ライフサイエンスコーパス: perfusion pressure

1 for mean intratracheal pressure and coronary perfusion pressure).

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

3 s that glaucoma is associated with decreased perfusion pressure.

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

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

6 ressor titration for maintenance of cerebral perfusion pressure.

7 icient to account for the increased coronary perfusion pressure.

8 ratio increased with reductions in cerebral perfusion pressure.

9 had a substantially elevated basal coronary perfusion pressure.

10 d in the setting of reduced levels of ATP or perfusion pressure.

11 ris and protects its capillary bed from high perfusion pressure.

12 Hg using norepinephrine to control cerebral perfusion pressure.

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

14 perfusion pressure, termed optimal cerebral perfusion pressure.

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

16 intaining intracranial pressure and cerebral perfusion pressure.

17 tween pressure reactivity index and cerebral perfusion pressure.

18 performed without compromise in the cerebral perfusion pressure.

19 refaction or decreased right coronary artery perfusion pressure.

20 ffect on intraspinal pressure or spinal cord perfusion pressure.

21 the vascular and tubular response to altered perfusion pressure.

22 ope dose significantly increased spinal cord perfusion pressure.

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

24 re (18 +/- 1 to 25 +/- 2; p = .04); cerebral perfusion pressure (16 +/- 3 to 18 +/- 3; p = .07); comm

25 re (20 +/- 1 to 26 +/- 1; p < .01); coronary perfusion pressure (18 +/- 1 to 25 +/- 2; p = .04); cere

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

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

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

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

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

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

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

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

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

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

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

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 Cerebral perfusion pressure and arterial PCO2 were maintained con

42 nial hypertension and assessment of cerebral perfusion pressure and autoregulation is the focus of on

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

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

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

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

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

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

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

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

55 secondary brain ischemia, in which cerebral perfusion pressure and oxygen delivery have gained new i

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 Vital organ perfusion pressures and end-tidal CO2 were significantly

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

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

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

67 cic pressure and markedly decreased coronary perfusion pressures and survival rates.

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

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

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

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

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

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

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

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

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

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

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

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

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

81 re was a strong correlation between coronary perfusion pressure (aortic to right atrial mean decompre

82 Because myocardial ATP levels and coronary perfusion pressure are reduced in CHF, this study was un

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 rodialysis to assess the effects of cerebral perfusion pressure augmentation on regional physiology a

87 Cerebral perfusion pressure augmentation resulted in a significan

88 Cerebral perfusion pressure augmentation significantly increased

89 Early aggressive cerebral perfusion pressure augmentation to a cerebral perfusion

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

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

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

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

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

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

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

97 ening condition due to elevation of cerebral perfusion pressure beyond the limits of autoregulation.

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

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

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

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

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 This SPS was altered during increased renal perfusion pressure, consistent with the podocyte dynamic

111 Despite a decrease in coronary perfusion pressure, coronary blood flow is increased.

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

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

114 ing the infusion produced a fall in cerebral perfusion pressure (CPP) and a significant decrease of t

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

116 wing that aggressive maintenance of cerebral perfusion pressure (CPP) can worsen outcome due to extra

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

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

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

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

121 dependently associated with optimal cerebral perfusion pressure curve absence.

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

123 8% of all 1,561 periods, an optimal cerebral perfusion pressure curve was absent.

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

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

126 associated with absence of optimal cerebral perfusion pressure curves.

127 es of epinephrine were given if the coronary perfusion pressure decreased below 15 mm Hg.

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

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

130 Coronary perfusion pressure (diastolic; aortic minus right atrial

131 Coronary perfusion pressure during CPR was not different between

132 1.06; P = .02), and low mean arterial ocular perfusion pressure during follow-up (HR, 1.172; P = .007

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

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

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

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

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

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

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

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

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

142 8.2%) was significantly higher than cerebral perfusion pressure group (18.2%; relative risk = 2.1; 95

143 The cerebral perfusion pressure group in comparison with intracranial

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

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

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

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

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

149 ith vasopressor therapy to maintain cerebral perfusion pressure >60 mmHg.

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

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

152 eceived mannitol and the target was cerebral perfusion pressure >or=60 mm Hg.

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

154 RBCT: Pbto2, intracranial pressure, cerebral perfusion pressure, hemoglobin oxygen saturation (Sao2),

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

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

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

158 inine vasopressin rapidly corrected cerebral perfusion pressure, improved cerebrovascular compliance,

159 fied the response to an increase in cerebral perfusion pressure in a region of interest around a brai

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

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

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

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

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

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

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

167 ST segment elevation and coronary perfusion pressure in the restored mice did not differ s

168 catecholamine infusions to maintain cerebral perfusion pressure in the setting of a high-dose propofo

169 ase in mean arterial pressure and thus renal perfusion pressure in this area of the kidney.

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

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

172 Mean arterial pressure and cerebral perfusion pressure increased significantly, and the requ

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

174 The cerebral perfusion pressure intervention resulted in a greater pe

175 ue compartments were reduced by the cerebral perfusion pressure intervention.

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

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

178 erebral blood flow even under relatively low perfusion pressures, it may be beneficial during global

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

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

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

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

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

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

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

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

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

188 Cerebral perfusion pressure<40 mm Hg following pediatric traumati

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

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

191 intaining tissue oxygenation during cerebral perfusion pressure management.

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

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

194 ic minus right atrial pressure) and cerebral perfusion pressure (mean arterial minus mean intracrania

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

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

197 rathoracic pressure (mm Hg/min) and coronary perfusion pressure (mm Hg) were 7.1+/-0.7, 11.6+/-0.7, 1

198 +/- 12, 8 +/- 3, p < 0.01); and 2) coronary perfusion pressures (mm Hg) were higher in ACD + ITD CPR

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

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

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

202 , 0.61; 95% CI, 0.58-0.64), all ICU cerebral perfusion pressure more than 40 mm Hg (adjusted relative

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

204 recommended to maintain an adequate cerebral perfusion pressure of >60 mm Hg.

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

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

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

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

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

210 70, we hypothesize that targeting a cerebral perfusion pressure of 70 mm Hg with the use of phenyleph

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

212 h positron emission tomography at a cerebral perfusion pressure of approximately 70 mm Hg and approxi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

230 Mean coronary perfusion pressure prior to defibrillation was significa

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

232 is tightly linked to sodium intake and renal perfusion pressure, reflecting the important role of the

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 Cerebral perfusion pressure, Sao2, and Fio2 were similar before a

239 crease appears to be independent of cerebral perfusion pressure, Sao2, and Fio2.

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 Changes in the descending aortic (systemic) perfusion pressure (SPP; flow constant) were used to ass

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

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

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

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

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

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

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

251 The Brain Trauma Foundation has revised perfusion pressure targets, and there are additional dat

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

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

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

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

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

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

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

259 In addition, no single cerebral perfusion pressure threshold was associated with a signi

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

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

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

266 alues appear to be elevated despite cerebral perfusion pressure values customarily considered to be a

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

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

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

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

271 The averaged coronary perfusion pressure was higher in the epinephrine (34 +/-

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 h arginine vasopressin vs. placebo, cerebral perfusion pressure was more rapidly corrected (p < .05).

275 Cerebral perfusion pressure was not restored until mannitol and p

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

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

278 Coronary perfusion pressure was significantly higher in the anima

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

280 Mean baseline ocular perfusion pressure was significantly increased during th

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

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

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

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

285 The systemic pressure and lobar arterial perfusion pressure were continuously monitored, electron

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

287 Flow rate and perfusion pressure were reproducible within a coefficien

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

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

290 he mean intratracheal pressures and coronary perfusion pressures were 7.1 +/- 0.7, 11.6 +/- 0.7, 17.5

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 hermia was not due to alteration of coronary perfusion pressure, which suggests that changes in the m

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