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1 licited, PF fatigue would be hastened due to peripheral vasoconstriction.
2 dministration of MP4, indicating the lack of peripheral vasoconstriction.
3  with a reduced cardiac output and excessive peripheral vasoconstriction.
4  causing an increase in arterial pressure by peripheral vasoconstriction.
5 28+/-9 mm Hg (P<0.001), primarily because of peripheral vasoconstriction.
6 ve response, which comprises bradycardia and peripheral vasoconstriction.
7  causing an increase in arterial pressure by peripheral vasoconstriction.
8 outinely experiences apnea, bradycardia, and peripheral vasoconstriction.
9 e leads to local vasodilation in addition to peripheral vasoconstriction.
10 lume or a (desirable) compensatory relief of peripheral vasoconstriction.
11 in uterine artery vascular resistance, fetal peripheral vasoconstriction, a reduction in oxygen deliv
12 e cold intolerant because they have impaired peripheral vasoconstriction and are unable to induce the
13 cular and metabolic responses, which include peripheral vasoconstriction and hyperglycaemia.
14                       In conclusion, blunted peripheral vasoconstriction and lower stroke volume cont
15 and regulate heat loss through modulation of peripheral vasoconstriction and piloerection.
16 ine and while upright, producing significant peripheral vasoconstriction and venoconstriction (20% ca
17 I, which include increase in blood pressure, peripheral vasoconstriction, and stimulation of aldoster
18                   Importantly, we identified peripheral vasoconstriction as a critical mechanism unde
19 ors and is characterized by both central and peripheral vasoconstriction as well as a resistance to n
20  only to the cutaneous circulation promoting peripheral vasoconstriction but also to the heart promot
21 he underlying mechanism seems to be enhanced peripheral vasoconstriction caused by attenuated cardiov
22 er cell-cell interaction, helping to promote peripheral vasoconstriction during HUT.
23 unclear if circulating adrenaline attenuates peripheral vasoconstriction during these manoeuvres.
24               These results suggest that rHb peripheral vasoconstriction elicited by rHb1.1 is signif
25 in cardiac contractility with an exaggerated peripheral vasoconstriction in the CHF state.
26                        Excessively increased peripheral vasoconstriction is a hallmark of heart failu
27 usside may improve myocardial performance if peripheral vasoconstriction is contributing to afterload
28  circulation and (b) whether the NE-mediated peripheral vasoconstriction is the main mechanism mediat
29  arterial pressure are mediated primarily by peripheral vasoconstriction, its chronic BP effects are
30                   During head-up tilt (HUT), peripheral vasoconstriction occurs.
31 rdia syndrome (POTS) is related to defective peripheral vasoconstriction of dependent extremities wit
32  XO-derived ROS in contributing to the fetal peripheral vasoconstriction, part of the fetal defence t
33                                              Peripheral vasoconstriction (PE and Ang II) is reduced i
34 52 to 146/66 mm Hg (P < .001/P < .05) due to peripheral vasoconstriction (systemic vascular resistanc
35  failure and may contribute to the increased peripheral vasoconstriction that characterizes this dise
36 -MSH doses effectively inhibited LPS-induced peripheral vasoconstriction, the principal heat-conservi
37       Both drugs also induced dose-dependent peripheral vasoconstriction, which appears to be a prima
38 lts from both direct neuronal activation and peripheral vasoconstriction, which redistributes arteria
39                                      Greater peripheral vasoconstriction with mental stress, denoted