ライフサイエンスコーパス: peripheral vasoconstriction

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1 ve response, which comprises bradycardia and 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 causing an increase in arterial pressure by peripheral vasoconstriction.

7 lume or a (desirable) compensatory relief of peripheral vasoconstriction.

8 licited, PF fatigue would be hastened due to peripheral vasoconstriction.

9 e cold intolerant because they have impaired peripheral vasoconstriction and are unable to induce the

10 cular and metabolic responses, which include peripheral vasoconstriction and hyperglycaemia.

11 In conclusion, blunted peripheral vasoconstriction and lower stroke volume cont

12 and regulate heat loss through modulation of peripheral vasoconstriction and piloerection.

13 ine and while upright, producing significant peripheral vasoconstriction and venoconstriction (20% ca

14 I, which include increase in blood pressure, peripheral vasoconstriction, and stimulation of aldoster

15 Importantly, we identified peripheral vasoconstriction as a critical mechanism unde

16 ors and is characterized by both central and peripheral vasoconstriction as well as a resistance to n

17 only to the cutaneous circulation promoting peripheral vasoconstriction but also to the heart promot

18 er cell-cell interaction, helping to promote peripheral vasoconstriction during HUT.

19 unclear if circulating adrenaline attenuates peripheral vasoconstriction during these manoeuvres.

20 These results suggest that rHb peripheral vasoconstriction elicited by rHb1.1 is signif

21 in cardiac contractility with an exaggerated peripheral vasoconstriction in the CHF state.

22 Excessively increased peripheral vasoconstriction is a hallmark of heart failu

23 usside may improve myocardial performance if peripheral vasoconstriction is contributing to afterload

24 circulation and (b) whether the NE-mediated peripheral vasoconstriction is the main mechanism mediat

25 arterial pressure are mediated primarily by peripheral vasoconstriction, its chronic BP effects are

26 During head-up tilt (HUT), peripheral vasoconstriction occurs.

27 rdia syndrome (POTS) is related to defective peripheral vasoconstriction of dependent extremities wit

28 XO-derived ROS in contributing to the fetal peripheral vasoconstriction, part of the fetal defence t

29 Peripheral vasoconstriction (PE and Ang II) is reduced i

30 52 to 146/66 mm Hg (P < .001/P < .05) due to peripheral vasoconstriction (systemic vascular resistanc

31 failure and may contribute to the increased peripheral vasoconstriction that characterizes this dise

32 -MSH doses effectively inhibited LPS-induced peripheral vasoconstriction, the principal heat-conservi

33 Both drugs also induced dose-dependent peripheral vasoconstriction, which appears to be a prima

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