Nitric oxide-dependent opposite effects of somatostatin on arterial and venous caliber in situ

1996 ◽  
Vol 271 (6) ◽  
pp. H2238-H2245
Author(s):  
M. Szentivanyi ◽  
G. L. Nadasy ◽  
L. Dezsi ◽  
G. Mozes ◽  
T. Tulassay ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Saphenous Vein ◽  
Vessel Diameter ◽  
Outer Diameter ◽  
Synthesis Inhibitor ◽  
Vascular Effects ◽  
Venous Diameter ◽  
Arteries And Veins ◽  
Saphenous Artery

The vascular effects of somatostatin (ST) and its mechanism of action are not well understood. In the present study, we investigated the direct effects of ST on the vascular tone of rat saphenous artery and vein using videomicroangiometry in situ. ST was administered either in superfusion or in infusion. We found opposite effects in arteries and veins: ST (10(-12)-10(-7) M) dilated the artery (outer diameter increased from 533 +/- 28 to 600 +/- 29 microns, administered in superfusion) and contracted the vein (from 709 +/- 26 to 640 +/- 26 microns and from 775 +/- 30 to 708 +/- 60 microns in superfusion and infusion, respectively). These effects of ST were completely abolished after deendothelization (air bolus maintained for 6 min in vessel lumen) and after local infusion of NG-nitro-L-arginine (L-NNA; 10(-4) M), a nitric oxide (NO) synthesis inhibitor. An NO-dependent basal vasodilator tone in the rat saphenous vein responsible for 10.9 +/- 0.3% of the total vessel diameter was found. After ST administration the venous diameter reduction was similar to that measured after deendothelization or L-NNA. We conclude that ST in situ induces NO release from endothelial cells of rat saphenous artery causing vasodilation, whereas, in contrast, it inhibits the basal NO-dependent vasodilator tone of the saphenous vein inducing vasoconstriction.

scholarly journals Nitrite anion stimulates ischemic arteriogenesis involving NO metabolism

2012 ◽  
Vol 303 (2) ◽  
pp. H178-H188 ◽  
Author(s):  
Shyamal C. Bir ◽  
Christopher B. Pattillo ◽  
Sibile Pardue ◽  
Gopi K. Kolluru ◽  
John Docherty ◽  
...  
Keyword(s):  
Sodium Nitrite ◽  
Vascular Remodeling ◽  
Vessel Diameter ◽  
Immunofluorescent Staining ◽  
Dependent Manner ◽  
Tissue Ischemia ◽  
Ischemic Tissue ◽  
Saphenous Artery ◽  
Profunda Femoris

Nitric oxide (NO) is a potential regulator of ischemic vascular remodeling, and as such therapies augmenting its bioavailability may be useful for the treatment of ischemic tissue diseases. Here we examine the effect of administering the NO prodrug sodium nitrite on arteriogenesis activity during established tissue ischemia. Chronic hindlimb ischemia was induced by permanent unilateral femoral artery and vein ligation. Five days postligation; animals were randomized to control PBS or sodium nitrite (165 μg/kg) therapy twice daily. In situ vascular remodeling was measured longitudinally using SPY angiography and Microfil vascular casting. Delayed sodium nitrite therapy rapidly increased ischemic limb arterial vessel diameter and branching in a NO-dependent manner. SPY imaging angiography over time showed that nitrite therapy enhanced ischemic gracillis collateral vessel formation from the profunda femoris to the saphenous artery. Immunofluorescent staining of smooth muscle cell actin also confirmed that sodium nitrite therapy increased arteriogenesis in a NO-dependent manner. The NO prodrug sodium nitrite significantly increases arteriogenesis and reperfusion of established severe chronic tissue ischemia.

Shear stress-induced nitric oxide antagonizes adenosine effects on intestinal metabolism

1999 ◽  
Vol 276 (5) ◽  
pp. G1227-G1234
Author(s):  
Chao Han ◽  
Zhi Ming ◽  
W. Wayne Lautt
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Constant Pressure ◽  
Lactate Production ◽  
Metabolic Effects ◽  
Stress Perfusion ◽  
Vascular Effects ◽  
No Donor ◽  
Isolated Segment

The influence of nitric oxide (NO) on adenosine-induced metabolic effects was studied in the intestine. Blood flow supplied an in situ- isolated segment of small intestine in anesthetized cats via the superior mesenteric artery (SMA) and was controlled by a vascular circuit. The SMA and portal samples were taken for analysis of oxygen and lactate. Adenosine (0.4 mg ⋅ kg−1 ⋅ min−1, intra-SMA) reduced oxygen consumption by 25.1 ± 2.9 from 73.1 ± 10.8 μmol ⋅ min−1 ⋅ 100 g−1 and increased lactate production by 13.3 ± 3.0 from 12.8 ± 4.6 μmol ⋅ min−1 ⋅ 100 g tissue−1 during constant-flow (CF, decreased shear stress) but not during constant-pressure (CP, increased shear stress) perfusion. Blockade of NO synthase using N ω-nitro-l-arginine methyl ester did not affect the metabolic effects of adenosine during CF but eliminated the differences seen between CP and CF perfusion. A NO donor, 3-morpholinosydnonimine, attenuated the metabolic effects of adenosine during CF perfusion. The results suggested that shear-induced NO antagonized metabolic effects of adenosine but that the inhibition of vascular effects by NO was not shear dependent since it occurred in both CP and CF perfusion.

scholarly journals Nitric oxide regulates retinal vascular tone in humans

2003 ◽  
Vol 285 (2) ◽  
pp. H631-H636 ◽  
Author(s):  
Guido T. Dorner ◽  
Gerhard Garhofer ◽  
Barbara Kiss ◽  
Elzbieta Polska ◽  
Kaija Polak ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Retinal Vessel ◽  
Vessel Diameter ◽  
Arterial Diameter ◽  
Retinal Vessel Diameter ◽  
Venous Diameter ◽  
Flicker Stimulation ◽  
Young Subjects

The purpose of the present study was to investigate the contribution of basal nitric oxide (NO) on retinal vascular tone in humans. In addition, we set out to elucidate the role of NO in flicker-induced retinal vasodilation in humans. Twelve healthy young subjects were studied in a three-way crossover design. Subjects received an intravenous infusion of either placebo or NG-monomethyl-l-arginine (l-NMMA; 3 or 6 mg/kg over 5 min), an inhibitor of NO synthase. Thereafter, diffuse luminance flicker was consecutively performed for 16, 32, and 64 s at a frequency of 8 Hz. The effect of l-NMMA on retinal arterial and venous diameter was assessed under resting conditions and during the hyperemic flicker response. Retinal vessel diameter was measured with a Zeiss retinal vessel analyzer. l-NMMA significantly reduced arterial diameter (3 mg/kg: –2%; 6 mg/kg: –4%, P < 0.001) and venous diameter (3 mg/kg: –5%; 6 mg/kg: –8%, P < 0.001). After placebo infusion, flicker induced a significant increase in retinal vessel diameter ( P < 0.001). At a flicker duration of 64 s, arterial diameter increased by 4% and venous diameter increased by 3%. l-NMMA did not abolish these hyperemic responses but blunted venous vasodilation ( P = 0.017) and arterial vasodilation ( P = 0.02) in response to flicker stimulation. Our data indicate that NO contributes to basal retinal vascular tone in humans. In addition, NO appears to play a role in flicker-induced vasodilation of the human retinal vasculature.

Acute depletion of heme by succinylacetone alters vascular responses but does not induce hypertension

2008 ◽  
Vol 86 (9) ◽  
pp. 613-619 ◽  
Author(s):  
Jonathan Soong ◽  
Michael A. Adams ◽  
Kanji Nakatsu
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Aminolevulinic Acid ◽  
Critical Role ◽  
High Dose ◽  
Compensatory Mechanisms ◽  
Irreversible Inhibitor ◽  
Synthesis Inhibitor ◽  
Vascular Effects ◽  
No Donor

Heme plays a critical role in blood pressure regulation because it is required by a number of enzymes that synthesize vascular modulators, including nitric oxide (NO), carbon monoxide (CO), guanosine 3′,5′-cyclic monophosphate (cGMP), endothelium-derived hyperpolarizing factor (EDHF), and prostacyclin. The goal of this study was to examine the vascular effects of a short-term depletion of heme achieved through administration of the heme-synthesis inhibitor succinylacetone (SA), an irreversible inhibitor of aminolevulinic acid dehydratase (ALAD). Rats were depleted of heme by using a 4-day treatment with SA. This treatment impacted hemoenzyme function, decreasing renal nitric oxide synthase (NOS) activity (as indicated by decreased in vitro NOS activity), and increasing kidney microsomal heme oxygenase (HO) activity by 27%. SA treatment also resulted in enhanced reduction in blood pressure after infusions of exogenous NO donor MAHMA NONOate (at high dose) and acetylcholine (at low doses). Nevertheless, this SA treatment was insufficient to produce an overt elevation of basal arterial pressure. This latter lack of effect may be the result of multiple compensatory mechanisms for the regulation of blood pressure.

A New Supermicrosurgery Training Model of Saphenous Artery and Great Saphenous Vein Anastomosis for Development of Advanced Microsurgical Skills

2017 ◽  
Vol 33 (06) ◽  
pp. 426-434 ◽  
Author(s):  
Can Bas ◽  
Joanna Cwykiel ◽  
Maria Siemionow
Keyword(s):  
Saphenous Vein ◽  
Great Saphenous Vein ◽  
Training Model ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
End To End ◽  
The One ◽  
The Right ◽  
Arteries And Veins ◽  
Saphenous Artery

Background This study aimed to confirm the feasibility and reliability of saphenous artery (SA) and great saphenous vein (GSV) anastomosis as a new supermicrosurgery training model and to compare the one-way-up anastomosis with the currently used end-to-end anastomosis technique. Methods Twenty supermicrosurgical anastomoses were performed in 10 Sprague Dawley rats. The external diameters of SA and GSV were measured using Leica LAS EZ software. The right-side SA and GSV anastomoses were performed using the standard end-to-end anastomosis technique. The left-side SA and GSV anastomoses were performed using the one-way-up technique with 11–0 monofilament-interrupted sutures. The duration of the surgery, patency rates, and technical challenges of the two anastomoses methods were compared. Results The mean external diameters of SA and GSV were 0.273 ± 0.03 and 0.291 ± 0.02 mm, respectively, which qualify these vessels for supermicrosurgical training. The vessels were easily accessible and both anastomosis techniques were feasible. The one-way-up technique was proven to be faster as compared with the end-to-end anastomosis technique (artery: 34 ± 2.55 vs. 40.4 ± 2.97 minutes, p = 0.02; and vein: 37 ± 4.85 vs. 44 ± 2.35 minutes, p = 0.05, respectively). Short-term patency rates for arteries and veins were 100% for both techniques. Seven-day anastomosis patency rates for arteries and veins were 80 and 100% for the end-to-end technique and 100 and 80% for the one-way-up technique, respectively. Conclusions We confirmed that saphenous pedicle is suitable for creating a supermicrosurgery training model for practicing the ultrafine motor skills. To the best of our knowledge, this is the first report on supermicrosurgery of SA and GSV in the rat model.

Morphometric characteristics of competent proximal valves of the great saphenous vein and superficial femoral vein in vivo according to ultrasound angioscanning data

2019 ◽  
Vol 18 (3) ◽  
pp. 16-22
Author(s):  
E. K. Gavrilov ◽  
H. L. Bolotokov ◽  
E. A. Babinets
Keyword(s):  
Saphenous Vein ◽  
Great Saphenous Vein ◽  
Femoral Vein ◽  
Lower Boundary ◽  
Average Diameter ◽  
Lower Limbs ◽  
Functional Test ◽  
Natural Form ◽  
Superficial Femoral Vein ◽  
Venous Diameter

Introduction. It seems relevant to study the ultrasound anatomy and physiology of the proximal valve segments of the superficial femoral vein (SFV) and the great saphenous vein (GSV) to develop effective reconstructive surgical interventions on venous valves in chronic vein diseases.The aim of the survey was to study the ultrasound anatomy of the venous wall, the size and shape of the proximal SFV and GSV valves are normal at rest and during the functional test Valsalva.Material and methods. Proximal valve SFV studies were performed in 144 lower limbs in 115 people (mean age 51.1 ± 14.4 years, 60 women and 55 men), proximal GSV valves studies - in 82 lower limbs in 67 persons (average age 45, 1 ± 13.3 years, 33 women, 34 men). A longitudinal and transverse ultrasound scanning of the femoral vein bifurcation and safenofemoral junction areas were performed, the structures of the proximal SFV and GSV valves were visualized, the valve shape was measured and the diameter of the veins was measured at the level valves at the base of the valves (inlet diameter), at the point of maximum ectasia (diameter of ectasia), at the upper border of the valve (diameter of the outlet), as well as measuring the length of the valve a (length to ectasia, the total length of the valve). The degree of ectasia over the valve was judged by calculating the relative venous diameter change (RVDC).Results. the average diameter of the SFV at the level of the lower boundary of its first valve was 10.01 ± 1.44 mm. The average diameter of the SFV at the level of the maximum ectasia of its first valve was 13,1±2 mm. The average value of the index of RVDC for SFV was 31%±10,4%. An increase in the diameter of the vein in the zone of supravalvular ectasia up to 20% corresponded to the spindle-shaped valve, more than 20% - to the clavate form, which was noted in the majority of the examined. The change in the relative venous diameter of the SFV on the Valsalva test was 38,2%±12,4%. The average diameter of the GSV at the base of the first valves was 6,07±1,25 mm. The average diameter of the GSV at the level of the maximum ectasia of the osteal valve was 9,44±1,69 mm. The average RVDC for GSV was 58%±24%.Conclusion. the natural form of proximal SFV and GSV valves is clavate with presence of the significant supravalvular ectasia, which was noted in the majority of the subjects alone and in all during the performance of the Valsalva functional test.

scholarly journals Selective estrogen receptor-α and estrogen receptor-β agonists rapidly decrease pulmonary artery vasoconstriction by a nitric oxide-dependent mechanism

2008 ◽  
Vol 295 (5) ◽  
pp. R1486-R1493 ◽  
Author(s):  
Tim Lahm ◽  
Paul R. Crisostomo ◽  
Troy A. Markel ◽  
Meijing Wang ◽  
Yue Wang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Estrogen Receptor ◽  
Pulmonary Artery ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Organ Bath ◽  
Sprague Dawley ◽  
Response Curves ◽  
Vascular Effects ◽  
M 10 ◽  
Dependent Mechanism

Both endogenous and exogenous estrogen decrease pulmonary artery (PA) vasoconstriction. Whether these effects are mediated via estrogen receptor (ER)-α or ER-β, and whether the contribution of ERs is stimulus-dependent, remains unknown. We hypothesized that administration of the selective ER-α agonist propylpyrazole triol (PPT) and/or the selective ER-β agonist diarylpropiolnitrile (DPN) rapidly decreases PA vasoconstriction induced by pharmacologic and hypoxic stimuli via a nitric oxide (NO)-dependent mechanism. PA rings ( n = 3–10/group) from adult male Sprague-Dawley rats were suspended in physiologic organ baths. Force displacement was measured. Vasoconstrictor responses to phenylephrine (10−8M − 10−5M) and hypoxia (Po2 35–45 mmHg) were determined. Endothelium-dependent and -independent vasorelaxation were measured by generating dose-response curves to acetylcholine (10−8M − 10−4M) and sodium nitroprusside (10−9M − 10−5M). PPT or DPN (10−9M − 5 × 10−5M) were added to the organ bath in the presence and absence of the NO-synthase inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) (10−4M). Selective ER-α activation (PPT, 5 × 10−5M) rapidly (<20 min) decreased phenylephrine-induced vasoconstriction. This effect, as well as PPT's effects on endothelium-dependent vasorelaxation, were neutralized by l-NAME. In contrast, selective ER-β activation (DPN, 5 × 10−5M) rapidly decreased phase II of hypoxic pulmonary vasoconstriction (HPV). l-NAME eliminated this phenomenon. Lower PPT or DPN concentrations were less effective. We conclude that both ER-α and ER-β decrease PA vasoconstriction. The immediate onset of effect suggests a nongenomic mechanism. The contribution of specific ERs appears to be stimulus specific, with ER-α primarily modulating phenylephrine-induced vasoconstriction, and ER-β inhibiting HPV. NO inhibition eliminates these effects, suggesting a central role for NO in mediating the pulmonary vascular effects of both ER-α and ER-β.

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