ライフサイエンスコーパス: vasoactive

1 te its effects on neuronal activity from its vasoactive actions.

2 both MRI, MR angiography and intracavernosal vasoactive agent administration can be questioned.

3 Both MRI and intravenous vasoactive agent administration may be helpful in suspic

4 dney disease, cancer, respiratory infection, vasoactive agent use, and receipt of renal replacement t

5 ng increased neurotransmission and releasing vasoactive agents (e.g., K(+)) from perivascular endfeet

6 5]), temporary pacemaker (OR, 6.4 [2.2-19]), vasoactive agents (OR, 1.5 [1.1-2.1]), acute (<24 hours)

7 ortality rates were associated with starting vasoactive agents 1-6 hours after onset.

8 Fluids and vasoactive agents are both used to treat septic shock, b

9 HR: 1.94 [95% CI: 1.26 to 2.98]), the use of vasoactive agents for bleeding (HR: 2.01 [95% CI: 0.91 t

10 Fluids and vasoactive agents had strong, interacting associations w

11 ever, there may be differential responses to vasoactive agents in AHF patients with reduced versus pr

12 Starting vasoactive agents in the initial hour may be detrimental

13 d flow in response to temperature changes or vasoactive agents is a feature of cardiovascular disease

14 uninvolved, skin indicates that these potent vasoactive agents may play a role in wealing and tissue

15 arterioles directly upstream in response to vasoactive agents or contraction of adjacent muscle fibr

16 , illness category, and need for intravenous vasoactive agents prior to the arrest.

17 Assessment score that takes into account all vasoactive agents used in current clinical practice, use

18 Mortality was lowest when vasoactive agents were begun 1-6 hours after onset, with

19 ascular leakage and expression of the potent vasoactive agents' calcitonin gene-related peptide (CGRP

20 9, 51.0%) including chemotherapy, inotropes, vasoactive agents, and sedatives were the most frequentl

21 significant change in the use of IV fluids, vasoactive agents, or blood products.

22 unit (ICU) stay for >24 hours, septic shock, vasoactive agents, positive-pressure ventilation, chest

23 uid administration, only thereafter starting vasoactive agents, while continuing aggressive fluid adm

24 ds being given with such early initiation of vasoactive agents.

25 ance network was dilated and unresponsive to vasoactive agents.

26 Thus, vasoactive agonists probably invoke unique mechanisms th

27 In this study, we examined the ability of vasoactive agonists to induce dynamic changes in vascula

28 orientation before and after treatment with vasoactive agonists.

29 vocal cord dysfunction, scombroid poisoning, vasoactive amine intolerance, carcinoid syndrome and pha

30 ologic and inflammatory responses, including vasoactive amine sensitization (VAAS) to histamine (HA),

31 ggregation and activation through release of vasoactive amines in the inflammatory response, resultin

32 Still, histamine and other vasoactive amines remained at low levels, thus not affec

33 ptidase that converts angiotensin I into the vasoactive and aldosterone-stimulating peptide angiotens

34 ue to many factors, such as the influence of vasoactive and anesthetic drugs, total muscular relaxati

35 with ERMs, we examine here the expression of vasoactive and inflammatory mediators in the vitreous of

36 cultured PAH and control P-EC proliferation, vasoactive and proinflammatory factor production, and cr

37 in AD have been typically attributed to the vasoactive and/or vasculotoxic effects of amyloid-beta (

38 r hemodynamic stabilization upon endoscopic, vasoactive, and antibiotic treatment.

39 s in patients receiving standard endoscopic, vasoactive, and antibiotic treatment.

40 d electrolyte fluid homeostasis, cleaves the vasoactive angiotensin-I, bradykinin, and a number of ot

41 Tyramine (TYR) is a vasoactive biogenic amine found in food products due to

42 LPA was first identified as a vasoactive compound because it induced transient hyperte

43 erivascular adipose tissue or PVAT) releases vasoactive compounds that regulate vascular smooth muscl

44 Numerous vasoactive cytokines are upregulated during sepsis, incl

45 e elaboration of reactive oxygen species and vasoactive cytokines, altering the inflammatory milieu i

46 ars, leading to the discovery of its role in vasoactive, cytoprotective and anti-inflammatory respons

47 t for invasive mechanical ventilation and/or vasoactive drug support for more than 24 hours following

48 Exclusions were receiving vasoactive drug(s) prior to hospital admission, having k

49 ability of CA in healthy older adults during vasoactive drug-induced changes in arterial pressure ass

50 Mechanical ventilation (47.9% of patients), vasoactive drugs (51.2%), and dialysis (25.9%) were asso

51 on, more patients in the HFOV group received vasoactive drugs (91% vs. 84%, P=0.01) and received them

52 nafil (P = 0.004), had a shorter duration of vasoactive drugs (P = 0.02), and less often failed treat

53 yndrome that compared the efficacy of active vasoactive drugs (terlipressin, midodrine, octreotide, n

54 pected to require mechanical ventilation and vasoactive drugs for at least 12 hours to either tight g

55 n optimization, 92 institutions (77.3%) used vasoactive drugs to achieve a target mean arterial blood

56 clusion and its duration, length of surgery, vasoactive drugs used, blood loss, and transfusion) were

57 Vasoactive drugs were used in 23 patients (68%) and rena

58 nd resuscitation with intravenous fluids and vasoactive drugs when needed.

59 ibing order of interventions withdrawn, with vasoactive drugs withdrawn first followed by gradual wit

60 ological variables, sedativeanalgesic drugs, vasoactive drugs, and medical/surgical therapies for int

61 ated by increased use of intravenous fluids, vasoactive drugs, and red-cell transfusions and reflecte

62 Mechanical ventilation, vasoactive drugs, and renal replacement therapy were adm

63 are-associated infection, the need for other vasoactive drugs, and the multiple organ dysfunction sco

64 f vasoactivity, using a small panel of known vasoactive drugs.

65 ared with other adrenergic and nonadrenergic vasoactive drugs.

66 plexus, an intervening neural structure with vasoactive effects, was not responsible for the increase

67 low (CBF) reflect neuronal activation or its vasoactive effects.

68 pose tissue (PVAT) has been shown to mediate vasoactive effects; however, a sex-dependent difference

69 n of astroglial metabolism (-35%, p < 0.01), vasoactive epoxyeicosatrienoic acids (EETs; -60%, p < 0.

70 rved that vitreous concentrations of classic vasoactive factors (e.g., vascular endothelial growth fa

71 ctivated receptor gamma regulates a panel of vasoactive factors communicating between diseased pulmon

72 in their gene expression and the release of vasoactive factors from endothelial cells.

73 During exercise there is a balance between vasoactive factors that facilitate increases in blood fl

74 that adipose tissue from Adipo-MROE secrete vasoactive factors that preferentially influence vascula

75 ic vasconstriction despite blockade of these vasoactive factors.

76 sive multiorgan dysfunction, ventilator- and vasoactive-free days at Day 28, functional status, and m

77 entilator-free days were 16 (IQR, 0-25), and vasoactive-free days were 23 (IQR, 12-28).

78 ortality (primary outcome); ventilator-free, vasoactive-free, and organ failure-free days; and length

79 The expression of an array of vasoactive genes was assessed in the thoracic aorta and

80 Calcium-dependent release of vasoactive gliotransmitters is widely assumed to trigger

81 n fraction underwent aggressive titration of vasoactive HF therapies with assessment of central aorti

82 gical effects of the RAS are mediated by the vasoactive hormone angiotensin II (AngII) via two recept

83 s have highlighted angiotensin II (AngII), a vasoactive hormone, as a potent HIF-1 activator in vascu

84 the glomerular filtration rate, P = 0.14, or vasoactive hormones were found.

85 The two vasoactive hormones, angiotensin II (ANG II; vasoconstri

86 ived stellakines and their responsiveness to vasoactive hormones.

87 faximin on hemodynamics, renal function, and vasoactive hormones.

88 fect glomerular filtration rate or levels of vasoactive hormones.

89 e, and suggest that TRPV1 may be a target of vasoactive inflammatory mediators.

90 s ratio, 0.82; 95% CI, 0.68-0.98), and fewer vasoactive infusion days (3.0 vs 3.3 d; p < 0.001) when

91 ed mechanical ventilation (74% of patients), vasoactive infusions (55%), and corticosteroids (45%).

92 Common therapies included the following: vasoactive infusions (88%), central venous catheters (86

93 oped cardiovascular dysfunction treated with vasoactive infusions a median of 5 days after T cell the

94 acute kidney injury, and shorter duration of vasoactive infusions when compared with exclusive use of

95 h CICU mortality included age <30 days, CHD, vasoactive infusions, ventricular tachycardia, mechanica

96 Forty-three patients (75%) had a change in Vasoactive-Inotrope Score after the fluid bolus, of whom

97 e support implantation, as assessed by their Vasoactive-Inotrope Score and number of organ failures.

98 ednisolone was associated with reductions in vasoactive inotropic requirements and in the incidence o

99 failure requiring a support equivalent to a Vasoactive Inotropic Score greater than 50 to reach a me

100 (6.0-17.0) and 9.0 (6.0-11.0); durations of vasoactive-inotropic and mechanical ventilation support

101 01/per point (1.01-1.02), p < 0.001; highest vasoactive-inotropic score, 1.02/per point (1.00-1.04),

102 al durations of stay, maximum and cumulative vasoactive-inotropic scores, duration of mechanical vent

103 the hypersecretion of insulin (5 patients), vasoactive intestinal peptide (5 patients), gastrin (2 p

104 T)-expressing interneurons are a subclass of vasoactive intestinal peptide (ChAT-VIP) neurons of whic

105 e product 9.5 (SGII[PGP9.5]) and peptidergic vasoactive intestinal peptide (SGII[VIP]), and cutaneous

106 stem cells, we found that costimulation with vasoactive intestinal peptide (V) and phorbol ester (P)

107 diated by the primary coupling neuropeptide, vasoactive intestinal peptide (VIP) and its canonical re

108 activity in the visual cortex contains both vasoactive intestinal peptide (VIP) and somatostatin (SS

109 Although VPAC1 and its ligand vasoactive intestinal peptide (VIP) are important in gas

110 Vasoactive intestinal peptide (VIP) has been widely acce

111 small proline-rich protein 1a (sprr1a), and vasoactive intestinal peptide (vip) in the trigeminal ga

112 t principal excitatory (EXC) neurons and the vasoactive intestinal peptide (VIP) interneurons that su

113 One solution to this problem could be the vasoactive intestinal peptide (VIP) interneurons, which

114 Vasoactive intestinal peptide (VIP) is a pleiotropic neu

115 Vasoactive intestinal peptide (VIP) is an anti-inflammat

116 Cells that express the neuropeptide vasoactive intestinal peptide (VIP) mediate retinal entr

117 Vasoactive intestinal peptide (VIP) mediates a broad ran

118 faceted approach in mice, we have identified vasoactive intestinal peptide (VIP) neurons as a novel c

119 ed by sound, while visual responses of L2/L3 vasoactive intestinal peptide (VIP) neurons were suppres

120 n interneurons expressing Cre recombinase in vasoactive intestinal peptide (VIP) or parvalbumin (PV)

121 synthase (NOS), serotonin, substance P (SP), vasoactive intestinal peptide (VIP) or vesicular acetylc

122 We show that vasoactive intestinal peptide (VIP) secreted by the inne

123 ng parvalbumin (PV), somatostatin (SST), and vasoactive intestinal peptide (VIP) show cell-type-speci

124 demonstrated their dependence upon G-coupled vasoactive intestinal peptide (VIP) signaling.

125 Vasoactive intestinal peptide (VIP) suppresses Th1 immun

126 decreased the area of nitrergic neurons and vasoactive intestinal peptide (VIP) varicosities.

127 a population of enteric neurons that express vasoactive intestinal peptide (VIP)(4).

128 Vasoactive Intestinal Peptide (VIP), a pulmonary vasodil

129 .5 (PGP 9.5), a general neuronal marker, and vasoactive intestinal peptide (VIP), a sudomotor nerve f

130 holinergic and alpha(1)-adrenergic agonists, vasoactive intestinal peptide (VIP), and the purinergic

131 opulations, expressing somatostatin (SOM) or vasoactive intestinal peptide (VIP), are active as popul

132 We explored the relation between vasoactive intestinal peptide (VIP), CRTH2, and eosinoph

133 essing parvalbumin (PV), somatostatin (SOM), vasoactive intestinal peptide (VIP), or neuropeptide Y.

134 ntal Cell, Nedvetsky et al. (2014) find that vasoactive intestinal peptide (VIP), secreted by parasym

135 al that locomotion increases the activity of vasoactive intestinal peptide (VIP), somatostatin (SST)

136 ma-aminobutyric acidergic neurons expressing vasoactive intestinal peptide (Vip), somatostatin (Sst),

137 ctionally important neuropeptides, including vasoactive intestinal peptide (VIP), which drives light

138 geted to the inhibitory synapses made by the vasoactive intestinal peptide (VIP)- and calretinin-posi

139 ow that disinhibitory circuits consisting of vasoactive intestinal peptide (VIP)-expressing and somat

140 Parvalbumin (PV)- and Vasoactive intestinal peptide (VIP)-expressing INs exhib

141 owever, targeting of somatostatin (SOM)- and vasoactive intestinal peptide (VIP)-expressing INs led t

142 tional ErbB4 deletion, we tested the role of vasoactive intestinal peptide (VIP)-expressing interneur

143 to light induces a gene program in cortical vasoactive intestinal peptide (VIP)-expressing neurons t

144 cuit inhibition and a subsequent increase in vasoactive intestinal peptide (VIP)-mediated disinhibiti

145 In contrast, activating vasoactive intestinal peptide (VIP)-positive interneuron

146 g animals revealed that locomotion activates vasoactive intestinal peptide (VIP)-positive neurons in

147 PEG5kDa-cholane) to a 28 amino acid peptide, vasoactive intestinal peptide (VIP).

148 ctly on nociceptors to induce the release of vasoactive intestinal peptide (VIP).

149 face (ALI) vs submerged] and the presence of vasoactive intestinal peptide (VIP).

150 tinorecipient cells that express and release vasoactive intestinal peptide (VIP).

151 originating from the SCN neurons expressing vasoactive intestinal peptide (VIP+ neurons).

152 ic factor (NDNF+) cells in L1a and MD drives vasoactive intestinal peptide (VIP+) cells in L1b.

153 ass of interneurons in DS - those expressing vasoactive intestinal peptide (VIP-IN) -is unknown.

154 In particular, the effects of vasoactive intestinal peptide and secretin on intra-acin

155 ibitory neurons that express parvalbumin and vasoactive intestinal peptide have mutually antagonistic

156 ed to the diminished light-induced c-fos and vasoactive intestinal peptide in the suprachiasmatic nuc

157 In SCN lacking vasoactive intestinal peptide or its receptor, mCry1 exp

158 Endogenous mediators, such as vasoactive intestinal peptide or prostaglandin E2 (PGE2)

159 duplications occurring within a single gene: vasoactive intestinal peptide receptor 2 (VIPR2).

160 hat, upon agonist stimulation, a GPCR called vasoactive intestinal peptide receptor 2 (VPAC2) is shed

161 Vasoactive intestinal peptide receptor 2 can elicit immu

162 olase, agonists of natriuretic peptide A and vasoactive intestinal peptide receptor 2, and a novel mi

163 Epithelial responsiveness to vasoactive intestinal peptide was increased after enteri

164 of parvalbumin (PV), somatostatin (SST), and vasoactive intestinal peptide were decreased in hypoxic-

165 Treatment with vasoactive intestinal peptide, an anti-inflammatory neur

166 rosine kinase, endothelial progenitor cells, vasoactive intestinal peptide, and miRNA in PAH therapeu

167 n mCry1 expression and its interactions with vasoactive intestinal peptide, cAMP, and PER at the hear

168 neuron-specific enolase, gastrin, glucagon, vasoactive intestinal peptide, pancreatic polypeptide, a

169 neurons were labeled in parvalbumin-Cre and vasoactive intestinal peptide-Cre mice.

170 rents activates muscarinic receptors on both vasoactive intestinal peptide-expressing (VIP) and parva

171 The relative weight of vasoactive intestinal peptide-expressing (Vip) interneur

172 Recent work has suggested that vasoactive intestinal peptide-expressing (VIP) interneur

173 Vasoactive intestinal peptide-expressing (VIP) interneur

174 In addition, vasoactive intestinal peptide-expressing axonal plexuses

175 Recent studies on vasoactive intestinal peptide-expressing inhibitory neur

176 Vasoactive intestinal peptide-expressing inhibitory neur

177 Vasoactive intestinal peptide-expressing interneurons (V

178 Finally, vasoactive intestinal peptide-expressing interneurons pr

179 tional connectivity of pyramidal neurons and vasoactive intestinal peptide-expressing interneurons wi

180 enhancers selective for parvalbumin (PV) and vasoactive intestinal peptide-expressing interneurons.

181 Optogenetic inhibition of vasoactive intestinal peptide-expressing neurons did not

182 ed controls is correlated with the number of vasoactive intestinal peptide-expressing SCN neurons.

183 The position of vasoactive intestinal peptide-immunoreactive fibers was

184 More input to vasoactive intestinal peptide-positive (VIP+) neurons th

185 n-positive, somatostatin-positive (SST+), or vasoactive intestinal peptide-positive (VIP+) neurons, t

186 uted preferentially to surround suppression, vasoactive intestinal peptide-positive interneurons were

187 s primarily signaled motor action (licking), vasoactive intestinal peptide-positive neurons responded

188 id delivery and other issues associated with vasoactive intestinal peptide.

189 ts parvalbumin (PV), somatostatin (SOM), and vasoactive intestinal peptitde (VIP)-expressing interneu

190 We demonstrate that interneurons expressing vasoactive intestinal polypeptide (VIP(+)) play a causal

191 Here, we show that interneurons expressing vasoactive intestinal polypeptide (VIP(+)) regulate the

192 hat type 3 IS (IS3) cells that coexpress the vasoactive intestinal polypeptide (VIP) and calretinin c

193 -dependent coupling process mediated by both vasoactive intestinal polypeptide (VIP) and GABAA signal

194 The neuropeptide vasoactive intestinal polypeptide (VIP) and its VPAC2 re

195 Inhibitory interneurons expressing vasoactive intestinal polypeptide (VIP) are known to dis

196 olar infusion of the VPAC1/2 receptor ligand vasoactive intestinal polypeptide (VIP) had no effect on

197 d determine the role of mast cells (MCs) and vasoactive intestinal polypeptide (VIP) in barrier regul

198 and alpha5-knockout mice, lower activity of vasoactive intestinal polypeptide (VIP) interneurons res

199 In mammals, vasoactive intestinal polypeptide (VIP) is known to have

200 Vasoactive intestinal polypeptide (VIP) is released from

201 e imaging, we show that SCN cells expressing vasoactive intestinal polypeptide (VIP) or its cognate r

202 ssion and odor detection performance require vasoactive intestinal polypeptide (VIP) or its receptor

203 There is evidence that vasoactive intestinal polypeptide (VIP) participates in

204 Both secretin and vasoactive intestinal polypeptide (VIP) receptors are re

205 In particular, while vasoactive intestinal polypeptide (VIP) signalling is es

206 ne hydroxylase, nitric oxide synthetase, and vasoactive intestinal polypeptide (VIP) to detect neural

207 Paradoxically, we found that vasoactive intestinal polypeptide (VIP), a neuropeptide

208 Strikingly, vasoactive intestinal polypeptide (VIP), a neuropeptide

209 rneurons expressing neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP), and the numeric

210 presence and colocalization of the peptides vasoactive intestinal polypeptide (VIP), calcitonin-gene

211 r GnIH inhibits the action of kisspeptin and vasoactive intestinal polypeptide (VIP), positive regula

212 circuit in frontal cortex that originates in vasoactive intestinal polypeptide (VIP)-expressing inter

213 stance P (SP)-IR varicosities and 9 +/- 1.3% vasoactive intestinal polypeptide (VIP)-IR varicosities

214 N, physiological evidence suggests that only vasoactive intestinal polypeptide (VIP)/gastrin-releasin

215 signaling pathways induced by kisspeptin and vasoactive intestinal polypeptide in GnRH neuronal cell

216 Although locomotion-induced vasoactive intestinal polypeptide positive (VIP) interne

217 Vasoactive intestinal polypeptide receptor (VIP1R) is a

218 oxylase, neuronal nitric oxide synthase, and vasoactive intestinal polypeptide to visualize neural el

219 s of somatostatin(+) (SST) (MGE-derived) and vasoactive intestinal polypeptide(+) (VIP) (CGE-derived)

220 the SCN: AVP (arginine vasopressin) and VIP (vasoactive intestinal polypeptide).

221 normal electrophysiology in the presence of vasoactive intestinal polypeptide, a potent stimulator o

222 s variant gene 1, substance P, somatostatin, vasoactive intestinal polypeptide, and parvalbumin.

223 for the specification of neuropeptide Y and vasoactive intestinal polypeptide, indicating that a sub

224 Immunoreactivity for vasoactive intestinal polypeptide, nitric oxide synthase

225 goal-oriented learning tasks, we found that vasoactive intestinal polypeptide-expressing (VIP(+)), d

226 Touch only weakly modulated vasoactive intestinal polypeptide-expressing (VIP) inter

227 re, we used a transgenic mouse line in which vasoactive intestinal polypeptide-expressing (VIP+) GABA

228 tory neurons reduced their activity, whereas vasoactive intestinal polypeptide-expressing interneuron

229 at in contrast to somatostatin-expressing or vasoactive intestinal polypeptide-expressing interneuron

230 we have confirmed an indispensable role for vasoactive intestinal polypeptide-expressing SCN (SCN(VI

231 inergic, adrenergic, and nitrergic axons and vasoactive intestinal polypeptide-positive terminals, so

232 dal cells and GABA interneurons coexpressing vasoactive intestinal polypeptide.

233 injured unmyelinated afferents labeled with vasoactive intestinal polypeptide.

234 hese also contained nitric oxide synthase or vasoactive intestinal polypeptide.

235 ments of synaptic activity in populations of vasoactive-intestinal peptide (VIP) interneurons express

236 training, either directly or via inhibiting vasoactive-intestinal-peptide-expressing interneurons, p

237 reduce the production of proinflammatory and vasoactive leukotrienes.

238 Vasoactive liabilities are typically assayed using wire

239 ple cytochrome P450 eicosanoids, is a potent vasoactive lipid whose vascular effects include stimulat

240 ial roles of inflammation, oxidative stress, vasoactive mediator imbalance, dysregulated endocannabin

241 scular permeability caused by the release of vasoactive mediator(s).

242 l infection, resulting in the release of the vasoactive mediators chymase and tryptase.

243 We conclude that therapies modulating vasoactive mediators or inflammatory cytokines may not a

244 degranulation with release and secretion of vasoactive mediators, enzymes, and cytokines.

245 ssure <90 mm Hg or the need for inotropic or vasoactive medication and the requirement for mechanical

246 ic drugs (odds ratio, 1.9; p = 0.03), higher vasoactive medication dose (odds ratio, 3.2; p = 0.02),

247 otein, Pediatric Index of Mortality 3 score, vasoactive medication, and invasive mechanical ventilati

248 mpt administration of intravenous fluids and vasoactive medications aimed at restoring adequate circu

249 Tailoring vasoactive medicines to patients with HF based upon bett

250 efined functional gene group (thrombophilic, vasoactive, metabolic, immune, and cell signalling).

251 rm the blood-brain barrier (BBB) and release vasoactive molecules that regulate vascular tone.

252 in the splanchnic vascular bed, with several vasoactive molecules, controlled at multiple levels, wor

253 onsequently, SERMs regulate the synthesis of vasoactive nitric oxide ((*)NO).

254 r diastolic dysfunction requiring continuous vasoactive or diuretic infusion, respiratory support, or

255 uscitation, fluid resuscitation > 5 L/24 hr, vasoactive or inotropic support, and renal replacement t

256 FXR expression and involved intrahepatic vasoactive pathways (e.g., endothelial nitric oxide synt

257 We report the identification of the vasoactive peptide apelin as a central regulator for end

258 lecular-weight kininogen (HK), releasing the vasoactive peptide bradykinin.

259 Serelaxin, recombinant human relaxin-2, is a vasoactive peptide hormone with many biological and haem

260 Adrenomedullin (ADM) is a circulating vasoactive peptide involved in vascular homeostasis and

261 drial ATP synthase F0 subunit component is a vasoactive peptide on its release from cells.

262 Endothelin-1 (ET-1) is a vasoactive peptide that is elevated in aqueous humor as

263 tected against barrier dysfunction caused by vasoactive peptide thrombin and proinflammatory bacteria

264 ds to overproduction of bradykinin, a potent vasoactive peptide.

265 Several endogenous vasoactive peptides act as adaptive mechanisms, and thei

266 ast, potentiation of endogenous compensatory vasoactive peptides can act to enhance the survival effe

267 , the two pathways are activated to generate vasoactive peptides that contribute in various ways to t

268 c imaging; they are constructed by combining vasoactive peptides with synthetic chemical appendages a

269 Neprilysin is an endopeptidase that degrades vasoactive peptides, including atrial natriuretic peptid

270 Endothelins are a family of vasoactive peptides, of which 3 distinct isoforms exist,

271 n of the natriuretic peptides and many other vasoactive peptides.

272 that this elevates systemic levels of their vasoactive products, including chymase, and promotes vas

273 pharmacologic PPAR-gamma activation, via its vasoactive properties, may protect the fetal growth unde

274 carbon monoxide-, or cytochrome p450-derived vasoactive prostanoid signaling but is associated with v

275 Elevated serum concentrations of the vasoactive protein endothelin-1 (ET-1) occur in the sett

276 Aqueous vasoactive protein levels were measured by protein array

277 Thirty-two vasoactive proteins were detected in aqueous in untreate

278 Aqueous levels of 55 vasoactive proteins were measured with protein array.

279 correlation between changes in levels of 13 vasoactive proteins with changes in EFT, including 3 kno

280 ynapses evokes the production and release of vasoactive signals from both neurons and astrocytes, whi

281 sponse to activation of endothelial cells by vasoactive signals such as endothelins.

282 ries is regulated by mechanical stresses and vasoactive signals.

283 function as a mechanical valve and source of vasoactive species to optimize throughput, we developed

284 reactivity, the response of the vessels to a vasoactive stimulus such as hypoxia and hyperoxia, can b

285 astrocytic activation, stimulates release of vasoactive substances and dilation of cerebral vasculatu

286 estration allowing for passage of diffusible vasoactive substances and interface of endothelial cell

287 It has been proposed that release of vasoactive substances by astrocytes couples neuronal act

288 of autophagy in the paracrine regulation of vasoactive substances from the endothelium.

289 lude that while astrocytes can still release vasoactive substances, vascular amyloid deposits render

290 lar function include more than production of vasoactive substances.

291 othelial cells targeted by mast cell-derived vasoactive substances.

292 ed mechanical ventilation, 90 (48%) received vasoactive support, and 4 (2%) died.

293 pulmonary hemorrhage, hypotension requiring vasoactive support, conduit disruption requiring covered

294 bolus, of whom 60% received higher level of vasoactive support.

295 hemodynamics, and the activity of endogenous vasoactive systems (AEVS) were measured prospectively in

296 st hoc analysis of ROSE AHF, the response to vasoactive therapies differed in patients with heart fai

297 lysis may enable better individualization of vasoactive therapies in chronic HF and reduced ejection

298 Concomitant vasoactive therapy (odds ratio = 1.633; p < 0.001), medi

299 >/= 60 mm Hg, using normal saline bolus and vasoactive therapy-dopamine, and if needed noradrenaline

300 There was no interaction between vasoactive treatment's effect and EF on change in cystat