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PubMed2003

Nonlinear changes of transmembrane potential during electrical shocks: role of membrane electroporation.

Defibrillation shocks induce nonlinear changes of transmembrane potential (DeltaVm) that determine the outcome of defibrillation. As shown earlier, strong shocks applied during action potential plateau cause nonmonotonic negative DeltaVm, where an initial hyperpolarization is followed by Vm shift to a more positive level. The biphasic negative DeltaVm can be attributable to (1) an inward ionic current or (2) membrane electroporation. These hypotheses were tested in cell cultures by measuring the effects of ionic channel blockers on DeltaVm and measuring uptake of membrane-impermeable dye. Experiments were performed in cell strands (width approximately 0.8 mm) produced using a technique of patterned cell growth. Uniform-field shocks were applied during the action potential plateau, and DeltaVm was measured by optical mapping. Shock-induced negative DeltaVm exhibited a biphasic shape starting at a shock strength of approximately 15 V/cm when estimated peak DeltaV-m was approximately -180 mV; positive DeltaVm remained monophasic. Application of a series of shocks with a strength of 23+/-1 V/cm resulted in uptake of membrane-impermeable dye propidium iodide. Dye uptake was restricted to the anodal side of strands with the largest negative DeltaVm, indicating the occurrence of membrane electroporation at these locations. The occurrence of biphasic negative DeltaVm was also paralleled with after-shock elevation of diastolic Vm. Inhibition of I(f) and I(K1) currents that are active at large negative potentials by CsCl and BaCl2, respectively, did not affect DeltaVm, indicating that these currents were not responsible for biphasic DeltaVm. These results provide evidence that the biphasic shape of DeltaVm at sites of shock-induced hyperpolarization is caused by membrane electroporation.

Action Potentials↗
PubMed1988

Structural and reactivity alterations of the renal vasculature of spontaneously hypertensive rats prior to and during established hypertension.

The renal vasculature of Wistar Kyoto spontaneously hypertensive rats (SHR), prior to (4-5 week) and during established hypertension (21 week) and those of age-matched Wistar Kyoto normotensive rats (WKY) were morphometrically and pharmacologically studied. Under dilated conditions, the vascular resistances (RVR) of the isolated kidneys of young and adult SHR were similar to WKY. Morphometric measurements of renal vasculature indicated that the cross-sectional area of the intima and adventitia and its subcomponents were similar in adult SHR and WKY. With the exception of the preglomerular arterioles, all the renal arteries of adult SHR exhibited elevated cross-sectional quantities of total media, medial smooth muscle cells (SMCs), and extracellular space. Analysis of the SMCs indicated the presence of increased numbers of SMC layers and/or an increase in the SMC volume-to-surface area ratio in arteries sampled from adult SHR. Vascular contraction produced by infusing norepinephrine, BaCl2, angiotensin II, or by stimulating the renal nerves elevated the RVR to a greater degree in adult SHR than in WKY. The sensitivity of the renal vasculature to the various contractile agents was similar in adult SHR and WKY. When compared with WKY, prehypertensive SHR also exhibited increased cross-sectional quantities of arterial media and elevated amplitudes of RVR change in response to norepinephrine and renal nerve stimulation. However, the vascular contractile sensitivity to norepinephrine was reduced. Our results indicate that renovascular wall thickening and the hypercontractile reactivity associated with such a change precedes hypertension in SHR. In prehypertensive SHR, elevations in RVR might be counterbalanced by a decreased norepinephrine sensitivity. An increase in the norepinephrine contractile sensitivity and further vascular thickening with age could elevate the RVR and establish hypertension.

Animals↗
PubMed1991

Effects of barium-induced cardiac contraction on large- and small-vessel intramyocardial blood volume.

We have measured the effects of barium-induced cardiac contraction on the intramyocardial blood volume content of all vessels and have independently measured the blood volume content of vessels with a diameter greater than 100 microns in rat myocardium. Measurements of total intramyocardial blood volume were made by using [125I]albumin as a plasma marker and technetium-99m as a red blood cell marker. In one group of rats (n = 8), diastolic arrest was induced by an intravenous injection of KCl; in a second group (n = 8), systolic arrest was induced by an intravenous injection of BaCl2. In both groups, the hearts were frozen in situ immediately after heart arrest while aortic pressure was decaying from its former physiological level. The left ventricular free wall was sectioned transmurally in a cryomicrotome, and the blood volume within each tissue sample was calculated from its radioactivity. The volume of blood in vessels larger than 100 microns was independently estimated from the exposed cross-sectional area of these vessels in photographs of the frozen tissue taken during tissue sectioning in the cryomicrotome. Total intramyocardial blood volume was found to decrease by about 42% from 8.6 +/- 1.3 ml/100 g (mean +/- SEM) in the KCl group to 5.0 +/- 0.7 ml/100 g in the BaCl2 group (p less than 0.01). Total volume was greater in the epicardial than in the endocardial layers of both groups (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Does vasospasm occur in small pial arteries and arterioles of rabbits?

BACKGROUND: Vasospasm is a serious complication associated with subarachnoid hemorrhage. Successful management of vasospasm will ultimately depend on a clear understanding of the scope of this phenomenon, including whether arterial elements of different calibers are equally affected. We therefore examined the responses to subarachnoid hemorrhage in rabbit basilar arteries, small pial arteries, and arterioles. SUMMARY OF REPORT: We compared the brain stem pial arteries of 10 perfusion-fixed male New Zealand White rabbits after experimental subarachnoid hemorrhage to those of five control rabbits using morphological analysis of cross-sections of plastic-embedded vessels. After subarachnoid hemorrhage, the internal elastic lamina was highly corrugated in all basilar arteries (mean diameter 319 +/- 51 microns). These arteries were severely constricted in comparison with the control group, in which the mean diameter was 691 +/- 17 microns, and corrugation of the internal elastic lamina was not present. In contrast, small pial arteries and arterioles very rarely demonstrated a vasoconstrictive configuration after subarachnoid hemorrhage. The contractility of the smaller vessels was confirmed by injecting 2 mg/kg BaCl2 intracisternally. Following BaCl2 injection, corrugation of the internal elastic lamina was detected in the small arteries and arterioles as well as the basilar arteries. CONCLUSIONS: We conclude that experimental chronic vasospasm after subarachnoid hemorrhage in rabbits tends to occur in large conducting arteries rather than in smaller pial arteries and arterioles.

Animals↗
PubMed1997

Role of potassium channels in relaxations of isolated canine basilar arteries to acidosis.

BACKGROUND AND PURPOSE: Concentration of hydrogen ions is an important regulator of cerebral arterial tone under physiological and pathological conditions. Previous studies demonstrated that in cerebral arteries, relaxations to hypercapnia are due to decrease in extracellular pH. The present study was designed to determine the role of potassium channels in mediation of cerebral arterial relaxations induced by extracellular acidosis. METHODS: Rings of canine basilar arteries without endothelium were suspended for isometric force recording. Acidosis (pH 7.3 to 7.0) was produced by incremental addition of hydrochloric acid (1.0N). The concentration of hydrogen ions was continuously monitored with a pH meter. RESULTS: During contractions to UTP, acidosis (pH 7.3 to 7.0) induced pH-dependent relaxations. These relaxations were abolished in arteries contracted by potassium chloride (20 mmol/L). A nonselective potassium channel inhibitor, BaCl2 (10(-4) and 10(-4) mol/L), and an ATP-sensitive potassium channel inhibitor, glyburide (5 x 10(-6) mol/L), significantly reduced relaxations to acidosis. Furthermore, BaCl2 (10(-4) mol/L) and glyburide (5 x 10(-6) mol/L) abolished relaxations to an ATP-sensitive potassium channel opener, cromakalim (10(-8) to 3 x 10(-5) mol/L). However, these potassium channel inhibitors did not affect relaxations to a voltage-dependent calcium channel inhibitor, diltiazem (10(-8) to 10(-4) mol/L), and glyburide (5 x 10(-6) mol/L) did not alter relaxations to a nitric oxide donor, SIN-1 (10(-9) to 10(-4) mol/L). A calcium-activated potassium channel inhibitor, charybdotoxin (10(-7) mol/L), and a delayed rectifier potassium channel inhibitor, 4-aminopyridine (10(-3) mol/L), did not affect relaxations to acidosis. CONCLUSIONS: These results suggest that extracellular acidosis causes relaxations of cerebral arteries in part by activation of potassium channels. ATP-sensitive potassium channels appear to contribute to acidosis-induced decrease in cerebral arterial tone.

4-Aminopyridine↗
PubMed1997

Role of potassium channels in relaxations of canine middle cerebral arteries induced by nitric oxide donors.

BACKGROUND AND PURPOSE: The mechanisms underlying smooth muscle relaxations of cerebral arteries in response to nitric oxide (NO) and cyclic GMP (cGMP) are still not completely understood. The present study was designed to determine the role of potassium channels in the relaxations to NO donors 3-morpholinosydnonimine (SIN-1) and sodium nitroprusside (SNP), as well as 8-bromo-3',5' -cGMP (a synthetic analogue of cGMP) and zaprinast (a selective cGMP phosphodiesterase inhibitor). METHODS: Rings of canine middle cerebral asteries without endothelium were suspended in Krebs-Ringer bicarbonate solution for isometric tension recording. The levels of cGMP were measured by radioimmunoassay. Relaxations to NO donors 8-bromo-cGMP and zaprinast were studied in the presence and in the absence of K+ channel blockers charybdotoxin (large-conductance Ca(2+)-activated K+ channels), glyburide (ATP-sensitive K+ channels), 4-aminopyridine (delayed rectifier K+ channels), and BaCl2 (multiple types of K+ channels). RESULTS: Concentration-dependent relaxations caused by NO donors (SIN-1 and SNP) were significantly reduced in arteries treated with BaCl2 (3 x 10(-4) mol/L) or charybdotoxin (3 x 10(-8) mol/L). Relaxations to 8-bromo-cGMP were not affected by the same concentrations of BaCl2 and charybdotoxin; however, they were reduced by higher concentrations of BaCl2 (3 x 10(-3) mol/L) or charybdotoxin (10(-7) mol/L). Zaprinast-induced relaxations were significantly reduced by BaCl2 (3 x 10(-4) mol/L) or charybdotoxin (3 x 10(-8) mol/L). Glyburide (10(-5) mol/L) and 4-aminopyridine (10(-3) mol/L) did not alter the relaxations to SIN-1 or SNP. The production of cGMP stimulated by SIN-1 in the vascular smooth muscle was not affected by BaCl2 (3 x 10(-3) mol/L) or charybdotoxin (10(-7) mol/L). CONCLUSIONS: These results indicate that in canine middle cerebral arteries, a significant portion of relaxations to NO liberated from nitrovasodilators is mediated by large-conductance Ca(2+)-activated K+ channels. Other K+ channels, sensitive to BaCl2, may also be involved in the mechanism of relaxations induced by NO.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1998

Altered function of inward rectifier potassium channels in cerebrovascular smooth muscle after ischemia/reperfusion.

BACKGROUND AND PURPOSE: Several recent studies have demonstrated that inward rectifier potassium channels (K(ir)s) are located on vascular smooth muscle of cerebral arteries in the rat. Activation of the K(ir)s dilates the arteries by relaxing the vascular smooth muscle. We tested the following hypothesis in the present study: function of inward rectifier potassium channels is altered after ischemia/reperfusion (I/R). METHODS: Temporary (2-hour) focal ischemia was induced in male Long-Evans rats (3% isoflurane anesthesia) by the intraluminal filament model. After 24 hours of reperfusion, ipsilateral and contralateral middle cerebral arteries (MCAs) were harvested and mounted on micropipettes, pressurized to 85 mm Hg, and luminally perfused. RESULTS: Resting diameters for contralateral (control) and ipsilateral (I/R) MCAs were not significantly different (215+/-4 microm and 211+/-5 microm [n = 6 and n = 7], respectively). Activation of the K(ir)s by abluminal administration of 15 mmol/L KCl to the control MCAs dilated the MCA by 34+/-4% (n = 8). Activation of the K(ir)s in I/R MCAs produced a dilation of only 11+/-3% (n = 8; P<0.001 compared with control). BaCl2 (75 micromol/L), a concentration-selective inhibitor of the K(ir)s, significantly attenuated the dilation produced by 15 mmol/L KCl in control MCAs but not in the I/R MCAs. Endothelial-mediated dilations elicited by the luminal administration of uridine triphosphate (10 micromol/L) produced similar dilations in both groups (32+/-5% for sham [n = 4] and 33+/-2% for I/R [n = 4]), indicating that dilator function in general was not altered in I/R vessels. CONCLUSIONS: We conclude that Kir function is altered after I/R. The Kir altered function is likely to exacerbate the brain injury occurring after I/R.

Animals↗
PubMed1999

P2u receptor-mediated release of endothelium-derived relaxing factor/nitric oxide and endothelium-derived hyperpolarizing factor from cerebrovascular endothelium in rats.

BACKGROUND AND PURPOSE: Stimulation of P2u purinoceptors by UTP on endothelium dilates the rat middle cerebral artery (MCA) through the release of endothelium-derived relaxing factor/nitric oxide (EDRF/NO) and an unknown relaxing factor. The purpose of this study was to determine whether this unknown relaxing factor is endothelium-derived hyperpolarizing factor (EDHF). METHODS: Rat MCAs were isolated, cannulated, pressurized, and luminally perfused. UTP was added to the luminal perfusate to elicit dilations. RESULTS: Resting outside diameter of the MCAs in one study was 209+/-7 micrometer (n=10). The MCAs showed concentration-dependent dilations with UTP administration. Inhibition of NO synthase with NG-nitro-L-arginine methyl ester (L-NAME) (1 micromol/L to 1 mmol/L) did not diminish the maximum response to UTP but did shift the concentration-response curve to the right. Scavenging NO with hemoglobin (1 or 10 micromol/L) or inhibition of guanylate cyclase with ODQ (1 or 10 micromol/L) had effects on the UTP-mediated dilations similar to those of L-NAME. In the presence of L-NAME, dilations induced by 10 micromol/L UTP were accompanied by 13+/-2 mV (P<0.009) hyperpolarization of the vascular smooth muscle membrane potential (-28+/-2 to -41+/-1 mV). Iberiotoxin (100 nmol/L), blocker of the large-conductance calcium-activated K channels, sometimes blocked the dilation, but its effects were variable. Charybdotoxin (100 nmol/L), also a blocker of the large-conductance calcium-activated K channels, abolished the L-NAME-insensitive component of the dilation to UTP. CONCLUSIONS: Stimulation of P2u purinoceptors on the endothelium of the rat MCA released EDHF, in addition to EDRF/NO, and dilated the rat MCA by opening an atypical calcium-activated K channel.

4-Aminopyridine↗
PubMed2001

Role of potassium channels in regulation of brain arteriolar tone: comparison of cerebrum versus brain stem.

BACKGROUND AND PURPOSE: Potassium channels are important regulators of resting tone in large cerebral arteries, but their activity and distribution may vary according to vessel location and species studied. In the cerebral microcirculation in vivo, however, these channels appear to be silent at rest. Our goal was to determine the activity of potassium channels of brain arterioles from 2 origins under basal conditions in vitro. METHODS: Penetrating cerebral (40. 9+/-2.2 microm control diameter) and brain stem (36.2+/-1.2 microm) arterioles of rats were prepared from middle cerebral and basilar arteries, respectively. The internal diameter of cannulated and pressurized vessel was monitored with the inverted microscope before and after administration of potassium channel inhibitors. In addition, we studied the effect of nitric oxide synthase inhibition on potassium channel activity. RESULTS: Cerebral and brain stem arterioles were significantly constricted by 4-aminopyridine and low concentration of BaCl(2) but not by glibenclamide. The addition of N:(omega)-nitro-L-arginine to 4-aminopyridine further decreased diameters of both arterioles. Tetraethylammonium ion caused a significant constriction of brain stem but not cerebral arteriole. The brain stem arteriole was further constricted by additional N:(omega)-nitro-L-arginine. CONCLUSIONS: Voltage-dependent and inward-rectifier, but not ATP-sensitive, potassium channels are active under basal conditions of rat cerebral and brain stem arterioles. There is a regional difference in the activity of calcium-activated potassium channels, which, at rest, are open in brain stem but silent in cerebral arterioles. In addition, basal endogenous nitric oxide may not contribute to the activation of voltage-dependent and calcium-activated potassium channels.

4-Aminopyridine↗
PubMed2005

Morphology and metabolism of hepatocytes microencapsulated with acrylic terpolymer-alginate using gelatin and poly(vinyl alcohol) as extracellular matrices.

Microcapsules with good mechanical stability were prepared using an appropriate mixture of alginate and acrylic terpolymer. It was found from the microscopic observation that the microcapsules had a porous structure with interconnected pores, with a size of 50-150 nm. The results of the permeability experiment of microcapsules using FITC-dextrans showed that the capsule had a molecular mass cut-off of 120 kDa. The hepatocytes encapsulated in both alginate and acrylic terpolymer with gelatin and PVA rapidly aggregated in the core. The aggregated cells showed high albumin synthesis and ammonia removal, suggesting good metabolic function.

Acrylates↗
PubMed1996

Prejunctional inhibition of cholinergic responses by prostaglandin E2 in human bronchi.

The effect of prostaglandin E2 (PGE2) on cholinergic responses elicited by electrical field stimulation (EFS) (8 Hz, 1 ms, 8 V for 10 s every 100 s) of human isolated human bronchi was studied. Indomethacin (1 microM) was found to produce approximately a 100% increase in the cholinergic response. In the presence of indomethacin, PGE2 (1-300 nM) was found to concentration-dependently inhibit the cholinergic responses to EFS. A maximal inhibition was obtained with 100 nM PGE2 which produced an 80% inhibition of the cholinergic response. By contrast 100 nM PGE2 was without significant effect on the concentration response curve to exogenously added acetylcholine. The inhibitory effect of PGE2 on the EFS-induced cholinergic responses was not modified by the large conductance Ca(2+)-activated K+ channel inhibitor charybdotoxin (100 nM). These results suggest that endogenously released prostaglandins, presumably PGE2, act to inhibit cholinergic responses by a prejunctional mechanism in human isolated bronchi. In contrast to other autocoids, this inhibition does not involve the activation of large-conductance Ca(2+)-activated K+ channels.

Acetylcholine↗
PubMed1998

ATP-independent membrane depolarization with ischemia in the oxygen-ventilated isolated rat lung.

We hypothesize that lung ischemic injury is related to cessation of flow leading to endothelial cell membrane depolarization and activation of oxidant-generating systems. Cell membrane potential was assessed in isolated, oxygen ventilated, Krebs-Ringer bicarbonate buffer-dextran-perfused rat lungs by lung surface fluorescence after infusion of bis-oxonol or 5,5',6,6'-tetrachloro-1, 1',3,3'-tetraethylbenzimidazolyl-carbocyanine iodide (JC-1), voltage-sensitive dyes. Surface fluorometry showed increased bis-oxonol fluorescence (34.7 +/- 3.3% above baseline) and decreased JC-1 fluorescence (24.5 +/- 4.5% below baseline) with ischemia, compatible with membrane depolarization. Fluorescence change was initiated within 1-2 min of the onset of ischemia and was rapidly reversible with reperfusion. Fluorescence changes varied with perfusion flow rate; maximal increase occurred with the transition from 1.8 ml/min to zero flow. Elevation of static intravascular pressure resulted in only a minor increase of bis-oxonol fluorescence. In situ subpleural fluorescence microscopy showed that endothelial cells are the major site of the increased bis-oxonol fluorescence signal with ischemia. These results indicate that endothelial cell membrane depolarization represents an early event with lung ischemia. Since the adenosine triphosphate content of lung was unchanged with ischemia in the O2-ventilated lungs, we postulate that membrane depolarization results from elimination of shear stress, possibly via inactivation of flow-sensitive K+-channels.

Adenosine Triphosphate↗
PubMed2004

Ordered nano-lslands on (La,Ba)MnO3 thin film surface by self-organization.

Self-organized nanostructures composed of discrete coherent islands were found on La0.67Ba0.33 MnO3 (LBMO) film surfaces. Our results revealed that rippled surface structures on LBMO films appeared during post-annealing at high temperature, and that the step edges of the rippled surfaces offer energetically favorable positions for the nucleation of coherent islands. The rippled surface serves as a template for the arrangement of coherent islands. This provides a new way to prepare ordered surface nanostructures in perovskite oxides without the necessity to employ any preprocessing techniques prior to the growth.

Barium Compounds↗
PubMed2005

Spontaneous ring-like self-assembly of BaF2 nanoparticles.

Self-assembly of BaF2 nanoparticles was described. BaF2 nanoparticles were prepared by microemulsion technology. The self-assembly of the particles is spontaneous without coating reagent on the surface or external force being applied during the procedure of sample preparation. XRD examination and ICP data showed the phase purity of the final product; FTIR spectroscopy confirmed that there was no organic species leaved in the product. By depositing one drop of colloid solution containing BaF2 particles on the TEM grid directly, we can get the ring-like self-assembly with larger particles dispersing peripherally to form a ring and smaller particles inside this ring forming circles.

Barium Compounds↗
PubMed2005

Supercritical fluid technology of nanoparticle coating for new ceramic materials.

This work highlights, for the first time, the coating of ferroelectric nanoparticles with a chemical fluid deposition process in supercritical fluids. BaTiO3 nanoparticles of about 50 nm are coated with a shell of a few nanometers of amorphous alumina and can be recovered as a dry powder for processing. The sintering of these core-shell nanoparticles gives access to a ceramic material with very interesting ferroelectric properties, in particular, dielectric losses below 1%.

Adsorption↗
PubMed2005

Supercritical fluid route for synthesizing crystalline Barium Strontium Titanate nanoparticles.

Pure and well-crystallized Barium Strontium Titanate (BST) nanoparticles with controlled Ba/Sr ratio have been successfully synthesized under supercritical conditions using a continuous-flow reactor in the temperature range of 150-380 degrees C at 26 MPa. To synthesize the Ba0.6Sr0.4TiO3 composition, alkoxides, ethanol and water were used. The resulting nanopowder consists of fine particles with an average particle size of 23 nm. The results show that the Ba/Sr ratio of this powder can be accurately controlled from the composition of precursor. The characterization of the as-synthesized Ba0.6Sr0.4TiO3 solid-solution and the dielectric properties of the sintered ceramics are here reported.

Barium Compounds↗
PubMed1997

Novel autocrine feedback control of catecholamine release. A discrete chromogranin a fragment is a noncompetitive nicotinic cholinergic antagonist.

Catecholamine secretory vesicle core proteins (chromogranins) contain an activity that inhibits catecholamine release, but the identity of the responsible peptide has been elusive. Size-fractionated chromogranins antagonized nicotinic cholinergic-stimulated catecholamine secretion; the inhibitor was enriched in processed chromogranin fragments, and was liberated from purified chromogranin A. Of 15 synthetic peptides spanning approximately 80% of chromogranin A, one (bovine chromogranin A344-364 [RSMRLSFRARGYGFRGPGLQL], or catestatin) was a potent, dose-dependent (IC50 approximately 200 nM), reversible secretory inhibitor on pheochromocytoma and adrenal chromaffin cells, as well as noradrenergic neurites. An antibody directed against this peptide blocked the inhibitory effect of chromogranin A proteolytic fragments on nicotinic-stimulated catecholamine secretion. This region of chromogranin A is extensively processed within chromaffin vesicles in vivo. The inhibitory effect was specific for nicotinic cholinergic stimulation of catecholamine release, and was shared by this chromogranin A region from several species. Nicotinic cationic (Na+, Ca2+) signal transduction was specifically disrupted by catestatin. Even high-dose nicotine failed to overcome the inhibition, suggesting noncompetitive nicotinic antagonism. This small domain within chromogranin A may contribute to a novel, autocrine, homeostatic (negative-feedback) mechanism controlling catecholamine release from chromaffin cells and neurons.

Amino Acid Sequence↗