ライフサイエンスコーパス: arteriole

1 supplied by a centrally placed thick-walled arteriole.

2 d in the absence of physical contact with an arteriole.

3 Xa after laser injury in the mouse cremaster arteriole.

4 al response to hyperglycemia at the efferent arteriole.

5 ontributes to functional dilatation in these arterioles.

6 the vascular smooth muscle layer of terminal arterioles.

7 alter the proper functioning of the adjacent arterioles.

8 phrine activation of alpha1ARs on peripheral arterioles.

9 lar remodeling in the precapillary pulmonary arterioles.

10 the glomeruli, peritubular capillaries, and arterioles.

11 stress secondary to metabolic dilatation of arterioles.

12 ar BAPTA causes vasoconstriction in adjacent arterioles.

13 versus CKD5 arterioles and in CKD5 versus PD arterioles.

14 nitrate (0.013-4.4 nmol/min) over resistance arterioles.

15 perivascular endfeet surrounding parenchymal arterioles.

16 ivascular regions of both large arteries and arterioles.

17 pid-induced endothelial dysfunction in human arterioles.

18 pitated with LOX-1 and CD32 from CRP-treated arterioles.

19 na is driven primarily by active dilation of arterioles.

20 and CD32 were detected in the endothelium of arterioles.

21 r impaired human platelet accrual in damaged arterioles.

22 merular microvessels, predominantly afferent arterioles.

23 ch as mesenteric arteries and larger retinal arterioles.

24 m-dependent vasomotor function in resistance arterioles.

25 gy characterized by concentrically thickened arterioles.

26 n prolonged vasodilation in distal pulmonary arterioles.

27 unologic, and stress-response cascades in PD arterioles.

28 the deleterious effects of Abeta on cerebral arterioles.

29 ssure and diameter data from porcine retinal arterioles.

30 injury of the carotid, aorta, and mesenteric arterioles.

31 ion declines with age in coronary resistance arterioles.

32 chanism is embolization and occlusion of end arterioles.

33 marily from venules, and the CBV signal from arterioles.

34 h wider retinal venules and narrower retinal arterioles.

35 venules (median RBC velocity in first-order arterioles, 5 minutes after administration was zero for

36 re/shell architecture previously observed in arterioles also occurs in venules, (2) plasma leakage pe

37 olated vascular smooth muscle cells from CAD arterioles, although mRNA or total cellular protein expr

38 tion alone is not sufficient to dilate these arterioles; an additional EC calcium-dependent signallin

39 tail bleeding times and impaired mesenteric arteriole and carotid artery thrombosis.

40 (-/-) mice demonstrated a marked decrease in arterioles and an increase in the number and volume of v

41 reases blood flow, capillaries dilate before arterioles and are estimated to produce 84% of the blood

42 d eNOS ser(1177) phosphorylation in terminal arterioles and capillaries (P < 0.05), but the latter ef

43 rease their energy supply by dilating nearby arterioles and capillaries.

44 ex vivo on human subcutaneous adipose tissue arterioles and endothelial cells.

45 ng associated with obliteration of pulmonary arterioles and formation of plexiform lesions composed o

46 t-and-pepper retinopathy, attenuation of the arterioles and generalized rod-cone dysfunction as deter

47 utive accumulation of HIF-2alpha in afferent arterioles and glomerular cells and HIF-1alpha in collec

48 ntial gene expression in control versus CKD5 arterioles and in CKD5 versus PD arterioles.

49 in the endothelium of muscularized pulmonary arterioles and in cultured pulmonary ECs from iPAH, cont

50 ronal fibers of spinal origin present around arterioles and in lymphocyte-containing areas of the whi

51 lazine treatment vasodilatates pre-capillary arterioles and increases microvascular perfusion, which

52 st area of fenestration within intramuscular arterioles and indicate that the anatomical architecture

53 in the walls of leptomeningeal and cortical arterioles and is likely a contributory factor to vascul

54 o ferric chloride (FeCl3)-injured mesenteric arterioles and laser-induced injury of cremaster muscle

55 rotein alpha-smooth muscle actin was high in arterioles and low in capillaries.

56 axation (EDR) was impaired in small coronary arterioles and mesenteric resistance artery from diabeti

57 ed activation of metabolic processes in CKD5 arterioles and of inflammatory, immunologic, and stress-

58 r processes along capillaries, pre-capillary arterioles and post-capillary venules.

59 cting both cerebral cortical capillaries and arterioles and resulting from Abeta deposition within th

60 or novel modes of activation of the AT1 R in arterioles and suggest that mechanically activated AT1 R

61 cts myogenic constriction in skeletal muscle arterioles and to determine underlying cellular mechanis

62 cts, lobules, microcysts, blood vessels, and arterioles and to identify invasive tumor through distin

63 as rapidly and completely stopped in all the arterioles and venules (median RBC velocity in first-ord

64 segment is determined by the distribution of arterioles and venules and their respective relative flo

65 id artery, the jugular vein, and cremasteric arterioles and venules in Apoe(-/-)and CatG-deficient mi

66 and wall shear stress (WSS) were measured in arterioles and venules, and compared between DR and C su

67 with specificity at the level of individual arterioles and venules.

68 ladder capillaries which connect peripheral arterioles and venules.

69 Narrower retinal arterioles and wider retinal venules conferred long-term

70 Narrower retinal arterioles and wider retinal venules have been associate

71 the vessel wall pulsatility of intracortical arterioles and widespread loss of perivascular AQP4 pola

72 n hearts, this causes a loss of arteries and arterioles and, despite a high capillary density, dimini

73 stained for smooth muscle actin (a marker of arterioles) and CD34 (an endothelial marker), with separ

74 l model of the sympathetic innervation of an arteriole, and used it to test the hypothesis that respi

75 lial endfeet contacting capillaries, but not arterioles, and that capillary dilations often follow sp

76 om well-known components, which assumes that arterioles are normally dilated in metabolically active

77 ich ADO induces dilation in small resistance arterioles are not established, or appear contradictory.

78 Here we show that parenchymal arterioles are responsible for 50% of the extracted O2 a

79 capillaries (37%), while for deeper regions arterioles are responsible for 61% of the total pressure

80 rted by local and spreading responses in the arterioles associated with those fibres.

81 ixed values, while the particles leaving the arteriole at the outlet are removed from the system.

82 Ca(2+) signaling regulates capillary but not arteriole blood flow.

83 channels in control tumors but a network of arterioles, bona fide capillaries, and venules in FGF9-e

84 sponsiveness to TNF-alpha in KRIT1 deficient arterioles, but not venules.

85 for arterial specification of the remodeling arteriole by mediating upregulation of the arterial endo

86 ntagonist of P2X1 receptors, dilated retinal arterioles by 32.1 +/- 2.6% (P < 0.001).

87 , an ATP hydrolysing enzyme, dilated retinal arterioles by 40.4 +/- 2.8%, while AOPCP (12.5 mm), an e

88 um), more selective P2X antagonists, dilated arterioles by 41.0 +/- 5.3% and 55.2 +/- 6.1% respective

89 trum P2 receptor antagonist, dilated retinal arterioles by 50.9 +/- 3.7% (P < 0.001).

90 reases extracellular ATP levels, constricted arterioles by 58.0 +/- 3.8% (P < 0.001 for both), demons

91 It dilates arterioles by activating large-conductance Ca(2+)-activa

92 inogen activator inhibitor-1 upregulation in arterioles by CRP.

93 of TGF-beta Furthermore, in the PD parietal arterioles, C1q and terminal complement complex abundanc

94 The results show that, independent of arterioles, capillaries actively dilate and regulate blo

95 cking the normal hierarchical arrangement of arterioles, capillaries and venules.

96 Unlike the arterioles, CD34-immunoreactive capillaries had dimensio

97 Rs was greater in upstream feed arteries and arterioles compared to downstream arterioles, with alpha

98 in time to thrombotic occlusion in cremaster arterioles compared with wild-type littermates, indicati

99 tory dilation observed in the normal retina, arterioles constrict in response to an oxygen deficiency

100 mal arteriole vascular tone, which result in arteriole constriction and dilation, respectively, alter

101 lood flow regulation, which assume that only arterioles control cerebral blood flow.

102 measured as the average diameter of retinal arterioles (CRAE) and venules (CRVE), and summarized as

103 ion of white matter hyperintensities via end-arteriole damage may protect against secondary brain atr

104 tion of 10 muM S1P, the diameter of afferent arterioles decreased to 35%+/-5% of the control diameter

105 ath-applied VP significantly constricted SON arterioles (Delta-41 +/- 7%) via activation of the V1a r

106 Arteriole density and wall motion abnormalities improved

107 ostischemic blood flow recovery and muscular arteriole density in immunodeficient mice.

108 Arteriole density was significantly higher in the peri-i

109 , infarct size, apoptosis, both vascular and arteriole density, and cell proliferation at week 4 afte

110 w recovery involves an increase in capillary/arteriole density, endothelial nitric oxide synthase/Akt

111 lowed by improved blood perfusion, capillary/arteriole density, skeletal muscle architecture, and cel

112 ricular function, myocardial metabolism, and arteriole density, while reducing infarct size, ventricu

113 In contrast, dilation of arterioles depends on NMDA receptor activation and Ca(2+

114 that acute COX-1 inhibition reduces resting arteriole diameter but fails to affect vasodilation in r

115 e responsible for the long-lasting change in arteriole diameter caused by theta burst neural activity

116 Fourth, fluctuations in arteriole diameter coherently drive fluctuations in bloo

117 ntrinsic ultra-slow (0.1 Hz) fluctuations in arteriole diameter, provides this link.

118 neurons and astrocytes that signal to alter arteriole diameter.

119 responsible for regulating capillary but not arteriole diameter.

120 ) and that the effect has an impact on basal arteriole diameter.SIGNIFICANCE STATEMENT The field of a

121 with FITC conjugated BSI-lectin labeling and arteriole diameters were compared before and five minute

122 Notably, efferent arterioles did not respond to S1P.

123 d, flow/pressure decreases evoke parenchymal arteriole dilation and increased resting pyramidal neuro

124 This hypothesis has been challenged, as arteriole dilation can occur in the absence of glial Ca(

125 elease at the perivascular endfoot, inducing arteriole dilation; K(+) undershoot in the synaptic spac

126 is reduced, light-evoked capillary, but not arteriole, dilation is abolished.

127 ibute to metabolic dilatation as they dilate arterioles directly upstream in response to vasoactive a

128 Arterioles displayed a vasoconstriction response to KCl

129 reatment midway between a FA and its primary arteriole eliminated ROV in the FA along with conducted

130 o endothelium midway between FAs and primary arterioles eliminated ROV only in FAs.

131 07, was also associated with central retinal arteriole equivalent (P=6.5x10(-12)).

132 an retinal vessel diameters (central retinal arteriole equivalent [CRAE] and central retinal venule e

133 al venule equivalent and the central retinal arteriole equivalent.

134 hich is also associated with central retinal arteriole equivalent.

135 ogenic responsiveness of renal preglomerular arterioles ex vivo and promoted cellular contraction in

136 or lipid-induced endothelial dysfunction in arterioles ex vivo.

137 PD arterioles exhibited particular upregulation of the comp

138 Endfeet with eHACSs were present only around arterioles exhibiting inversion of NVC.

139 III1H,8-10 and FNIII1H applied to EC-denuded arterioles failed to produce any dilatation indicating t

140 We found that, in first- and second-order arterioles, flicker evoked large (7.5 and 5.0%), rapid (

141 dicator of the dilatory capacity of cerebral arterioles for a vasomotor stimulus for maintaining a sp

142 cular unit (synaptic region, astrocytes, and arteriole) for the cortex of the young brain.

143 y promote endothelial cell proliferation and arteriole formation.

144 dent vasodilatation was impaired in coronary arterioles from aged rats (maximal relaxation to bradyki

145 mistry demonstrated ceramide accumulation in arterioles from both healthy patients and patients with

146 In arterioles from CAD subjects, H2O2-induced dilation was

147 induces arteriolargenesis - the formation of arterioles from capillaries - in a model of physiologica

148 dothelial dysfunction, whereas in resistance arterioles from glycolytic muscle, alterations in both n

149 Internal diameter changes of resistance arterioles from human adipose and atrial tissue were mea

150 dings were validated in omental and parietal arterioles from independent pediatric control (n=5), CKD

151 hibited alpha-adrenergic vasoconstriction in arterioles from mice and hypertensive humans, an effect

152 After exposure to BIBR-1532, arterioles from non-CAD subjects maintained the magnitud

153 with advancing age are heterogeneous between arterioles from oxidative and glycolytic muscles.

154 In resistance arterioles from oxidative muscle, loss of nitric oxide s

155 signalling contribute to the dysfunction in arterioles from oxidative muscles as compared with those

156 ctional adaptations that occur in resistance arterioles from oxidative muscles differ from those that

157 Remodeled pulmonary arterioles from SU-5416/hypoxia-PAH rats and monocrotali

158 a physiological mechanism of vasodilation in arterioles from subjects with CAD.

159 hibitor) abolished flow-mediated dilation in arterioles from subjects without CAD, whereas polyethyle

160 We microdissected omental arterioles from tissue layers not directly exposed to PD

161 nd a panniculitis with sparse, subtle, intra-arteriole, gray amorphous deposits that, on analysis by

162 In human arterioles, H2O2-induced dilation is impaired in CAD, wh

163 Neighbouring penetrating arterioles had different orientation preferences.

164 f ageing, smooth muscle actin-immunoreactive arterioles had thicker walls (P < 0.05), larger perimete

165 that functional vasodilatation in resistance arterioles has an endothelial cell (EC)-dependent compon

166 s to the disease site i.e., distal pulmonary arterioles has been one of the major challenges in achie

167 tanding of blood flow regulation by cerebral arterioles has evolved rapidly.

168 contrast, most in vivo studies of downstream arterioles have disproved these hypotheses and instead h

169 udies testing these hypotheses in downstream arterioles have failed to find evidence of intrinsic O2

170 nt where a large number of the pre-capillary arterioles have low perfusion, low haematocrit, and are

171 on has been reported in most skeletal muscle arterioles; however, unique alterations in signalling co

172 1.20 per 1-SD increase) and narrower retinal arterioles (HR, 1.06; 95% CI, 1.01-1.11; HR, 1.14; 95% C

173 Middle cerebral arterioles imaged in situ through cranial window also co

174 Venous segments were deviated toward the arterioles in 6 of the 7 cases.

175 aged Ca(2+) produced dilation of penetrating arterioles in a manner attenuated by scavenging D-serine

176 pacities were applied directly to resistance arterioles in cremaster muscles of anaesthetized (pentob

177 Yet the diameters of arterioles in distant (>5 mm), mirrored transhemispheric

178 vasoreactivity was absent in control tumors, arterioles in FGF9-expressing tumors could constrict and

179 as well as surface arteries and penetrating arterioles in rat visual cortex (where orientation maps

180 d flow regulation suggests the dilatation of arterioles in response to tissue hypoxia via the emissio

181 The ability of arterioles in situ to respond to occupancy of a specific

182 eptors, particularly on endothelial cells of arterioles in the brain and immune cells, which is in li

183 al activity and communicating it to upstream arterioles in the form of an electrical vasodilatory sig

184 blood flow and large numbers of newly formed arterioles in the hindlimb ischemia mouse model.

185 Arterioles in the peripheral microcirculation are exquis

186 is, or the lumenal expansion of pre-existing arterioles in the presence of an upstream occlusion, is

187 ncreases in flow/pressure within parenchymal arterioles increased the firing activity of a subtype of

188 Flow/pressure increases within parenchymal arterioles increased vascular tone and simultaneously de

189 om both neurons and astrocytes, which dilate arterioles, increasing in turn cerebral blood flow (CBF)

190 ed greater volume, with evidence of tortuous arterioles indicative of arteriogenesis (n=6-8 per group

191 ontraction while observing feed arteries and arterioles initiated ROV, which increased with contracti

192 elet accumulation in laser-induced cremaster arteriole injury, and PDI(ss-oo) mice had attenuated pla

193 The field of astrocyte-neuron and astrocyte-arteriole interactions is currently in a state of refine

194 cise, vasodilatation ascends from downstream arterioles into upstream feed arteries (FAs).

195 nal membrane of smooth muscle cells in renal arterioles is elicited.

196 gs suggest that vascular tone in rat retinal arterioles is maintained by tonic release of ATP from th

197 tment with gAd improved insulin responses in arterioles isolated from HFD rats, which was blocked by

198 ast with LacZ-positive cells in the afferent arterioles, LacZ-positive cells in the glomerular tuft d

199 tion and structural remodelling of pulmonary arterioles, leading to chronic elevation of pulmonary ar

200 This renders arterioles less responsive to K(+) released from astrocy

201 ate cerebral blood flow at the capillary and arteriole levels.

202 mitter pathway by which astrocytes influence arteriole lumen diameter.

203 phages, accompanied by enhanced formation of arterioles, may be responsible for shift of Hmox1(-/-) m

204 plus spironolactone in vivo, which decreased arteriole muscularization and pulmonary hypertension in

205 ease in pulmonary artery pressure and distal arteriole muscularization.

206 We found leukostasis with retinal arteriole occlusion in all treated eyes.

207 labeling of renin cells along renal afferent arterioles of adult mice.

208 c 3D simulations to study plasma skimming in arterioles of diameters 20 to 32 microns.

209 in the endothelial layer of capillaries and arterioles of human skeletal muscle.

210 sopressin-mediated vascular responses in SON arterioles of hypothalamic brain slices of Wistar or VP-

211 al oxygen uptake takes place in precapillary arterioles of less than 30 mum in diameter before the bl

212 erstitial cells, in the remodelled pulmonary arterioles of rats, cows and humans susceptible to hypox

213 s of ministrokes targeted to individual pial arterioles on motor function in Thy-1 line 18 channelrho

214 3 +/- 0.6, in mmHg) was greater than that of arterioles or collecting lymphatic vessels exposed to un

215 The extent to which smooth muscle-covered arterioles or pericyte-covered capillaries control vasom

216 create occlusions of individual penetrating arterioles or venules in rat cortex.

217 vessels and minute flows down to 0.3 mm/s in arterioles or venules were readily detectable at depths

218 nuated retinal vascular pulsation amplitude (arterioles P = .028; venules P < .0001).

219 contribute to the regulation of parenchymal arteriole (PA) tone in response to hemodynamic stimuli (

220 NVC was modeled by measuring parenchymal arteriole (PA) vasodilation in response to neuronal stim

221 assessed using ultrasound, and capillary and arteriole parameters were assessed using immunohistochem

222 Here, using parenchymal arterioles (PAs) from within the brain, we determined th

223 nction and structure of cerebral parenchymal arterioles (PAs), a major target of cerebral small vesse

224 PD fluid and used adjacent sections of four arterioles per patient for transcriptomic and proteomic

225 med by immunohistochemistry and evaluated on arterioles, peritubular capillaries, glomeruli, and tubu

226 d Mito-TEMPO impaired FID in healthy adipose arterioles pretreated with ceramide, whereas N(omega)-ni

227 ressed increased StAR in remodeled pulmonary arterioles, providing a basis for investigating hypoxia-

228 comparable at flash settings of 27 to 76 Ws (arterioles' range: 85%-92%; venules' range: 45%-53%).

229 val in vitro Optimal inhibition of pulmonary arteriole Raptor was achieved by treatment with Staramin

230 Renal preglomerular arterioles regulate vascular tone to ensure a large pres

231 TGF-induced vasoconstriction of the afferent arteriole results from the enhanced effect of several va

232 monary hypertension the loss of precapillary arterioles results from vascular injury causing endothel

233 Microarray analysis of mutant arterioles revealed upregulation of genes usually expres

234 dimensional model of HGPS that replicates an arteriole-scale tissue engineered blood vessel (TEBV) us

235 Whether blood flow is controlled solely by arteriole smooth muscle, or also by capillary pericytes,

236 Decidual spiral arteriole (SpA) remodeling is essential to ensure optima

237 s the average pulsation amplitude of retinal arterioles (SRAP) and venules (SRVP).

238 zed by increased blood pressure in the small arterioles supplying blood to lungs for oxygenation.

239 nd vasoconstriction of specific arteries and arterioles supplying bone.

240 ed resistance arteries and large first-order arterioles support the hypotheses that O2 -dependent inh

241 d resistance arteries and large, first-order arterioles support the hypothesis that these vessels are

242 The luminal diameter of a common terminal arteriole (TA) controls blood flow through up to 20 capi

243 scent HSCs associate specifically with small arterioles that are preferentially found in endosteal bo

244 FAs reflects hyperpolarization of downstream arterioles that conducts along the endothelium into prox

245 be a pathogenetic change in aged human brain arterioles that impacts multiple brain areas and contrib

246 dy rat isolated first-order cremaster muscle arterioles the AT1 R inhibitor candesartan (10(-7) -10(-

247 hypertension (PAH), correlate with pulmonary arteriole thickening, which suggests that mTORC1 regulat

248 ions to produce the same response allows the arteriole to respond to key homeostatic requirements usi

249 he relative contributions of capillaries and arterioles to blood flow regulation remain unclear, eluc

250 the blood oxygenation process from pulmonary arterioles to capillaries and venules in two-dimensional

251 cytotrophoblast progenitors remodel maternal arterioles to promote blood flow to the placenta.

252 esponsiveness of the aorta and small retinal arterioles to the vasoconstriction-inducing drug U46619

253 perficial layer, allowing rapid transit from arterioles to venules.

254 ganized, including venules, capillaries, and arterioles, to supply all of the cells with sufficient n

255 n the retrotrapezoid nucleus (RTN) maintains arteriole tone during high CO2/H(+) and disruption of th

256 On the other hand, decreasing parenchymal arteriole tone increased resting cortical pyramidal neur

257 e, we demonstrate that increased parenchymal arteriole tone significantly increased intracellular cal

258 ytes can control basal synaptic strength and arteriole tone via their resting Ca(2+) activity.

259 ot Ca(2+) was coincident with an increase in arteriole tone, and both the Ca(2+) drop and the tone ch

260 hat, in response to increases in parenchymal arteriole tone, astrocyte intracellular Ca(2+) increased

261 During increases in parenchymal arteriole tone, the pyramidal neuron response was unaffe

262 ascular resistance, which largely depends on arteriole tone.

263 cyte Ca(2+) and that this phenomenon changed arteriole tone.

264 d non-dividing (Ki-67(-)), were distant from arterioles, transition zone vessels, and bone surfaces.

265 ased saturation measurements in both retinal arterioles (up to 110%) and venules (up to 92%), with a

266 ed vasodilatation of the FA initiated on the arteriole using ACh microiontophoresis.

267 ulation despite robust dilations of adjacent arterioles using cyto-GCaMP3 and Lck-GCaMP6s, the most s

268 Mitochondrial H2O2 production was assayed in arterioles using mito peroxy yellow 1.

269 that astrocytes provide tonic regulation of arterioles using resting intracellular Ca(2+) in a manne

270 In arterioles, V, WSR, and WSS were lower in NDR (P </= 0.0

271 evoked increases or decreases in parenchymal arteriole vascular tone, which result in arteriole const

272 hies are divided into two groups-nerve large arteriole vasculitis and nerve microvasculitis-on the ba

273 Inorganic nitrite dilates small resistance arterioles via hypoxia-facilitated reduction to vasodila

274 ow by providing steady-state vasodilation to arterioles via resting astrocyte Ca(2+) and the continuo

275 n of HENA (45 muM) dilated the pial cerebral arterioles via selective BK-channel targeting.

276 fenestration area in second and first order arterioles vs. feed and popliteal arteries (58% and 16%

277 his electrical homogeneity arises, a virtual arteriole was developed that introduces variation in the

278 Rather, blood sourced by penetrating arterioles was effectively drained by the penetrating ve

279 Flow-mediated dilation (FMD) of coronary arterioles was investigated in DM (n = 41) and non-DM (n

280 is models in mesenterium or cremaster muscle arterioles, we demonstrate that Bambi-deficient mice for

281 and laser-induced injury of cremaster muscle arterioles, we herein show that thrombi formed in Cc2(-/

282 dies of intact or EC-denuded skeletal muscle arterioles, we show that ADO acts via A2A receptors loca

283 flow and vasodilatory responses of coronary arterioles were evaluated in all groups at the end of tr

284 Porcine coronary arterioles were isolated for vasoreactivity study, dihyd

285 Human coronary and adipose arterioles were isolated for videomicroscopy.

286 eeding times and thrombus formation in small arterioles were largely unaffected by reductions of PC u

287 duced thrombus formation in cremaster muscle arterioles were measured in wild-type (WT) and IL-6-defi

288 The diameters of primary arterioles were monitored under control conditions and f

289 st- (1A), second- (2A) and third- (3A) order arterioles were studied in response to single tetanic co

290 ar smooth muscle cells in the lumen of small arterioles, which failed to undergo outward expansion.

291 at rest, but is attenuated in remodeled lung arterioles, which may be of relevance in pulmonary hyper

292 -independent vasodilation in non-CAD adipose arterioles, which was reduced by paxilline, a large-cond

293 -independent vasodilation in non-CAD adipose arterioles, which was reduced by paxilline, a large-cond

294 Intraluminal treatment of pressurized arterioles with a pathophysiological level of CRP (7 mic

295 a preferential occlusion of the precapillary arterioles with infiltration of neutrophils, macrophages

296 teries and arterioles compared to downstream arterioles, with alpha2 ARs more effective than alpha1 A

297 effective in promoting the formation of new arterioles within the granulation tissue.

298 Occlusion of individual arterioles within the motor cortex led to a ministroke t

299 co-fluctuations in the diameter of pairs of arterioles within the same hemisphere diminish to chance

300 eling of a venous segment close to a retinal arteriole without arteriovenous overlap were imaged by a