). An index of skin blood flow was measured using laser-Doppler flowmetry during local heating (42°C). Nitric oxide (NO)-dependent vasodilation was directly quantified after perfusion of the nonspecific NO synthase inhibitor NG-nitro-l-arginine methyl ester (15 mM). A third fiber was perfused with increasing concentrations (10−10– 10−2M) of norepinephrine to elicit adrenoreceptor-mediated cutaneous vasoconstriction. NO-dependent vasodilation was attenuated in patients with psoriasis (57 ± 5% and 39 ± 7% maximum cutaneous vascular conductance in control subjects and adults with psoriasis, respectively, P < 0.01). l-Ascorbate did not improve NO-dependent vasodilation ( P > 0.05). There was no group difference in maximal vasoconstriction or microvascular sensitivity to norepinephrine ( P > 0.05). These data suggest that NO bioavailability is reduced in otherwise healthy individuals with psoriasis, which contributes to systemic microvascular dysfunction.NEW & NOTEWORTHY In adults with psoriasis, reduced nitric oxide bioavailability mediates impaired endothelium-dependent vasodilation, independent of increases in oxidative stress. Furthermore, the degree of psoriatic symptomology is directly related to greater reductions in nitric oxide-dependent vasodilation.

scholarly journals Endothelial nitric oxide synthase control mechanisms in the cutaneous vasculature of humans in vivo

2008 ◽  
Vol 295 (1) ◽  
pp. H123-H129 ◽  
Author(s):  
Dean L. Kellogg ◽  
Joan L. Zhao ◽  
Yubo Wu
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
Local Heating ◽  
Ringer Solution ◽  
Whole Body ◽  
Control Mechanisms ◽  
Local Skin ◽  
Doppler Flowmetry ◽  
Whole Body Heat Stress ◽  
Body Heat

Nitric oxide (NO) participates in locally mediated vasodilation induced by increased local skin temperature (Tloc) and in sympathetically mediated vasodilation during whole body heat stress. We hypothesized that endothelial NOS (eNOS) participates in the former, but not the latter, response. We tested this hypothesis by examining the effects of the eNOS antagonist NG-amino-l-arginine (l-NAA) on skin blood flow (SkBF) responses to increased Tloc and whole body heat stress. Microdialysis probes were inserted into forearm skin for drug delivery. One microdialysis site was perfused with l-NAA in Ringer solution and a second site with Ringer solution alone. SkBF [laser-Doppler flowmetry (LDF)] and blood pressure [mean arterial pressure (MAP)] were monitored, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF ÷ MAP). In protocol 1, Tloc was controlled with LDF/local heating units. Tloc initially was held at 34°C and then increased to 41.5°C. In protocol 2, after a normothermic period, whole body heat stress was induced (water-perfused suits). At the end of both protocols, 58 mM sodium nitroprusside was perfused at both microdialysis sites to cause maximal vasodilation for data normalization. In protocol 1, CVC at 34°C Tloc did not differ between l-NAA-treated and untreated sites ( P > 0.05). Local skin warming to 41.5°C Tloc increased CVC at both sites. This response was attenuated at l-NAA-treated sites ( P < 0.05). In protocol 2, during normothermia, CVC did not differ between l-NAA-treated and untreated sites ( P > 0.05). During heat stress, CVC rose to similar levels at l-NAA-treated and untreated sites ( P > 0.05). We conclude that eNOS is predominantly responsible for NO generation in skin during responses to increased Tloc, but not during reflex responses to whole body heat stress.

Prostanoids contribute to cutaneous active vasodilation in humans

2006 ◽  
Vol 291 (3) ◽  
pp. R596-R602 ◽  
Author(s):  
Gregg R. McCord ◽  
Jean-Luc Cracowski ◽  
Christopher T. Minson
Keyword(s):  
Core Body Temperature ◽  
Local Heating ◽  
Ringer Solution ◽  
Control Site ◽  
Whole Body ◽  
Nitric Oxide Synthase Inhibitor ◽  
Doppler Flowmetry ◽  
Forearm Skin ◽  
Synthase Inhibitor ◽  
Hyperemic Response

The specific mechanisms by which skin blood flow increases in response to a rise in core body temperature via cutaneous active vasodilation are poorly understood. The primary purpose of this study was to determine whether the cyclooxygenase (COX) pathway contributes to active vasodilation during whole body heat stress ( protocol 1; n = 9). A secondary goal was to verify that the COX pathway does not contribute to the cutaneous hyperemic response during local heating ( protocol 2; n = 4). For both protocols, four microdialysis fibers were placed in forearm skin. Sites were randomly assigned and perfused with 1) Ringer solution (control site); 2) ketorolac (KETO), a COX-1/COX-2 pathway inhibitor; 3) NG-nitro-l-arginine methyl ester (l-NAME), a nitric oxide synthase inhibitor; and 4) a combination of KETO and l-NAME. During the first protocol, active vasodilation was induced using whole body heating with water-perfused suits. The second protocol used local heaters to induce a local hyperemic response. Red blood cell flux (RBC flux) was indexed at all sites using laser-Doppler flowmetry, and cutaneous vascular conductance (CVC; RBC flux/mean arterial pressure) was normalized to maximal vasodilation at each site. During whole body heating, CVC values at sites perfused with KETO (43 ± 9% CVCmax), l-NAME (35 ± 9% CVCmax), and combined KETO/l-NAME (22 ± 8% CVCmax) were significantly decreased with respect to the control site (59 ± 7% CVCmax) ( P < 0.05). Additionally, CVC at the combined KETO/l-NAME site was significantly decreased compared with sites infused with KETO or l-NAME alone ( P < 0.05). In the second protocol, the hyperemic response to local heating did not differ between the control site and KETO site or between the l-NAME and KETO/l-NAME site. These data suggest that prostanoids contribute to active vasodilation, but do not play a role during local thermal hyperemia.

scholarly journals Nitric Oxide-mediated Cutaneous Microvascular Function is not Altered in Young Adults Following Mild-to-Moderate SARS CoV-2 Infection.

2022 ◽  
Author(s):  
Gabrielle A. Dillon ◽  
S. Tony Wolf ◽  
Lacy M. Alexander
Keyword(s):  
Nitric Oxide ◽  
Vascular Dysfunction ◽  
Local Heating ◽  
Cross Sectional Study ◽  
Healthy Adults ◽  
Microvascular Function ◽  
Cross Sectional ◽  
Doppler Flowmetry ◽  
Healthy Control ◽  
Underlying Mechanisms

Vascular dysfunction has been reported in adults who have recovered from COVID-19. To date, no studies have investigated the underlying mechanisms of persistent COVID-19-associated vascular dysfunction. PURPOSE: To quantify nitric oxide (NO)-mediated vasodilation in healthy adults who have recovered from SARS-CoV-2 infection. We hypothesized that COVID-19-recovered adults would have impaired NO-mediated vasodilation compared to adults who have not had COVID-19. METHODS: We performed a cross-sectional study including: 10 (5M/5W, 24 ± 4yrs) healthy control (HC) adults who were unvaccinated for COVID-19, 11 (4M/7W, 25 ± 6yrs) healthy vaccinated (HV) adults, and 12 (5M/7W, 22 ± 3yrs) post-COVID-19 (PC, 19 ± 14wks) adults. COVID-19 symptoms severity (survey) were assessed. A standardized 39°C local heating protocol was used to assess NO-dependent vasodilation via perfusion (intradermal microdialysis) of 15 mM NG-nitro-l-arginine methyl ester during the plateau of the heating response. Red blood cell flux was measured (laser-Doppler flowmetry) and cutaneous vascular conductance (CVC = flux/mmHg) was expressed as a percentage of maximum (28mM sodium nitroprusside + 43°C). RESULTS: The local heating plateau (HC: 61 ± 20%, HV: 60 ± 19%, PC: 67 ± 19%, p=0.80) and NO-dependent vasodilation (HC: 77 ± 9%, HV: 71 ± 7%, PC: 70 ± 10%, p=0.36) were not different among groups. Neither symptom severity (25 ± 12 AU) nor time since diagnosis correlated with the NO-dependent vasodilation (r=0.46, p=0.13; r=0.41, p=0.19, respectively). CONCLUSION: Healthy adults who have had mild-to-moderate COVID-19 do not have altered NO-mediated cutaneous microvascular function.

Flow-mediated dilatation following wrist and upper arm occlusion in humans: the contribution of nitric oxide

2001 ◽  
Vol 101 (6) ◽  
pp. 629-635 ◽  
Author(s):  
Sagar N. DOSHI ◽  
Katerina K. NAKA ◽  
Nicola PAYNE ◽  
Christopher J.H. JONES ◽  
Moira ASHTON ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Peak Flow ◽  
Ultrasound Probe ◽  
Upper Arm ◽  
Flow Mediated Dilatation ◽  
Synthase Inhibitor ◽  
Increased Blood Flow ◽  
Similar Peak

Flow-mediated dilatation (FMD) of the brachial artery assessed by high-resolution ultrasound is widely used to measure endothelial function. However, the technique is not standardized, with different groups using occlusion of either the wrist or the upper arm to induce increased blood flow. The validity of the test as a marker of endothelial function rests on the assumption that the dilatation observed is endothelium-dependent and mediated by nitric oxide (NO). We sought to compare the NO component of brachial artery dilatation observed following wrist or upper arm occlusion. Dilatation was assessed before and during intra-arterial infusion of the NO synthase inhibitor NG-monomethyl-l-arginine (l-NMMA) following occlusion of (i) the wrist (distal to ultrasound probe) and (ii) the upper arm (proximal to ultrasound probe) for 5min in ten healthy males. Dilatation was significantly greater after upper arm occlusion (upper arm, 11.62±3.17%; wrist, 7.25±2.49%; P = 0.003). During l-NMMA infusion, dilatation after wrist occlusion was abolished (from 7.25±2.49% to 0.16±2.24%; P < 0.001), whereas dilatation after upper arm occlusion was only partially attenuated (from 11.62±3.17% to 7.51±2.34%; P = 0.006). The peak flow stimulus was similar after wrist and upper arm occlusion. We conclude that dilatation following upper arm occlusion is greater than that observed after wrist occlusion, despite a similar peak flow stimulus. l-NMMA infusion revealed that FMD following wrist occlusion is mediated exclusively by NO, while dilatation following upper arm occlusion comprises a substantial component not mediated by NO, most probably related to tissue ischaemia around the brachial artery. FMD following wrist occlusion may be a more valid marker of endothelial function than dilatation following upper arm occlusion.

scholarly journals Oral atorvastatin therapy increases nitric oxide-dependent cutaneous vasodilation in humans by decreasing ascorbate-sensitive oxidants

2011 ◽  
Vol 301 (3) ◽  
pp. R763-R768 ◽  
Author(s):  
Lacy A. Holowatz ◽  
W. Larry Kenney
Keyword(s):  
Nitric Oxide ◽  
Local Heating ◽  
Oxidant Stress ◽  
Microvascular Dysfunction ◽  
Local Skin ◽  
Cutaneous Vasodilation ◽  
Before And After ◽  
Atorvastatin Therapy ◽  
Oxide Synthase ◽  
Cutaneous Vascular Conductance

Elevated low-density lipoproteins (LDL) are associated with cutaneous microvascular dysfunction partially mediated by increased arginase activity, which is decreased following a systemic atorvastatin therapy. We hypothesized that increased ascorbate-sensitive oxidant stress, partially mediated through uncoupled nitric oxide synthase (NOS) induced by upregulated arginase, contributes to cutaneous microvascular dysfunction in hypercholesterolemic (HC) humans. Four microdialysis fibers were placed in the skin of nine HC (LDL = 177 ± 6 mg/dl) men and women before and after 3 mo of a systemic atorvastatin intervention and at baseline in nine normocholesterolemic (NC) (LDL = 95 ± 4 mg/dl) subjects. Sites served as control, NOS inhibited, L-ascorbate, and arginase-inhibited+L-ascorbate. Skin blood flow was measured while local skin heating (42°C) induced NO-dependent vasodilation. After the established plateau in all sites, 20 mM ≪ngname≫ was infused to quantify NO-dependent vasodilation. Data were normalized to maximum cutaneous vascular conductance (CVC) (sodium nitroprusside + 43°C). The plateau in vasodilation during local heating (HC: 78 ± 4 vs. NC: 96 ± 2% CVCmax, P < 0.01) and NO-dependent vasodilation (HC: 40 ± 4 vs. NC: 54 ± 4% CVCmax, P < 0.01) was reduced in the HC group. Acute L-ascorbate alone (91 ± 5% CVCmax, P < 0.001) or combined with arginase inhibition (96 ± 3% CVCmax, P < 0.001) augmented the plateau in vasodilation in the HC group but not the NC group (ascorbate: 96 ± 2; combo: 93 ± 4% CVCmax, both P > 0.05). After the atorvastatin intervention NO-dependent vasodilation was augmented in the HC group (HC postatorvastatin: 64 ± 4% CVCmax, P < 0.01), and there was no further effect of ascorbate alone (58 ± 4% CVCmax, P > 0.05) or combined with arginase inhibition (67 ± 4% CVCmax, P > 0.05). Increased ascorbate-sensitive oxidants contribute to hypercholesteromic associated cutaneous microvascular dysfunction which is partially reversed with atorvastatin therapy.

Role of nitric oxide in gut ischemia-reperfusion-induced hepatic microvascular dysfunction

1997 ◽  
Vol 273 (5) ◽  
pp. G1007-G1013 ◽  
Author(s):  
Yoshinori Horie ◽  
Robert Wolf ◽  
D. Neil Granger
Keyword(s):  
Nitric Oxide ◽  
Important Determinant ◽  
Leukocyte Adhesion ◽  
Ischemia Reperfusion ◽  
Protective Action ◽  
Microvascular Dysfunction ◽  
Artery Occlusion ◽  
No Donor ◽  
Synthase Inhibitor

The overall objective of this study was to assess the contribution of an altered bioavailability of nitric oxide (NO) to the leukocyte adhesion and hypoxic stress elicited in the liver by gut ischemia-reperfusion (I/R). The accumulation of leukocytes, number of nonperfused sinusoids (NPS), and NADH autofluorescence were monitored (by intravital microscopy) in mouse liver after 15 min of superior mesenteric artery occlusion and 60 min of reperfusion. Leukostasis, NPS, and NADH autofluorescence (indicating hypoxia) were all increased in the liver at 60 min after gut I/R. The NO synthase inhibitor N G-monomethyl-l-arginine (l-NMMA) exaggerated the liver leukostasis elicited by gut I/R, responses that were prevented by coadministration of l-arginine. The NO donor diethylenetriamine-NO (DETA-NO) andl-arginine were both effective in attenuating the gut I/R-induced leukostasis and increased NADH autofluorescence, whereas neither DETA nord-arginine exerted a protective action. These findings indicate that NO is an important determinant of the liver leukostasis, impaired sinusoidal perfusion, and tissue hypoxia elicited by gut I/R.

Does local heating-induced nitric oxide production attenuate vasoconstrictor responsiveness to lower body negative pressure in human skin?

2007 ◽  
Vol 102 (5) ◽  
pp. 1839-1843 ◽  
Author(s):  
David A. Low ◽  
Manabu Shibasaki ◽  
Scott L. Davis ◽  
David M. Keller ◽  
Craig G. Crandall
Keyword(s):  
Nitric Oxide ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Local Heating ◽  
Ringer Solution ◽  
No Production ◽  
Lower Body ◽  
Forearm Skin ◽  
Per Se ◽  
Cutaneous Vascular Conductance

We tested the hypothesis that local heating-induced nitric oxide (NO) production attenuates cutaneous vasoconstrictor responsiveness. Eleven subjects (6 men, 5 women) had four microdialysis membranes placed in forearm skin. Two membranes were perfused with 10 mM of NG-nitro-l-arginine (l-NAME) and two with Ringer solution (control), and all sites were locally heated to 34°C. Subjects then underwent 5 min of 60-mmHg lower body negative pressure (LBNP). Two sites (a control and an l-NAME site) were then heated to 39°C, while the other two sites were heated to 42°C. At the l-NAME sites, skin blood flow was elevated using 0.75–2 mg/ml of adenosine in the perfusate solution (Adn + l-NAME) to a similar level relative to control sites. Subjects then underwent another 5 min of 60-mmHg LBNP. At 34°C, cutaneous vascular conductance (CVC) decreased (Δ) similarly at both control and l-NAME sites during LBNP (Δ7.9 ± 3.0 and Δ3.4 ± 0.8% maximum, respectively; P > 0.05). The reduction in CVC to LBNP was also similar between control and Adn + l-NAME sites at 39°C (control Δ11.4 ± 2.5 vs. Adn + l-NAME Δ7.9 ± 2.0% maximum; P > 0.05) and 42°C (control Δ1.9 ± 2.7 vs. Adn + l-NAME Δ 4.2 ± 2.7% maximum; P > 0.05). However, the decrease in CVC at 42°C, regardless of site, was smaller than at 39°C ( P < 0.05). These results do not support the hypothesis that local heating-induced NO production attenuates cutaneous vasoconstrictor responsiveness during high levels of LBNP. However, elevated local temperature, per se, attenuates cutaneous vasoconstrictor responsiveness to LBNP, presumably through non-nitric oxide mechanisms.

scholarly journals Cyclooxygenase and nitric oxide synthase dependence of cutaneous reactive hyperemia in humans

2007 ◽  
Vol 293 (1) ◽  
pp. H425-H432 ◽  
Author(s):  
Marvin S. Medow ◽  
Indu Taneja ◽  
Julian M. Stewart
Keyword(s):  
Nitric Oxide ◽  
Peak Flow ◽  
Reactive Hyperemia ◽  
Laser Doppler ◽  
Doppler Flowmetry ◽  
Time To Peak ◽  
Flow Parameters ◽  
Cox Inhibitor ◽  
Cutaneous Circulation ◽  
Synthase Inhibitor

We tested the hypothesis that cyclooxygenases (COXs) or COX products inhibit nitric oxide (NO) synthesis and thereby mask potential effects of NO on reactive hyperemia in the cutaneous circulation. We performed laser-Doppler flowmetry (LDF) with intradermal microdialysis in 12 healthy volunteers aged 19–25 yr. LDF was expressed as the percent cutaneous vascular conduction (%CVC) or as the maximum %CVC (%CVCmax) where CVC is LDF/mean arterial pressure. We tested the effects of the nonisoform-specific NO synthase inhibitor nitro-l-arginine (NLA, 10 mM), the nonspecific COX inhibitor ketorolac (Keto, 10 mM), combined NLA + Keto, and NLA + sodium nitroprusside (SNP, 28 mM) on baseline and reactive hyperemia flow parameters. We also examined the effects of isoproterenol, a β-adrenergic agonist that causes prostaglandin-independent vasodilation to correct for the increase in baseline flow caused by Keto. When delivered directly into the intradermal space, Keto greatly augments all aspects of the laser-Doppler flow response to reactive hyperemia: peak reactive hyperemic flow increased from 41 ± 5 to 77 ± 7%CVCmax, time to peak flow increased from 17 ± 3 to 56 ± 24 s, the area under the reactive hyperemic curve increased from 1,417 ± 326 to 3,376 ± 876%CVCmax·s, and the time constant for the decay of peak flow increased from 100 ± 23 to 821 ± 311 s. NLA greatly attenuates the Keto response despite exerting no effects on baseline LDF or on reactive hyperemia when given alone. Low-dose NLA + SNP duplicates the Keto response. Isoproterenol increased baseline and peak reactive flow. These results suggest that COX inhibition unmasks NO dependence of reactive hyperemia in human cutaneous circulation.

scholarly journals Microcirculation as a goal of correction in macroangiopathy (atherogenesis)

2020 ◽  
pp. 80-81
Author(s):  
O.B. Dynnyk
Keyword(s):  
Nitric Oxide ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Carotid Artery ◽  
Laser Doppler Flowmetry ◽  
Common Carotid Artery ◽  
Carotid Arteries ◽  
Clinical Settings ◽  
Healthy Individuals ◽  
Doppler Flowmetry

Background. The microcirculatory system (MCS) is a network of blood vessels that includes arterioles, capillaries, venules, and terminal lymphatic vessels. Microcirculation is characterized by the constant variability. Factors of atherogenesis development due to MCS dysfunction include shear stress, hyperglycemia, dyslipidemia, systemic and local inflammation, hypoxia and endothelial dysfunction mediated by oxidative stress. Laser Doppler flowmetry (LDF) is used to study microcirculation in the clinical settings. The advantages of LDF include simplicity, accessibility and non-invasiveness. Objective. To describe the features of microcirculation disorders and their elimination. Materials and methods. Analysis of literature data on this topic; own study. The study involved 98 patients (59 females; 39 males) with a mean age of 52.0 years. The first group consisted of patients with coronary heart disease (CHD) and chronic heart failure of I-IIA grades, the second – of relatively healthy individuals. All patients underwent LDF, ultrasound examination of the carotid arteries, and determination of anthropometric parameters. Results and discussion. MCS dysfunction is not only a risk factor for atherogenesis, but also a trigger for its acute complications (myocardial infarction, stroke, sudden death). Nitric oxide (NO) deficiency plays an important role in this. A potential target of therapeutic influence in the treatment of coronary heart disease is not only macrovascular system, but also vasa vasorum. The condition of the latter determines the course of atherosclerosis. According to the results of our own study, patients with CHD demonstrated a muscle mass decrease, an increase in waist and hip circumference, and in body mass index. In addition, the groups differed in thickness of the intima-media complex of both common carotid arteries (right common carotid artery: CHD group – 0.79±0.18 mm; group of relatively healthy individuals – 0.69±0.13 mm, p<0,05; left common carotid artery: CHD group – 0.81±0.19 mm, group of relatively healthy individuals – 0.70±0.14 mm, p<0,05). When assessing the indicators of wavelet analysis of LDF, a significant decrease in the rate of microcirculation and capillary blood flow reserve is revealed in the CHD group, as well as an increase in peripheral vascular resistance. According to previous own studies, sorbitol (Reosorbilact, “Yuria-Pharm”) and pentoxifylline (Latren, “Yuria-Pharm”) can be used to correct microcirculation disorders. The use of these drugs leads to vasodilation of precapillary sphincters and improvement of regional microperfusion. Conclusions. 1. Disorders of MCS are the pathogenetic factors of the atherogenesis. 2. Laser Doppler flowmetry is used to study microcirculation in the clinical settings. 3. In patients with CHD there is an increase in neuro- and myotonus of the MCS, which is associated with the impaired release of nitric oxide. 4. Changes in microcirculation contribute to the development of atherosclerosis, which should be taken into account when choosing treatment for such patients. 5. Sorbitol (Reosorbilact) and pentoxifylline (Latren) can be used to correct microcirculation disorders.

Sex differences and role of nitric oxide in blood flow of canine urinary bladder

1999 ◽  
Vol 276 (2) ◽  
pp. R407-R413 ◽  
Author(s):  
Michel A. Pontari ◽  
Michael R. Ruggieri
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Intravesical Pressure ◽  
Bladder Mucosa ◽  
Arterial Infusion ◽  
Nitric Oxide Synthase Inhibitor ◽  
Doppler Flowmetry ◽  
Muscle Perfusion ◽  
Anesthetized Dogs ◽  
Synthase Inhibitor

Continuous measurements were made of bladder blood flow by laser Doppler flowmetry in anesthetized dogs during bladder filling and emptying. In both mucosa and muscle, perfusion was inversely proportional to intravesical pressure. There was significantly greater perfusion in the bladder mucosa of males than females at baseline and up to 10 cm water filling pressure but not in the muscle. Intra-arterial infusion of the nitric oxide synthase inhibitor N G-nitro-l-arginine produced a significant decrease in resting bladder perfusion in the mucosa only, with no differences seen in the response to intravesical pressure. Intra-arterial infusion ofl-arginine produced a significant increase in the level of perfusion in the mucosa seen immediately after the bladder was drained. No changes were observed in muscle perfusion afterl-arginine. These results suggest that the perfusion of the bladder mucosa differs by gender and is regulated differently than the bladder muscle, possibly related to the different function of the two layers.

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