Contrast Medium-Induced Vasoconstrictions

1995 ◽  
Vol 36 (2) ◽  
pp. 198-203 ◽  
Author(s):  
J. Karstoft ◽  
L. Bååth ◽  
I. Jansen ◽  
L. Edvinsson
Keyword(s):  
Smooth Muscle ◽  
Calcium Antagonist ◽  
Contrast Media ◽  
Contrast Medium ◽  
Vessel Wall ◽  
Nerve Terminals ◽  
Buffer Solution ◽  
Low Concentrations ◽  
Isolated Arteries

Angiographic contrast media (CM) may cause both vasodilatation and vasoconstriction. This study evaluates a contrast medium-induced vasoconstriction that occurs when isolated arteries are exposed directly to a CM. Segments of rabbit coronary arteries were mounted in tissue baths containing buffer solution. During the experiments the buffer solution was exchanged with iohexol iso-osmolar with plasma, which caused a temporary vasoconstriction of the vessel segments. The constriction did not depend on the degree of oxygenation of iohexol. The endothelium was not involved in the vasoconstriction. Prazosin slightly decreased the vasoconstriction and a small part of the constriction might thus depend on liberation of norepinephrine by iohexol. The constriction was totally inhibited by the calcium antagonist nifedipine, while it was augmented by addition of low concentrations of KCl to ihoexol. It is concluded that the otherwise safe CM iohexol causes vasoconstriction in vitro by depolarizing the smooth muscle cells and the nerve terminals in the vessel wall.

A study of rat intracerebral arterioles: methods, morphology, and reactivity

1982 ◽  
Vol 243 (4) ◽  
pp. H598-H606 ◽  
Author(s):  
R. G. Dacey ◽  
B. R. Duling
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vessel Wall ◽  
Cell Layer ◽  
Muscle Tone ◽  
Vessel Diameter ◽  
Cell Nuclei

Penetrating, intracerebral arterioles from rat were isolated, cannulated, and studied in vitro. Vessel wall elements were found to consist of an endothelial cell layer, one smooth muscle cell layer, and a thin adventitial layer or leptomeningeal sheath. Smooth muscle cell nuclei were oriented perpendicular to the vessel's longitudinal axis; endothelial cell nuclei were parallel to the axis. Mean vessel diameter with the smooth muscle inactivated (passive diameter) was 36.7 +/- 1.6 (SE) micrometer. Spontaneous smooth muscle tone developed at 37 degrees C and reduced vessel diameter to 70 +/- 4% of passive diameter. Vessels were activated by the extraluminal application of 140 mM KCl solution at pH 8.00, which produced a transient contraction that decayed within 30 s to a steady contraction of somewhat less intensity. Changes in intravascular pressure were used to alter wall tension of the vessels. Tension in the vessel wall was computed, and length-tension curves for the arteriolar smooth muscle were approximated. Length-tension relationships similar to those seen in other smooth-muscle preparations were found with maximal estimated force development of 1.29 x 10(-5) N . m-2. Alterations of bath pH caused changes in vessel diameter that were inversely related to extraluminal pH and varied by approximately 77% in the range from pH 6.85 to 8.00. Adenosine dilated vessels to 140 +/- 6% of control diameter at a concentration of 10(-5) M. The mechanical characteristics and the reactivity to H+, K+, and adenosine of these vessels were quantitatively consistent with in vitro data from larger cerebral vessels and in vivo data from pial arteries.

scholarly journals Sympathetic nerves and the endothelium influence the vasoconstrictor effect of low concentrations of ouabain in pressurized small arteries

2010 ◽  
Vol 298 (6) ◽  
pp. H2093-H2101 ◽  
Author(s):  
Hema Raina ◽  
Qingli Zhang ◽  
Albert Y. Rhee ◽  
Thomas L. Pallone ◽  
W. Gil Wier
Keyword(s):  
Smooth Muscle ◽  
Sympathetic Nerve ◽  
Arterial Wall ◽  
Sympathetic Nerves ◽  
Nerve Terminals ◽  
Arterial Smooth Muscle ◽  
Low Concentrations ◽  
Endogenous Ouabain ◽  
Adrenoceptor Blocker ◽  
Arterial Endothelium

We hypothesized that in salt-dependent forms of hypertension, endogenous ouabain acts on arterial smooth muscle to cause enhanced vasoconstriction. Here, we tested for the involvement of the arterial endothelium and perivascular sympathetic nerve terminals in ouabain-induced vasoconstriction. Segments of rat mesenteric or renal interlobar arteries were pressurized to 70 mmHg at 37°C and exposed to ouabain (10−11–10−7 M). Removal of the endothelium enhanced ouabain-induced vasoconstriction by as much as twofold (at an ouabain concentration of 10−9 M). A component of the ouabain-induced vasoconstriction is due to the enhanced spontaneous release of norepinephrine (NE) from nerve terminals in the arterial wall. The α1-adrenoceptor blocker prazosin (10−6 M) decreased ouabain-induced vasoconstrictions by as much as 50%. However, neither the contraction induced by sympathetic nerve activity (SNA) nor the NE release evoked by SNA (measured directly by carbon fiber amperometry) was increased by ouabain (<10−7 M). Nevertheless, the converse case was true: after brief bursts of SNA, vasoconstrictor responses to ouabain were transiently increased (1.75-fold). This effect may be mediated by neuropeptide Y and Y1 receptors on smooth muscle. In arteries lacking the endothelium and exposed to prazosin, ouabain (10−11 M and greater) caused vasoconstriction, indicating a direct effect of very “low” concentrations of ouabain on arterial smooth muscle. In conclusion, in intact arteries, the endothelium opposes ouabain (10−11–10−7M)-induced vasoconstriction, which is caused by both enhanced spontaneous NE release and direct effects on smooth muscle. Ouabain (<10−7M) does not enhance SNA-mediated contractions, but SNA enhances ouabain-induced contractions. The effects of endogenous ouabain may be accentuated in forms of hypertension that involve sympathetic nerve hyperactivity and/or endothelial dysfunction.

Role of vessel wall in acute resetting of aortic baroreceptors

1985 ◽  
Vol 248 (6) ◽  
pp. H843-H852 ◽  
Author(s):  
P. A. Munch ◽  
A. M. Brown
Keyword(s):  
Smooth Muscle ◽  
Vessel Wall ◽  
Muscle Tone ◽  
Photoelectric Device ◽  
Wall Structures ◽  
Before And After ◽  
Sympathetic Efferents ◽  
Aortic Baroreceptors

Previously we found that baroreceptor (BR) pressure-frequency (PF) curves rapidly (5 min) reset to changes in mean arterial pressure (MAP) exclusive of sympathetic efferents or circulating hormones. Since BRs are mechanically coupled to vessel wall structures, resetting may be due to changes in the wall. This was examined using an in vitro rat aortic arch-aortic nerve preparation and a photoelectric device to measure arch diameter. Pressure-diameter (PD) curves were constructed at selected MAPs following the resetting protocol used previously [Am. J. Physiol. 244 (Heart Circ. Physiol. 13): H672-H680, 1983]. Overall there was no consistent relationship between the PD curves and MAP, which was in sharp contrast to BR PF resetting. To determine if smooth muscle tone could affect aortic or BR function, the arch was constricted or relaxed with norepinephrine (NE) or sodium nitroprusside (NP), respectively. BR PF and aortic PD curves were constructed before and after drug treatment. NE reduced and NP increased discharge at given pressures. Diameter-frequency (DF) plots were not altered by either drug. PD and PF curves at constant MAP were stable after the initial responses to NP relaxation were completed. Subsequent MAP elevations in NP reset BRs to higher pressures, whereas PD curves shifted to lower pressures. Hence, DF plots shifted to higher diameters. These results show that neither smooth muscle activity nor mechanical changes in the whole wall can account for BR rapid resetting. The process probably occurs in the receptors.

Pharmacological and morphological effects of in vitro transluminal balloon angioplasty on normal and vasospastic canine basilar arteries

1995 ◽  
Vol 83 (3) ◽  
pp. 522-530 ◽  
Author(s):  
Patrick D. S. Chan ◽  
J. Max Findlay ◽  
Bozena Vollrath ◽  
David A. Cook ◽  
Michael Grace ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Balloon Angioplasty ◽  
Vessel Wall ◽  
Ionophore A23187 ◽  
Content Type ◽  
Basilar Arteries ◽  
Scanning Em ◽  
Fine Print

✓ Despite growing clinical use of transluminal balloon angioplasty (TBA) to treat cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH), the precise mechanism of action of balloon dilation on the cerebral arterial wall is unknown. In this experiment the authors examined the pharmacological and morphological changes in 10 normal and 12 vasospastic canine basilar arteries following in vitro silicone microballoon TBA. For the SAH group in which the double-hemorrhage model was used, vasospasm was confirmed by angiography and the animals were killed on Day 7 after the first SAH. In vitro TBA was performed on basilar arteries from normal and SAH dogs immediately after sacrifice and removal of the brain. The procedure was performed while the arteries were maintained in oxygenated Krebs buffer. In the pharmacological studies, potassium chloride, prostaglandin F2α, serotonin, and noradrenaline were used as vasoconstrictors, and bradykinin and calcium ionophore A23187 were used to produce an endothelium-dependent dilation. In both normal and vasospastic groups, the pharmacological responses of dilated segments of basilar arteries were compared to those of nondilated segments of the same arteries. Vessels from all groups were examined using scanning electron microscopy (EM) and transmission EM. Scanning EM was used to study the intact vessel wall, the smooth-muscle cell layer obtained after digestion with hydrochloric acid, and the extracellular matrix obtained after digestion with bleach. Cross-sections of the vessel wall were examined using transmission EM. The most striking finding was that immediately after in vitro TBA of both normal and vasospastic canine basilar arteries, there was a significant reduction (p < 0.05) of responses to both vasoconstrictors and vasorelaxants. As revealed by scanning EM and transmission EM, both normal and vasospastic vessels dilated with TBA showed flattening and patchy denudation of the endothelium, and straightening and occasional rupturing of the internal elastic lamina. In addition, vasospastic vessels dilated with TBA showed decreased surface rippling and mild stretching and straightening of smooth-muscle cells, and mild thinning of the tunica media. There was no gross vascular disruption or obvious change in the extracellular matrix of the vessel walls of either normal or vasospastic arteries after TBA. These results suggest that functional impairment of vasoreactivity in the vessel wall as a result of mechanical stretching of the smooth-muscle layer plays a more important role than structural alteration, at least in the immediate dilation produced in vasospastic arteries byTBA.

scholarly journals Effect of contrast media on radioimmunoassay of beta-endorphin in cerebrospinal fluid.

1984 ◽  
Vol 30 (2) ◽  
pp. 311-314 ◽  
Author(s):  
V S Fang ◽  
R G Fessler ◽  
J R Rachlin ◽  
F D Brown
Keyword(s):  
Cerebrospinal Fluid ◽  
Electrical Stimulation ◽  
Contrast Media ◽  
Contrast Medium ◽  
Plasma Samples ◽  
Previous Suggestion ◽  
Beta Endorphin ◽  
Standard Curve ◽  
Low Concentrations ◽  
The Mean

Abstract An effect of metrizamide, a contrast medium, on results of beta-endorphin radioimmunoassay was examined. We found that 1, 5, and 10 microL of the medium added to 100 microL of standard containing 0 to 500 pg of beta-endorphin shifted the standard curve to the left in proportion to the metrizamide concentration. Three other contrast media showed a similar effect at low concentrations of beta-endorphin. This effect of contrast media artificially increased results in radioimmunoassay of beta-endorphin in cerebrospinal fluid, the mean overestimate being 121.9% (range, 0 to 435%). For plasma samples, this effect of contrast media resulted in an average 11.7% overestimate of beta-endorphin (range, -16% to 41%). These observations bring into question the validity of a previous suggestion that an increase in beta-endorphin in cerebrospinal fluid after intracerebral electrical stimulation is the mechanism for stimulation-produced analgesia.

Role of Na(+)-Ca2+ exchange in the regulation of vascular smooth muscle tension

1993 ◽  
Vol 264 (4) ◽  
pp. H1028-H1040 ◽  
Author(s):  
E. D. Motley ◽  
R. J. Paul ◽  
M. A. Matlib
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Nerve Terminal ◽  
Muscle Tension ◽  
Second Phase ◽  
Nerve Terminals ◽  
Free Solution

To determine the role of the Na(+)-Ca2+ exchange systems of nerve terminal and sarcolemmal membrane on development of tension in rabbit aortic rings, internal or external Na+ concentration was changed with either ouabain or Na(+)-free solution, respectively. Ouabain produced a verapamil-insensitive but external Na(+)- and Ca(2+)-dependent biphasic tension with distinct lag periods both of which were shortened by depolarization with KCl. The first phase of tension was inhibited by prazosin, phentolamine, in vitro neurolysis with 6-hydroxydopamine and in vivo treatment with reserpine to deplete catecholamines in nerve terminals. Therefore, first phase of tension was attributed to catecholamines released from nerve terminals induced by increased axoplasmic Ca2+ concentration mediated by the neural Na(+)-Ca2+ exchanger due to the increased axoplasmic Na+ concentration resulting from inhibition of the Na(+)-Ka+ pump with ouabain. In the absence of the first phase of tension, the second phase of tension was enhanced by caffeine, presumably by preventing sequestration of the sarcolemmal Na(+)-Ca2+ exchanger-mediated increase in cytosolic Ca2+ concentration in vascular smooth muscle cells. The prazosin-insensitive tension was dependent on the external Na+ concentration and was also attributed to the sarcolemmal Na(+)-Ca2+ exchanger of vascular smooth muscle. The magnitude of the increase in tension with ouabain or Na(+)-free solution attributed to the sarcolemmal Na(+)-Ca2+ exchanger of vascular smooth muscle was larger than that mediated by the exchanger of the nerve terminal. It was concluded that the Na(+)-Ca2+ exchange systems of both the nerve terminal and the vascular smooth muscle sarcolemma contribute to the development of tension by different mechanisms and to different extents when internal or external Na+ concentration was changed.

Vasoconstriction of Isolated Arteries Induced by Angiographic Contrast Media

1995 ◽  
Vol 36 (3) ◽  
pp. 312-316 ◽  
Author(s):  
J. Karstoft ◽  
L. Bååth ◽  
I. Jansen ◽  
L. Edvinsson
Keyword(s):  
Smooth Muscle ◽  
Contrast Media ◽  
Smooth Muscle Cells ◽  
Coronary Arteries ◽  
Muscle Cells ◽  
Ion Content ◽  
Ionic Media ◽  
Ionic Monomer ◽  
Isolated Arteries

Angiographic contrast media (CM) may cause both vasodilatation and vasoconstriction, effects that can only be partly be explained by the media's hyperosmolality. The present study describes a CM-induced vasoconstriction of isolated rabbit coronary arteries that depends on chemotoxicity and ion content of the CM. Rings of arteries were mounted in tissue baths and the constrictions induced by different CM were measured. Iotrolan and iodixanol (nonionic dimers) caused the most powerful constrictions followed by iohexol (non-ionic monomer) and mannitol. Ioxaglate (ionic dimer) and diatrizoate (ionic monomer) caused no or weak constrictions. By comparing these findings with previous studies, it is concluded that non-ionic media cause vasoconstriction due to depolarization of the smooth muscle cells, an effect that for iohexol can be counteracted by addition of 30 mM NaCl. The ionic media seem to cause hyperpolarization of the cells. This difference between non-ionic and ionic CM might be one of the reasons for the lower tendency of non-ionic CM to cause vasodilatation clinically.

Development of margination of platelet-sized particles in red blood cell suspensions flowing through Y-shaped bifurcating microchannels

Biorheology ◽  
2021 ◽  
Vol 57 (2-4) ◽  
pp. 101-116
Author(s):  
Masako Sugihara-Seki ◽  
Tenki Onozawa ◽  
Nozomi Takinouchi ◽  
Tomoaki Itano ◽  
Junji Seki
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Vessel Wall ◽  
Flow Direction ◽  
Spherical Particles ◽  
Free Layer ◽  
Low Concentrations ◽  
Asymmetric Distributions ◽  
Cell Free Layer

BACKGROUND: In the blood flow through microvessels, platelets exhibit enhanced concentrations in the layer free of red blood cells (cell-free layer) adjacent to the vessel wall. The motion of platelets in the cell-free layer plays an essential role in their interaction with the vessel wall, and hence it affects their functions of hemostasis and thrombosis. OBJECTIVE: We aimed to estimate the diffusivity of platelet-sized particles in the transverse direction (the direction of vorticity) across the channel width in the cell-free layer by in vitro experiments for the microchannel flow of red blood cell (RBC) suspensions containing platelet-sized particles. METHODS: Fluorescence microscope observations were performed to measure the transverse distribution of spherical particles immersed in RBC suspensions flowing through a Y-shaped bifurcating microchannel. We examined the development of the particle concentration profiles along the flow direction in the daughter channels, starting from asymmetric distributions with low concentrations on the inner side of the bifurcation at the inlet of the daughter channels. RESULTS: In daughter channels of 40 μm width, reconstruction of particle margination revealed that a symmetric concentration profile was attained in ∼30 mm from the bifurcation, independent of flow rate. CONCLUSIONS: We presented experimental evidence of particle margination developing in a bifurcating flow channel where the diffusivity of 2.9-μm diameter particles was estimated to be ∼40 μm2/s at a shear rate of 1000 s−1 and hematocrit of 0.2.

Effects of extracellular calcium on canine tracheal smooth muscle

1986 ◽  
Vol 61 (2) ◽  
pp. 706-711 ◽  
Author(s):  
S. J. Gunst ◽  
J. M. Pisoni
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Extracellular Calcium ◽  
Tracheal Smooth Muscle ◽  
Inhibitory Effects ◽  
Contractile Responses ◽  
Low Concentrations ◽  
K Depletion

Strips of canine tracheal smooth muscle were studied in vitro to determine the effects of changes in the extracellular calcium (Cao) concentration on tonic contractions induced by acetylcholine and 5-hydroxytryptamine. Strips were contracted with graded concentrations of the above agents in 2.4 mM Ca, after which CaCl2 was administered to achieve final concentrations of 5.0, 10.0, and 20.0 mM. Increases in Cao to 5 mM or above caused significant relaxation of muscles contracted with 5-hydroxytryptamine but did not significantly relax muscles contracted with acetylcholine. Increases in Cao also caused significant relaxation of muscles contracted with low concentrations of K+ (20 or 30 mM). However, in 60 or 120 mM K+, increases in Cao resulted predominantly in muscle contraction. Inhibition of the Na+-K+-ATPase by ouabain (10(-5) M) or K+ depletion reversed the effects of Cao from relaxation to contraction in tissues contracted with 5-hydroxytryptamine. Increases in Cao also caused contraction rather than relaxation in the presence of verapamil (10(-6) M). We conclude that calcium has both excitatory and inhibitory effects on the contractile responses of canine tracheal smooth muscle. The inhibitory effects of Ca2+ appear to be linked to the activity of the membrane Na+-K+-ATPase.

scholarly journals Substance P released from intrinsic airway neurons contributes to ozone-enhanced airway hyperresponsiveness in ferret trachea

2003 ◽  
Vol 95 (2) ◽  
pp. 742-750 ◽  
Author(s):  
Zhong-Xin Wu ◽  
Brian E. Satterfield ◽  
Richard D. Dey
Keyword(s):  
Smooth Muscle ◽  
Substance P ◽  
Airway Hyperresponsiveness ◽  
Sensory Nerve ◽  
Sensory Innervation ◽  
Tracheal Smooth Muscle ◽  
Nerve Terminals ◽  
Air Exposure ◽  
Cholinergic Agonist

Exposure to ozone (O3) induces airway hyperresponsiveness mediated partly through the release of substance P (SP) from nerve terminals in the airway wall. Although substantial evidence suggests that SP is released by sensory nerves, SP is also present in neurons of airway ganglia. The purpose of this study was to investigate the role of intrinsic airway neurons in O3-enhanced airway responsiveness in ferret trachea. To remove the effects of sensory innervation, segments of ferret trachea were maintained in culture conditions for 24 h before in vitro exposure to 2 parts/million of O3 or air for 1 h. Sensory nerve depletion was confirmed by showing that capsaicin did not affect tracheal smooth muscle responsiveness to cholinergic agonist or contractility responses to electrical field stimulation (EFS). Contractions of isolated tracheal smooth muscle to EFS were significantly increased after in vitro O3 exposure, but the constrictor response to cholinergic agonist was not altered. Pretreatment with CP-99994, an antagonist of the neurokinin 1 receptor, attenuated the increased contraction to EFS after O3 exposure but had no effect in the air exposure group. The number of SP-positive neurons in longitudinal trunk ganglia, the extent of SP innervation to superficial muscular plexus nerve cell bodies, and SP nerve fiber density in tracheal smooth muscle all increased significantly after O3 exposure. The results show that release of SP from intrinsic airway neurons contributes to O3-enhanced tracheal smooth muscle responsiveness by facilitating acetylcholine release from cholinergic nerve terminals.

Sign in / Sign up

Export Citation Format

Share Document