ライフサイエンスコーパス: perfusion pressure

1 cit (mean Deltaarea under the curve-cerebral perfusion pressure).

2 terpreted as the value of "optimal" cerebral perfusion pressure.

3 intaining intracranial pressure and cerebral perfusion pressure.

4 performed without compromise in the cerebral perfusion pressure.

5 refaction or decreased right coronary artery perfusion pressure.

6 ffect on intraspinal pressure or spinal cord perfusion pressure.

7 the vascular and tubular response to altered perfusion pressure.

8 ope dose significantly increased spinal cord perfusion pressure.

9 s that glaucoma is associated with decreased perfusion pressure.

10 hich is not modulated by changes in cerebral perfusion pressure.

11 d-tidal CO2 as well as coronary and cerebral perfusion pressure.

12 egulation to a sudden step increase in renal perfusion pressure.

13 ressor titration for maintenance of cerebral perfusion pressure.

14 icient to account for the increased coronary perfusion pressure.

15 ratio increased with reductions in cerebral perfusion pressure.

16 uld close a slit and prevent leakage at high perfusion pressure.

17 sure in the brain without impairing cerebral perfusion pressure.

18 tween pressure reactivity index and cerebral perfusion pressure.

19 lity and relaxation while restoring coronary perfusion pressure.

20 sure, pressure reactivity index, or cerebral perfusion pressure.

21 perfusion pressure, termed optimal cerebral perfusion pressure.

22 lic, diastolic, and mean blood pressures and perfusion pressures.

23 er kg/m(2); 95% CI, 0.38 to 1.59), and renal perfusion pressure (0.42 per mm Hg; 95% CI, 0.25 to 0.59

24 , nutrition (162 of 199 [81%]), and cerebral perfusion pressure (128 of 199 [64%]).

25 e-minute survival was higher in the coronary perfusion pressure-20 group (8 of 8) compared to depth 3

26 fusion pressures were higher in the coronary perfusion pressure-20 group compared to depth 33 mm (p =

27 gies: 1) Hemodynamic directed care (coronary perfusion pressure-20): chest compressions with depth ti

28 significantly reduced impairment of cerebral perfusion pressure (23+/-2 vs. 10+/-3 mmHg, p=0.006) and

29 Coronary perfusion pressures (29.5 +/- 2.7 mm Hg vs. 22.4 +/- 1.6

30 measured by ultrasound dilution at different perfusion pressures (30, 40, 50, and 60 mm Hg), duration

31 l perfusion pressure 70 compared to cerebral perfusion pressure 40.

32 te/pyruvate ratios were improved at cerebral perfusion pressure 70 compared to cerebral perfusion pre

33 rebral blood flow was higher in the cerebral perfusion pressure 70 group but did not reach statistica

34 Spinal cord perfusion pressure 90 to 100mm Hg and tissue glucose >4.

35 ntrolling intracranial pressure and cerebral perfusion pressure according to a local protocol.

36 wing incremental reductions in arteriovenous perfusion pressure across the retinal circulation.

37 ine is often used for management of cerebral perfusion pressure after traumatic brain injury, but can

38 elevant to glaucoma pathogenesis than ocular perfusion pressure alone.

39 ation induced an increase in baseline portal perfusion pressure and a decrease in vasodilation to ace

40 Both the increase in tracheal perfusion pressure and action potential discharge in res

41 show that astrocytes detect falling cerebral perfusion pressure and activate CNS autonomic sympatheti

42 Cerebral perfusion pressure and arterial PCO2 were maintained con

43 conventional precordial leads, like coronary perfusion pressure and end tidal PCO2, were predictive o

44 l rates were associated with higher coronary perfusion pressure and ETco2 during CPR.

45 ion at any given flow rate but indicates low perfusion pressure and limited autoregulatory reserve.

46 to examine the relationship between cerebral perfusion pressure and low, high, or normal mean middle

47 e acutely sensitive to decreases in cerebral perfusion pressure and may function as intracranial baro

48 ost episodes of hypoxia occur while cerebral perfusion pressure and mean arterial pressure are within

49 ounders of the relationship between cerebral perfusion pressure and mean middle cerebral artery flow

50 ounders of the relationship between cerebral perfusion pressure and mean middle cerebral artery flow

51 ound strong relationships between low ocular perfusion pressure and OAG prevalence, as well as OAG in

52 dies report similar associations between low perfusion pressure and OAG progression.

53 ociations were found between systolic ocular perfusion pressure and OAG, POAG, or PEXG, regardless of

54 A possible connection between ocular perfusion pressure and open-angle glaucoma (OAG) has bee

55 his study determined the optimum spinal cord perfusion pressure and optimum tissue glucose concentrat

56 sociation was found between diastolic ocular perfusion pressure and PEXG, regardless of the use of an

57 cance was found between low diastolic ocular perfusion pressure and POAG (OR = 0.84 per 10 mm Hg, 95%

58 The relationship between cerebral perfusion pressure and pressure reactivity index normall

59 y a defect in the relationship between renal perfusion pressure and sodium excretion.

60 e effect of various maneuvers on spinal cord perfusion pressure and spinal cord function and assessed

61 tial resuscitation rapidly restored cerebral perfusion pressure and stabilized hemodynamics with impr

62 efore LPS prevented the increase in baseline perfusion pressure and totally normalized the vasodilati

63 ntly shown to increase coronary and cerebral perfusion pressures and higher rates of return of sponta

64 ), diastolic (OR = 1.9), and mean (OR = 3.6) perfusion pressures and low diastolic blood pressure (OR

65 mpedance threshold device increased cerebral perfusion pressures and lowered diastolic intracranial p

66 e probe, to monitor continuously spinal cord perfusion pressure, and a microdialysis catheter, to mon

67 erived mean velocity index based on cerebral perfusion pressure, and autoregulation reactivity index

68 index, mean velocity index based on cerebral perfusion pressure, and autoregulation reactivity index

69 Cerebral blood flow, cerebral perfusion pressure, and autoregulatory index decreased m

70 reductions in cerebral blood flow, cerebral perfusion pressure, and autoregulatory index during hypo

71 tery diameter, cerebral blood flow, cerebral perfusion pressure, and elevated intracranial pressure a

72 flow, coronary perfusion pressure, cerebral perfusion pressure, and end-tidal CO2 were increased wit

73 pressure, arterial blood pressure, cerebral perfusion pressure, and impaired cerebral autoregulation

74 al curvature ratio, cataract surgery, ocular perfusion pressure, and peak expiratory flow rate were a

75 olic blood pressure and mean arterial ocular perfusion pressure, and use of systemic beta-blockers we

76 ndently predicted by end-tidal CO2, coronary perfusion pressure, and ventricular fibrillation wavefor

77 End-tidal CO2, coronary perfusion pressure, and ventricular fibrillation wavefor

78 variates included age, sex, diastolic ocular perfusion pressure, antihypertensive treatment, intraocu

79 ion resulted in higher intra-arrest coronary perfusion pressure, aortic pressures, and brain tissue o

80 as a result of chronically elevated cerebral perfusion pressure are hypothesized to precede the onset

81 hemodilution, and hypertension/high systolic perfusion pressure are more beneficial in CRVO, suggesti

82 ntracranial pressure and inadequate cerebral perfusion pressure are not infrequent during extraventri

83 Although the associations of OAG to perfusion pressure are strong, consistent, and biologica

84 We also identified spinal cord perfusion pressure as a key determinant of drug entry in

85 oninvasive technologies for ICP and cerebral perfusion pressure assessment are being tested in the cl

86 ral responses that maintain blood volume and perfusion pressure at levels optimal for survival.

87 Early aggressive cerebral perfusion pressure augmentation to a cerebral perfusion

88 We investigated whether a cerebral perfusion pressure autoregulation range-which uses a con

89 ions is essential for effective tailoring of perfusion pressure-based treatment strategies.

90 No difference in coronary perfusion pressure before delivering of the shock was ob

91 The percentage of time with cerebral perfusion pressure below (%cerebral perfusion pressure <

92 nt guidelines recommend maintaining cerebral perfusion pressure between 40 mm Hg-60 mm Hg.

93 he 20 mmHg threshold, and to target cerebral perfusion pressure between 50 and 70 mmHg.

94 anscranial Doppler velocity, PaCO2, cerebral perfusion pressure between the different steps.

95 ndependent of possible differences in ocular perfusion pressures between the 2 treatment arms.

96 not prevent the increase in baseline portal perfusion pressure, but attenuated the development of si

97 ve as phenylephrine for maintaining cerebral perfusion pressure, but intracranial pressure and brain

98 ntly with intracranial pressure and cerebral perfusion pressure, but not with pressure reactivity ind

99 the middle of the handgrip task), and ocular perfusion pressure by 25%+/-6% (averaged across the enti

100 We then manipulated forearm arterial perfusion pressure by adjusting the position of the exer

101 al spectrum, we manipulated forearm arterial perfusion pressure by altering the arm position above or

102 Increasing spinal cord perfusion pressure by approximately 10mm Hg increased th

103 Renal perfusion pressure can directly regulate sodium reabsorp

104 suscitation substantially decreased coronary perfusion pressure, cardiac index, and myocardial blood

105 y underlie the observed increase in cerebral perfusion pressure, carotid blood flow, and survival rat

106 In both groups, carotid blood flow, coronary perfusion pressure, cerebral perfusion pressure, and end

107 lly recorded intracranial pressure, cerebral perfusion pressure, cerebrovascular pressure reactivity

108 ne (P </= .006) and greater nocturnal ocular perfusion pressure compared with timolol treatment (P =

109 in greater diurnal sitting and supine ocular perfusion pressures compared with baseline (P </= .006)

110 acterized by intracranial pressure, cerebral perfusion pressure, compensatory reserve index, and auto

111 14), systolic arterial pressure and cerebral perfusion pressure corrected immediately (both p < 0.05)

112 matic spinal cord injury, higher spinal cord perfusion pressure correlated with increased limb motor

113 -fitting method that determined the cerebral perfusion pressure (CPP) at which the pressure reactivit

114 artery diameter, cortical CBF, and cerebral perfusion pressure (CPP) concomitant with elevated intra

115 ral balloon catheter until negative cerebral perfusion pressure (CPP) was obtained.

116 Cerebral perfusion pressure (CPP), calculated as mean arterial bl

117 CBF is related to cerebral perfusion pressure (CPP).

118 the continuous updating of optimal cerebral perfusion pressure (CPPopt) for patients after severe tr

119 ime, its ability to give an optimal cerebral perfusion pressure (CPPopt) recommendation, and its rela

120 dependently associated with optimal cerebral perfusion pressure curve absence.

121 between the absence of the optimal cerebral perfusion pressure curve and physiological variables, cl

122 8% of all 1,561 periods, an optimal cerebral perfusion pressure curve was absent.

123 utcome being absence of the optimal cerebral perfusion pressure curve.

124 Sequential optimal cerebral perfusion pressure curves were used to create a color-co

125 associated with absence of optimal cerebral perfusion pressure curves.

126 lds showed no significant impact on cerebral perfusion pressure deficit (mean Deltaarea under the cur

127 receptor antagonist) normalized the coronary perfusion pressure, demonstrating that the elevated endo

128 1.06; P = .02), and low mean arterial ocular perfusion pressure during follow-up (HR, 1.172; P = .007

129 ure was unaltered and that on renal vascular perfusion pressure enhanced in endotoxemic rats at both

130 Increasing femoral perfusion pressure (FPP) by moving from the supine to th

131 ithout a posture-induced increase in femoral perfusion pressure (FPP).

132 Handgrip exercise changes ocular perfusion pressure free of potential drug side effect an

133 indicates disturbed autoregulation, regional perfusion pressure gradients, or redistribution of flow

134 of 100 mm Hg and vasopressors to a coronary perfusion pressure greater than 20 mm Hg (BP care); or o

135 tration of vasopressors to maintain coronary perfusion pressure greater than 20 mm Hg; 2) Depth 33 mm

136 ial pressure greater than 70 mm Hg, cerebral perfusion pressure greater than 50 mm Hg, PaO2 150 +/- 5

137 ic directed resuscitation targeting coronary perfusion pressures greater than 20 mm Hg during 10 minu

138 8.2%) was significantly higher than cerebral perfusion pressure group (18.2%; relative risk = 2.1; 95

139 The cerebral perfusion pressure group in comparison with intracranial

140 D) significantly (P<0.05) decreased coronary perfusion pressure (group C, 12.8+/-4.78 mm Hg; group D,

141 lower limit of reactivity), above (%cerebral perfusion pressure > upper limit of reactivity), or with

142 geted therapy (n = 55) (maintaining cerebral perfusion pressure >/= 60 mm Hg, using normal saline bol

143 ral artery flow velocity occur with cerebral perfusion pressure >40 mm Hg in severe pediatric traumat

144 rebral artery flow velocity despite cerebral perfusion pressure >40 mm Hg.

145 rginine vasopressin was titrated to cerebral perfusion pressure >70 mm Hg (randomized and blinded) pl

146 trose were administered to maintain cerebral perfusion pressure >70 mm Hg, filling pressure >12 mm Hg

147 90 mm Hg, vasopressors titrated to coronary perfusion pressure >= 20 mm Hg) or depth-guided cardiopu

148 rain herniation; and maintenance of cerebral perfusion pressure (>40 mm Hg) for 72 h after the diagno

149 cations associated with targeting a cerebral perfusion pressure>70, we hypothesize that targeting a c

150 er sufficient chest compressions and to keep perfusion pressure high.

151 ine perfusion solution and 25% physiological perfusion pressures (HMP, n=5).

152 I = 1.32 to 4.87, P = .005), and mean ocular perfusion pressure (HR = 1.21/mm Hg lower, 95% CI = 1.12

153 ationship of cerebral blood flow to cerebral perfusion pressure in a swine model of pediatric hypoxic

154 nce of Kir6.1 did not elevate basal coronary perfusion pressure in eKO mice.

155 described in previous studies on the role of perfusion pressure in glaucoma.

156 re run to assess the role of systolic ocular perfusion pressure in OAG, POAG, and PEXG.

157 vated intracranial pressure and low cerebral perfusion pressure in obstructive intraventricular hemor

158 e cerebral artery flow velocity and cerebral perfusion pressure in pediatric traumatic brain injury.

159 and nocturnal periods, and increases ocular perfusion pressure in the diurnal, but not the nocturnal

160 Studies suggest that reduced ocular perfusion pressure in the optic nerve head (ONH) increas

161 o the Ohm's law locally decrease hydrostatic perfusion pressures in the pulmonary microvasculature du

162 ncreased more in those with larger diastolic perfusion pressure increase and in AC compared to OA eye

163 weight, systemic blood pressure, and ocular perfusion pressure increased significantly with age, but

164 compared to timolol 0.5%, lower mean ocular perfusion pressure increased the risk for reaching a pro

165 nges occurred in the presence of reduced leg perfusion pressure, indicating that these augmentations

166 Sex, mean ocular perfusion pressure, intraocular pressure, mean deviation

167 iopulmonary resuscitation, adequate coronary perfusion pressure is essential for establishing return

168 Besides time, mean ocular perfusion pressure is significantly associated with this

169 Adherence to the cerebral perfusion pressure key performance indicator was also as

170 Each 1 mm Hg increase in cerebral perfusion pressure led to a decrease in the jugular veno

171 anial pressure greater than 20 plus cerebral perfusion pressure less than 60 mm Hg were associated wi

172 y-30 modified Rankin Scale, whereas cerebral perfusion pressure less than 65 and less than 75 mm Hg w

173 anial pressure greater than 20 plus cerebral perfusion pressure less than 70 mm Hg were associated wi

174 l pressure, percentage of time with cerebral perfusion pressure less than lower limit of reactivity w

175 ac unloading properties, reductions in renal perfusion pressures limit their clinical effectiveness.

176 timation of the "lower" and "upper" cerebral perfusion pressure limits of cerebrovascular pressure au

177 tomatically the "lower" and "upper" cerebral perfusion pressure limits of reactivity, respectively.

178 Low diastolic, systolic and mean perfusion pressures, low diastolic blood pressure, and h

179 ic piglets had a significant decrease in the perfusion pressure lower limit of autoregulation compare

180 cerebral perfusion pressure below (%cerebral perfusion pressure < lower limit of reactivity), above (

181 th unfavorable outcome (odds ratio %cerebral perfusion pressure < lower limit of reactivity, 1.04; 95

182 ebral perfusion pressure threshold, cerebral perfusion pressure <60 mm Hg was not associated with hig

183 Cerebral perfusion pressure<40 mm Hg following pediatric traumati

184 In severe traumatic brain injury, cerebral perfusion pressure management based on cerebrovascular p

185 ndividualized autoregulation-guided cerebral perfusion pressure management may be a plausible alterna

186 intaining tissue oxygenation during cerebral perfusion pressure management.

187 Low diastolic ocular perfusion pressure may be associated with increased risk

188 ure control for the optimization of cerebral perfusion pressure may constitute the most important the

189 ntracranial pressure and inadequate cerebral perfusion pressure may contribute to poor outcomes in hy

190 gen tension, intracranial pressure, cerebral perfusion pressure, mean arterial pressure, and jugular

191 Cerebral perfusion pressures, measured in nine additional pigs, w

192 find a way of improving the optimal cerebral perfusion pressure methodology by introducing a new visu

193 dition to intracranial pressure and cerebral perfusion pressure monitoring leads to better outcomes a

194 pressure [IOP], axial length and mean ocular perfusion pressure [MOPP]) and systemic parameters (bloo

195 w Outcome Scale: all operating room cerebral perfusion pressure more than 40 mm Hg (adjusted relative

196 , 0.61; 95% CI, 0.58-0.64), all ICU cerebral perfusion pressure more than 40 mm Hg (adjusted relative

197 sessed the time-weighted average of the mean perfusion pressure (MPP) deficit (i.e., the percentage d

198 e/pyruvate ratio was not related to cerebral perfusion pressure, nor was the percent time-burden of e

199 Cerebral perfusion pressure, nutrition, and hypocarbia targets ar

200 and its flow adjusted to maintain a coronary perfusion pressure of 10 mm Hg.

201 d cell injury volumes compared to a cerebral perfusion pressure of 40 mm Hg in an immature swine mode

202 an arterial pressure of 78+/-5 mm Hg, ocular perfusion pressure of 67+/-4 mm Hg at rest (mean+/-SD, n

203 erfusion pressure augmentation to a cerebral perfusion pressure of 70 mm Hg in pediatric traumatic br

204 Targeting a cerebral perfusion pressure of 70 mm Hg resulted in a greater red

205 70, we hypothesize that targeting a cerebral perfusion pressure of 70 mm Hg with the use of phenyleph

206 min for 2.0 Hz and increased global cerebral perfusion pressure of 91 mm Hg for 0 Hz, 100.5 mm Hg for

207 lic blood pressure of 100 mm Hg and coronary perfusion pressure of greater than 20 mm Hg improved 24-

208 and vasopressor dosing to maintain coronary perfusion pressure of greater than 20 mm Hg or 2) guidel

209 terial pressure, and both the renal vascular perfusion pressure of perfused kidneys in vitro and rena

210 States of low perfusion pressure of the kidney associate with hyperpla

211 Measurements were made at perfusion pressures of 10 mmHg, 20 mmHg, 30 mmHg, and 40

212 Measurements were made at perfusion pressures of 10, 20, 30 and 40 mm Hg.

213 is appears necessary to establish a cerebral perfusion pressure on the order of 100 mm Hg at the cran

214 The aim of this study was to compare ocular perfusion pressure (OPP) and ophthalmic artery flow (OAF

215 raocular pressure (IOP) and decreased ocular perfusion pressure (OPP) are risk factors for glaucoma d

216 Systemic blood pressure (BP) and ocular perfusion pressure (OPP) parameters were also determined

217 5% CI, 1.70-11.75), and low diastolic ocular perfusion pressure (OPP) throughout the study (OR, 0.39;

218 ease in blood pressure leads to lower ocular perfusion pressure (OPP), which may significantly increa

219 c (DBP) blood pressure and on 24-hour ocular perfusion pressure (OPP).

220 cluding intraocular pressure (IOP) or ocular perfusion pressure (OPP).

221 l perfusion pressure target-called "cerebral perfusion pressure optimal".

222 stant level despite fluctuations of cerebral perfusion pressure or arterial blood pressure.

223 e association with axial length, mean ocular perfusion pressure, or IOP was assessed using a linear m

224 edia thickness (P = .04), and reduced ocular perfusion pressure (P < .001).

225 on-brain oxygen tension gradient to cerebral perfusion pressure (p = 0.004) when comparing normoxia t

226 There were trends for rising cerebral perfusion pressure (p = 0.03) and intracranial pressure

227 METHODS AND MAIN Cerebral perfusion pressure-pressure reactivity index curves were

228 Mean coronary perfusion pressure prior to defibrillation was significa

229 ned that the placenta in the reduced uterine perfusion pressure rat model of preeclampsia is hypoxic,

230 eted to arterial blood pressure and coronary perfusion pressure rather than optimal guideline care wo

231 Proportion of cerebral perfusion pressure readings from less than 65 to less th

232 Proportion of cerebral perfusion pressure readings from less than 65 to less th

233 As ocular perfusion pressure reflects the vascular status at the o

234 olor-coded maps of autoregulation - cerebral perfusion pressure relationship evolution over time.

235 volumes significantly increased with higher perfusion pressures, remained constant over time, and si

236 control groups to attain the target coronary perfusion pressure, resulting in comparable left anterio

237 We studied the impact of renal perfusion pressure (RPP) on the development of renal inj

238 egnant (NP) and preeclamptic reduced uterine perfusion pressure (RUPP) Sprague Dawley rats on gestati

239 itor intraspinal pressure (ISP), spinal cord perfusion pressure (SCPP), tissue metabolism and inflamm

240 e perfusion performed using subphysiological perfusion pressures seems to offer some advantages over

241 Of all factors tested, only mean ocular perfusion pressure showed a significant association with

242 Systemic perfusion pressure (SPP) measured in the descending aort

243 rt the hypothesis that the concept of ocular perfusion pressure status may be more relevant to glauco

244 sting for intracranial pressure and cerebral perfusion pressure, systemic glucose concentration (adju

245 After 8 hrs, in both groups, cerebral perfusion pressure, systolic arterial pressure, and hear

246 tifying "one" autoregulation-guided cerebral perfusion pressure target-called "cerebral perfusion pre

247 We compared cerebral perfusion pressure-targeted approach with the convention

248 s were randomized to receive either cerebral perfusion pressure-targeted therapy (n = 55) (maintainin

249 Cerebral perfusion pressure-targeted therapy, which relied on mor

250 Perfusion pressure, temperature, and circuit flow were m

251 vidualized target for management of cerebral perfusion pressure, termed optimal cerebral perfusion pr

252 re IOP reduction and more increase of ocular perfusion pressure than timolol.

253 f an individually targeted level of cerebral perfusion pressure that aims to restore impaired cerebra

254 acholine caused strong increases in tracheal perfusion pressure that were accompanied by action poten

255 cardiac workload and reduced coronary artery perfusion pressure that, in turn, may lead to microvascu

256 rly values of intracranial pressure/cerebral perfusion pressure, the compensatory reserve index, and

257 ion that sodium excretion is driven by renal perfusion pressure, the so-called 'renal function curve'

258 ation with intracranial pressure or cerebral perfusion pressure; the correlation with pressure reacti

259 be a plausible alternative to fixed cerebral perfusion pressure threshold management in severe trauma

260 When examined by cerebral perfusion pressure threshold, cerebral perfusion pressur

261 related to any particular sustained cerebral perfusion pressure threshold.

262 We hypothesized that increased cerebral perfusion pressure through phenylephrine sex dependently

263 tracranial pressure-time burden and cerebral perfusion pressure-time burden should be tested prospect

264 dialysis was started after fall of cerebral perfusion pressure to 45 mmHg and continued for 8 h.

265 essure reactivity index and optimal cerebral perfusion pressure using ICM+ software (Cambridge Enterp

266 The cerebral perfusion pressure values at which this "U-shaped curve"

267 Burden of low cerebral perfusion pressure was also associated with poor short-

268 oxic episodes were more common when cerebral perfusion pressure was below 60 mm Hg (relative risk = 3

269 The mean ocular perfusion pressure was calculated for each eye at each o

270 Ocular perfusion pressure was defined as 2/3[diastolic BP + 1/3

271 Coronary perfusion pressure was higher in the BP care group (poin

272 he association between physical activity and perfusion pressure was independent of IOP, but largely m

273 One hour after injury, cerebral perfusion pressure was manipulated with the vasoconstric

274 Cerebral perfusion pressure was not restored until mannitol and p

275 te, intracranial pressure (ICP) and cerebral perfusion pressure was recorded during the stepwise elev

276 In subgroup analyses, diastolic ocular perfusion pressure was significantly associated with POA

277 Coronary perfusion pressure was significantly higher in the anima

278 ure were similar between groups but cerebral perfusion pressure was significantly higher in the posit

279 Mean baseline ocular perfusion pressure was significantly increased during th

280 circulation after a shock, although coronary perfusion pressure was significantly related to both amp

281 ng, a postural change that increases retinal perfusion pressure, was measured.

282 By intervening to increase spinal cord perfusion pressure, we could increase the amplitude of m

283 tissue oxygen tension gradient, and cerebral perfusion pressure were 14 mm Hg (SD, 4), 53 mm Hg (SD,

284 lar venous bulb oxygen tension, and cerebral perfusion pressure were 29 mm Hg (SD, 9), 45 mm Hg (SD,

285 Mean IOP and calculated ocular perfusion pressure were compared for the diurnal and noc

286 End-tidal CO2 and coronary perfusion pressure were not predictive of return of spon

287 Intracranial pressure and cerebral perfusion pressure were recorded every 4 hours, analyzed

288 Flow rate and perfusion pressure were reproducible within a coefficien

289 d flow responding to the elevations of renal perfusion pressure were significantly blunted by 50% and

290 pulmonary resuscitation, aortic and coronary perfusion pressure were similar between groups but cereb

291 Coronary perfusion pressures were higher in the coronary perfusio

292 , adenosine and levcromakalim, decreased the perfusion pressure whereas the K(ATP) channel blocker gl

293 rease in the autoregulation range toward low perfusion pressure, which is consistent with observation

294 at an initial salt-induced increase in renal perfusion pressure, which is likely independent of immun

295 sion imaging or a significant fall in distal perfusion pressure with hyperemia-induced vasodilatation

296 n (p < .01), resulting in decreased coronary perfusion pressure with leaning.

297 ese data indicate that elevation of cerebral perfusion pressure with phenylephrine sex dependently pr

298 ressure, intracranial pressure, and cerebral perfusion pressure, with real-time calculations of press

299 or within these reactivity limits (%cerebral perfusion pressure within limits of reactivity) was calc

300 ult from the shifting distributions of local perfusion pressures within the network of capillary vess