Remote effects of pressure changes in arterioles

1995 ◽  
Vol 268 (3) ◽  
pp. H1379-H1382 ◽  
Author(s):  
R. J. Rivers

Blood is distributed to match the demands of the tissue in accordance with the local effectors of pressure, flow, nerves, and metabolites. Influences of these effectors are integrated and communicated to larger vessels to create a coordinated upstream response that allows for the blood required to meet the metabolic demands of the tissue. Each effector's contribution to the communicated response is unknown. In the present study in situ segments of arteriole, within the cheek pouch of the anesthetized hamster, were isolated from the pressure and flow of the surrounding vasculature while maintaining electrotonic continuity. Pressure was transiently increased or decreased (-70 to +120 cmH2O) for 60 s. These pressure changes within the isolated segment caused myogenic responses within the isolated segment as well as changes in diameter at remote arteriolar locations (ranging from -8 to 5 microns) that were outside the isolated segment and insulated from the changes in pressure. The size of the remote response correlated significantly with the change in pressure inside the isolated segment. This demonstrates that the effects of pressure changes in arterioles are communicated to neighboring portions of the vasculature.

1997 ◽  
Vol 272 (6) ◽  
pp. H2895-H2901 ◽  
Author(s):  
R. J. Rivers

Conducted vasodilation occurs remotely from a site of microapplication of a drug. Intravascular pressure is required for a conducted response in vivo, yet in vitro studies in unpressurized arterioles show pressure is not essential. To determine how pressure affects conducted vasodilation, intra-arteriolar pressure was controlled within an in situ isolated segment (average length 950 +/- 96 microns, average baseline diameter 28 +/- 2.1 microns) of arterioles in the hamster cheek pouch. Methacholine (10(-4) M, 5 s) was microapplied either onto the isolated segment or remotely, with local and conducted vasodilation measured at both locations. Increasing pressure in the lumen of the segment (0-80 cmH2O) increased the segment local dilation to methacholine, and the segment-conducted dilation plateaued (at 4.1 +/- 0.8 micron) when segment pressure reached 20 cmH2O. Any local (16 +/- 1.5 microns) and conducted (4.4 +/- 1.3 microns) dilations viewed outside the segment were unaffected by segment pressure and persisted in its absence. Thus segment pressure affected only electromechanical transduction of the conducted response. Thus vasomotor signals move throughout the vasculature regardless of tone, but tone is essential to transduce the response.


2001 ◽  
Author(s):  
Richard L. Johnson ◽  
Paul C. Johnson ◽  
Tim L. Johnson ◽  
Neil Thomas ◽  
Andrea Leason

2016 ◽  
Vol 52 (4) ◽  
pp. 3113-3126 ◽  
Author(s):  
Vincent Allègre ◽  
Emily E. Brodsky ◽  
Lian Xue ◽  
Stephanie M. Nale ◽  
Beth L. Parker ◽  
...  

1998 ◽  
Vol 274 (1) ◽  
pp. R237-R242
Author(s):  
Xiao-Pei Gao

The purpose of this study was to determine whether tannic acid elicits neurogenic plasma exudation from the oral mucosa in vivo and, if so, whether this response is transduced in part by thel-arginine-nitric oxide (NO) biosynthetic pathway. Using intravital microscopy, we found that suffusion of tannic acid elicits significant concentration-dependent leaky site formation and increase in clearance of fluorescein isothiocyanate-dextran (molecular mass 70 kDa) from the in situ hamster cheek pouch ( P < 0.05). These effects are significantly attenuated by two selective, but structurally distinct, nonpeptide neurokinin-1 (NK1) receptor antagonists, CP-96,345 and RP-67580, but not by CP-96,344, the 2R,3R enantiomer of CP-96,345. N G-nitrol-arginine methyl ester (l-NAME), an NO synthase inhibitor, but notd-NAME, significantly attenuates tannic acid-induced responses.l-Arginine, but notd-arginine, reverses the attenuating effects of l-NAME. We conclude that tannic acid elicitsl-arginine-NO biosynthetic pathway-dependent neurogenic plasma exudation from the in situ hamster cheek pouch.


1998 ◽  
Vol 275 (2) ◽  
pp. R588-R595
Author(s):  
Hiroyuki Ikezaki ◽  
Hayat Önyüksel ◽  
Israel Rubinstein

The purpose of this study was to determine whether vasoactive intestinal peptide (VIP) modulates vasoconstriction elicited by phenylephrine and ANG II in vivo and, if so, to begin to elucidate the mechanisms underlying this phenomenon. Using intravital microscopy, we found that suffusion of phenylephrine and ANG II elicits significant vasoconstriction in the in situ hamster cheek pouch that is potentiated by VIP-(10—28), a VIP receptor antagonist, but not by VIP-(1—12) ( P< 0.05). Aqueous VIP has no significant effects on phenylephrine- and ANG II-induced vasoconstriction. However, VIP on sterically stabilized liposomes (SSL), a formulation where VIP assumes a predominantly α-helix conformation, significantly attenuates this response. Maximal effect is observed within 30 min and is no longer seen after 60 min. Empty SSL are inactive. Indomethacin has no significant effects on responses induced by VIP on SSL. The vasodilators ACh, nitroglycerin, calcium ionophore A-23187, 8-bromo-cAMP, and isoproterenol have no significant effects on phenylephrine- and ANG II-induced vasoconstriction. Collectively, these data suggest that vasoconstriction modulates VIP release in the in situ hamster cheek pouch and that α-helix VIP opposes α-adrenergic- and ANG II-induced vasoconstriction in this organ in a reversible, prostaglandin-, NO-, cGMP-, and cAMP-independent fashion.


2005 ◽  
Vol 20 (10) ◽  
pp. 2745-2753 ◽  
Author(s):  
Yung-Shou Ho ◽  
Fong-Shung Huang ◽  
Fu-Hsing Lu

In this research, the influences of the oxygen impurity contained in the commercially available nitrogen gas on the reactions of chromium pellets with nitrogen were investigated in the temperature range 600–1350 °C. A small amount of oxygen competed with the majority N2 to react with chromium in the annealing process. Analyzing the in situ oxygen partial pressure changes during annealing proved that the dissolution of oxygen in Cr and/or resultant CrxN (CrN or Cr2N) was exothermic and the solubility decreased with increasing temperature. It was found that the oxygen partial pressure decreased drastically to about 10−22 atm when specimens were annealed at 600 °C compared to a mere 10−5 atm for a blank test, while its value increased with temperature. The oxidation involved simultaneous dissolution of oxygen in specimens and formation of oxide scale. Moreover, comparing the aforementioned results with those obtained from additional annealing experiments preformed in argon gas showed that the formation of Cr2O3 might stem mainly from oxidation of the resultant nitrides instead of the metallic chromium.


1999 ◽  
Vol 276 (5) ◽  
pp. R1359-R1365 ◽  
Author(s):  
Hiroyuki Ikezaki ◽  
Manisha Patel ◽  
Hayat Önyüksel ◽  
Syed R. Akhter ◽  
Xiao-Pei Gao ◽  
...  

The purpose of this study was to determine whether exogenous calmodulin potentiates vasoactive intestinal peptide (VIP)-induced vasodilation in vivo and, if so, whether this response is amplified by association of VIP with sterically stabilized liposomes. Using intravital microscopy, we found that calmodulin suffused together with aqueous and liposomal VIP did not potentiate vasodilation elicited by VIP in the in situ hamster cheek pouch. However, preincubation of calmodulin with liposomal, but not aqueous, VIP for 1 and 2 h and overnight at 4°C before suffusion significantly potentiated vasodilation ( P < 0.05). Calmodulin-induced responses were significantly attenuated by calmidazolium, trifluoperazine, and N G-nitro-l-arginine methyl ester (l-NAME) but notd-NAME. The effects ofl-NAME were reversed byl- but notd-arginine. Indomethacin had no significant effects on calmodulin-induced responses. Calmodulin had no significant effects on adenosine-, isoproterenol-, acetylcholine-, and calcium ionophore A-23187-induced vasodilation. Collectively, these data indicate that exogenous calmodulin amplifies vasodilation elicited by phospholipid-associated, but not aqueous, VIP in the in situ peripheral microcirculation in a specific, calmodulin active sites-, and nitric oxide-dependent fashion. We suggest that extracellular calmodulin, phospholipids, and VIP form a novel functionally coordinated class of endogenous vasodilators.


1999 ◽  
Vol 87 (2) ◽  
pp. 619-625 ◽  
Author(s):  
Xiao-Pei Gao ◽  
Syed R. Akhter ◽  
Hiroyuki Ikezaki ◽  
Dennis Hong ◽  
Israel Rubinstein

The purpose of this study was to determine whether dexamethasone attenuates the acute increase in macromolecular efflux from the oral mucosa elicited by an aqueous extract of smokeless tobacco (STE) in vivo, and, if so, whether this response is specific. Using intravital microscopy, we found that 20-min suffusion of STE elicited significant, concentration-related leaky site formation and an increase in clearance of fluorescein isothiocyanate-labeled dextran (FITC-dextran; mol mass 70 kDa) from the in situ hamster cheek pouch ( P < 0.05). This response was significantly attenuated by dexamethasone (10 mg/kg iv). Dexamethasone also attenuated the bradykinin-induced leaky site formation and the increase in clearance of FITC-dextran from the cheek pouch. However, it had no significant effects on adenosine-induced responses. Dexamethasone had no significant effects on baseline arteriolar diameter and on bradykinin-induced vasodilation in the cheek pouch. Collectively, these data indicate that dexamethasone attenuates, in a specific fashion, the acute increase in macromolecular efflux from the in situ oral mucosa evoked by short-term suffusion of STE. We suggest that corticosteroids mitigate acute oral mucosa inflammation elicited by smokeless tobacco.


1998 ◽  
Vol 275 (1) ◽  
pp. R56-R62 ◽  
Author(s):  
Hiroyuki Ikezaki ◽  
Sudhir Paul ◽  
Hayat Alkan-Önyüksel ◽  
Manisha Patel ◽  
Xiao-Pei Gao ◽  
...  

The purpose of this study was to determine whether a monoclonal anti-vasoactive intestinal peptide (VIP) antibody, which binds VIP with high affinity and specificity and catalyzes cleavage of the peptide in vitro, attenuates VIP vasorelaxation in vivo and, if so, whether insertion of VIP on the surface of sterically stabilized liposomes (SSL), which protects the peptide from trypsin- and plasma-catalyzed cleavage in vitro, curtails this response. Using intravital microscopy, we found that suffusion of monoclonal anti-VIP antibody (clone c23.5, IgG2ak), but not of nonimmune antibody (myeloma cell line UPC10, IgG2ak) or empty SSL, significantly attenuates VIP-induced vasodilation in the in situ hamster cheek pouch ( P < 0.05). By contrast, anti-VIP antibody has no significant effects on vasodilation elicited by isoproterenol, nitroglycerin, and calcium ionophore A-23187, agonists that activate intracellular effector systems in blood vessels that mediate, in part, VIP vasoreactivity. Suffusion of VIP on SSL, but not of empty SSL, restores the vasorelaxant effects of VIP in the presence of anti-VIP antibody. Collectively, these data suggest that VIP catalysis by high affinity and specific VIP autoantibodies displaying protease-like activity constitutes a novel mechanism whereby VIP vasoreactivity is regulated in vivo.


SPE Journal ◽  
2016 ◽  
Vol 22 (01) ◽  
pp. 172-183 ◽  
Author(s):  
Mahmood Bataee ◽  
Sonny Irawan ◽  
Syahrir Ridha ◽  
Hamed Hematpour ◽  
Zakaria Hamdi

Summary Accurate evaluation of failure pressure is crucial in the design of injection wells. Besides, in-situ stresses play an important role in obtaining the results. Pressure and rock stresses are related together as the role of effective-stress theorem. In fact, pressure changes with stress alteration caused by change in porosity and permeability. Therefore, it should be obtained with the coupling method. Moreover, to calculate pressure, temperature, and stress in the fully coupling method, a huge matrix should be solved, and it takes long processing time to implement it. Therefore, this study developed a wellbore geomechanical model for stability during injection by use of the iterative coupling method. The processing speed was enhanced in this study because the parameters were calculated separately. The parameters of pressure, temperature, saturation, and stress were obtained for the multiphase-flow condition with numerical modeling. Furthermore, in this study, the finite-difference method (FDM) had been used to solve pressure, temperature, and saturation, whereas the finite-volume method (FVM) was applied to solve the wellbore stress. On top of that, the iterative coupling method was used to improve the accuracy of the stress results. As a result, a correction of approximately 20 psi (0.14 MPa) was noted for pressure in relation to stress, which is 1 psi (6.89 kPa). Moreover, the Drucker-Prager failure criterion was used to model the fracturing on the basis of the stress results. Other than that, sensitivity analysis on horizontal maximum (σH) and minimum (σh) stresses showed that by increasing σH, the maximum injection pressures to avoid fracturing had been reduced, whereas in the case for σh, an increment was observed.


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