Effect of NO, phenylephrine, and hypoxemia on ductus venosus diameter in fetal sheep

2000 ◽  
Vol 279 (3) ◽  
pp. H1166-H1171 ◽  
Author(s):  
Torvid Kiserud ◽  
Takashi Ozaki ◽  
Hidenori Nishina ◽  
Charles Rodeck ◽  
Mark A. Hanson
Keyword(s):  
Nitric Oxide ◽  
Carotid Artery ◽  
Common Carotid Artery ◽  
Umbilical Vein ◽  
Ductus Venosus ◽  
Adrenergic Agonist ◽  
Fetal Sheep ◽  
Vasoactive Substances ◽  
Ultrasound Measurements

To study the regulation of the ductus venosus (DV) inlet in vivo, we measured the effect of vasoactive substances and hypoxemia on its diameter in nine fetal sheep in utero at 0.9 gestation under ketamine-diazepam anesthesia. Catheters were inserted into an umbilical vein and a fetal common carotid artery, and a flowmeter was placed around the umbilical veins. Ultrasound measurements of the diameter of the fetal DV during normoxic baseline conditions [fetal arterial Po2(Pao2) 24 mmHg] were compared with measurements during infusion of sodium nitroprusside (SNP; 1.3, 2.6, and 6.5 μg · kg−1· min−1) or the α1-adrenergic agonist phenylephrine (6.5 μg · kg−1· min−1) into the umbilical vein or during hypoxemia (fetal PaO2reduced to 10 mmHg). SNP increased the DV inlet diameter by 23%, but phenylephrine had no effect. Hypoxemia caused a 61% increase of the inlet diameter and a distension of the entire vessel. We conclude that the DV inlet is tonically constricted, because nitric oxide dilates it but an α1-adrenergic agonist does not potentiate constriction. Hypoxemia causes a marked distension of the entire DV.

scholarly journals Endothelial Nitric Oxide Synthase Pathophysiology after Nonocclusive Common Carotid Artery Thrombosis in Rats

2002 ◽  
Vol 22 (5) ◽  
pp. 612-619 ◽  
Author(s):  
Gary H. Danton ◽  
Ricardo Prado ◽  
Jessie Truettner ◽  
Brant D. Watson ◽  
W. Dalton Dietrich
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Carotid Artery ◽  
Middle Cerebral Artery ◽  
Common Carotid Artery ◽  
Endothelial Nitric Oxide Synthase ◽  
Carotid Artery Thrombosis ◽  
Artery Thrombosis ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Although vascular dysregulation has been documented in patients with extracranial vascular disease, transient ischemic attacks, and stroke, the pathomechanisms are poorly understood. To model thromboembolic stroke in rats, photochemically induced nonocclusive common carotid artery thrombosis (CCAT) was used to generate a platelet thrombus in the carotid artery of anesthetized rats. After CCAT, platelet aggregates break off the thrombus, travel to the distal cerebral vasculature, damage blood vessels, and cause small infarctions. The authors hypothesized that deficits in the endothelial nitric oxide synthase (eNOS) pathway may be responsible for vascular dysfunction after embolic stroke. To examine the functional status of the eNOS system, they measured eNOS-dependent dilation after CCAT by applying acetylcholine through a cranial window over the middle cerebral artery. The authors also measured eNOS mRNA and protein in the middle cerebral artery to determine whether functional changes were caused by alterations in expression. eNOS-dependent dilation was reduced at 6 hours, elevated at 24 hours, and returned to baseline 72 hours after CCAT. Endothelial nitric oxide synthase mRNA increased at 2 hours and was followed by a rise in protein 24 hours after CCAT. Changes in the eNOS system may account for some of the observed vascular deficits in patients with cerebrovascular disease.

Hydrogen sulfide downregulates the aortic l-arginine/nitric oxide pathway in rats

2007 ◽  
Vol 293 (4) ◽  
pp. R1608-R1618 ◽  
Author(s):  
Bin Geng ◽  
Yuying Cui ◽  
Jing Zhao ◽  
Fang Yu ◽  
Yi Zhu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Umbilical Vein ◽  
Transcript Abundance ◽  
Inhibitory Effect ◽  
Akt Phosphorylation ◽  
Enos Activity ◽  
Nos Inhibitors

The aim of the present study was to investigate the effect of hydrogen sulfide (H2S) signaling by nitric oxide (NO) in isolated rat aortas and cultured human umbilical vein endothelial cells (HUVECs). Both administration of H2S and NaHS, as well as endogenous H2S, reduced NO formation, endothelial nitric oxide synthase (eNOS) activity, eNOS transcript abundance, and l-arginine (l-Arg) transport (all P < 0.01). The kinetics analysis of eNOS activity and l-Arg transport showed that H2S reduced Vmax values (all P < 0.01) without modifying Km parameters. Use of selective NOS inhibitors verified that eNOS [vs. inducible NOS (iNOS) and neuronal NOS (nNOS)] was the specific target of H2S regulation. H2S treatment (100 μmol/l) reduced Akt phosphorylation and decreased eNOS phosphorylation at Ser1177. H2S reduced l-Arg uptake by inhibition of a system y+ transporter and decreased the CAT-1 transcript. H2S treatment reduced protein expression of eNOS but not of nNOS and iNOS. Pinacidil (KATP channel opener) exhibited the similar inhibitory effects on the l-Arg/NOS/NO pathway. Glibenclamide (KATP channel inhibitor) partly blocked the inhibitory effect of H2S and pinacidil. An in vivo experiment revealed that H2S downregulated the vascular l-Arg/eNOS/NO pathway after intraperitoneal injection of NaHS (14 μmol/kg) in rats. Taken together, our findings suggest that H2S downregulates the vascular l-Arg/NOS/NO pathway in vitro and in vivo, and the KATP channel could be involved in the regulatory mechanism of H2S.

scholarly journals Normalization of Endothelial and Inducible Nitric Oxide Synthase Expression in Brain Microvessels of Spontaneously Hypertensive Rats by Angiotensin II AT1 Receptor Inhibition

2003 ◽  
Vol 23 (3) ◽  
pp. 371-380 ◽  
Author(s):  
Haruki Yamakawa ◽  
Miroslava Jezova ◽  
Hiromichi Ando ◽  
Juan M. Saavedra
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Carotid Artery ◽  
Common Carotid Artery ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Brain Microvessels ◽  
Receptor Inhibition ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Inhibition of angiotensin II AT1 receptors protects against stroke, reducing the cerebral blood flow decrease in the periphery of the ischemic lesion. To clarify the mechanism, spontaneously hypertensive rats (SHR) and normotensive control Wistar Kyoto (WKY) rats were pretreated with the AT1 receptor antagonist candesartan (0.3 mg · kg−1 · d−1) for 28 days, a treatment identical to that which protected SHR from brain ischemia, and the authors studied middle cerebral artery (MCA) and common carotid morphology, endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) messenger RNA (mRNA), and protein expression in cerebral microvessels, principal arteries of the Willis polygon, and common carotid artery. The MCA and common carotid artery of SHR exhibited inward eutrophic remodeling, with decreased lumen diameter and increased media thickness when compared with WKY rats. In addition, there was decreased eNOS and increased iNOS protein and mRNA in common carotid artery, circle of Willis, and brain microvessels of SHR when compared with WKY rats. Both remodeling and alterations in eNOS and iNOS expression in SHR were completely reversed by long-term AT1 receptor inhibition. The hemodynamic, morphologic, and biochemical alterations in hypertension associated with increased vulnerability to brain ischemia are fully reversed by AT1 receptor blockade, indicating that AT1 receptor activation is crucial for the maintenance of the pathologic alterations in cerebrovascular circulation during hypertension, and that their blockade may be of therapeutic advantage.

Evaluating endothelial function of the common carotid artery: An in vivo human model

2009 ◽  
Vol 19 (3) ◽  
pp. 205-210 ◽  
Author(s):  
S. Mazzucco ◽  
F. Bifari ◽  
M. Trombetta ◽  
G.C. Guidi ◽  
M. Mazzi ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Endothelial Function ◽  
Common Carotid Artery ◽  
Human Model ◽  
The Common

Progressive Attenuation of the Longitudinal Kinetics in the Common Carotid Artery: Preliminary in Vivo Assessment

2015 ◽  
Vol 41 (1) ◽  
pp. 339-345 ◽  
Author(s):  
Guillaume Zahnd ◽  
Simone Balocco ◽  
André Sérusclat ◽  
Philippe Moulin ◽  
Maciej Orkisz ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Common Carotid Artery ◽  
The Common ◽  
In Vivo Assessment

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.

Vascular hyporesponsiveness in simulated microgravity: role of nitric oxide-dependent mechanisms

2000 ◽  
Vol 88 (2) ◽  
pp. 507-517 ◽  
Author(s):  
D. Sara Sangha ◽  
N. D. Vaziri ◽  
Y. Ding ◽  
R. E. Purdy
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Carotid Artery ◽  
Femoral Artery ◽  
Simulated Microgravity ◽  
Fold Increase ◽  
Mechanical Removal ◽  
Inducible Nos

Simulated microgravity depresses the ability of arteries to constrict to norepinephrine (NE). In the present study the role of nitric oxide-dependent mechanisms on the vascular hyporesponsiveness to NE was investigated in peripheral arteries of the rat after 20 days of hindlimb unweighting (HU). Blood vessels from control rats and rats subjected to HU (HU rats) were cut into 3-mm rings and mounted in tissue baths for the measurement of isometric contraction. Mechanical removal of the endothelium from carotid artery rings, but not from aorta or femoral artery rings, of HU rats restored the contractile response to NE toward control. A 10-fold increase in sensitivity to ACh was observed in phenylephrine-precontracted carotid artery rings from HU rats. In the presence of the nitric oxide synthase (NOS) substratel-arginine, the inducible NOS inhibitor aminoguanidine (AG) restored the contractile responses to NE to control levels in the femoral, but not carotid, artery rings from HU rats. In vivo blood pressure measurements revealed that the peak blood pressure increase to NE was significantly greater in the control than in the HU rats, but that to AG was less than one-half in control compared with HU rats. These results indicate that the endothelial vasodilator mechanisms may be upregulated in the carotid artery, whereas the inducible NOS expression/activity may be increased in the femoral artery from HU rats. These HU-mediated changes could produce a sustained elevation of vascular nitric oxide levels that, in turn, could contribute to the vascular hyporesponsiveness to NE.

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