ライフサイエンスコーパス: myocardial reperfusion

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1 to be more effective in thrombus removal and myocardial reperfusion.

2 ay be considered a reference test for failed myocardial reperfusion.

3 ence has accumulated in randomized trials of myocardial reperfusion.

4 uced in wild-type mice at 2 to 6 hours after myocardial reperfusion.

5 s that free radical generation occurs during myocardial reperfusion.

6 us cannulation of the right atrium and after myocardial reperfusion.

7 Myocardial reperfusion after ischemia (I/R), although an

8 Suboptimal myocardial reperfusion after PCI in STEMI is common and

9 the rate of distal embolization and impaired myocardial reperfusion after percutaneous coronary inter

10 ht to determine the prognostic importance of myocardial reperfusion after various contemporary interv

11 in loading dose before elective PCI improves myocardial reperfusion and injury indexes, suggesting a

12 tPA provided additional benefit in terms of myocardial reperfusion, as evidenced by greater resoluti

13 l increases in intracellular Ca(2)(+) during myocardial reperfusion can cause cardiomyocyte death and

14 ation myocardial infarction; however, failed myocardial reperfusion commonly passes undetected in up

15 o tissue injury and repair including stroke, myocardial reperfusion damage, ischemia, cancer, amyloid

16 ow phenomenon." Therefore, GPI might improve myocardial reperfusion, distinct from its effects on epi

17 n and platelet lysis improves epicardial and myocardial reperfusion in AMI.

18 e ischemic area at risk increased during rat myocardial reperfusion in vivo.

19 tandard clinical measures of the efficacy of myocardial reperfusion, including the ischemic time, ST-

20 ma has been shown to be cardioprotective for myocardial reperfusion injury and ischemia and may play

21 currently under investigation for preventing myocardial reperfusion injury have the potential to impr

22 l and antithrombotic properties that reduces myocardial reperfusion injury in animal models of myocar

23 itric oxide bioavailability, and ameliorated myocardial reperfusion injury in the setting of severe h

24 dings suggest that the blood contribution to myocardial reperfusion injury is amplified in diabetes.

25 Myocardial reperfusion injury is associated with the inf

26 Myocardial reperfusion injury is mediated in part by acc

27 itself induce cardiomyocyte death, known as myocardial reperfusion injury, for which there is still

28 associated with oxidative stress, including myocardial reperfusion injury, heart transplantation, st

29 ity resulting in increased cytoprotection in myocardial reperfusion injury.

30 he protective functional phenotype of MIF in myocardial reperfusion injury.

31 uld prevent neutrophil activation and reduce myocardial reperfusion injury.

32 ming may not utilize ADO's potential against myocardial reperfusion injury.

33 ibution of nondiabetic and diabetic blood to myocardial reperfusion injury.

34 elopment for the treatment of hepatitis C or myocardial reperfusion injury.

35 Myocardial reperfusion is believed to be associated with

36 the poor prognosis is due to lower rates of myocardial reperfusion is unknown.

37 complement activation is a key regulator of myocardial reperfusion ischemic injury.

38 /- 82.6 pmol/mmol by 15 minutes after global myocardial reperfusion (P < .05) and dropped to 181.2 +/

39 Now that we have entered the third decade of myocardial reperfusion therapy, we can expect iterative

40 ly, this was achieved when dosing well after myocardial reperfusion (up to 3 h after), the same time

41 and limiting MI size is timely and effective myocardial reperfusion using either thombolytic therapy

42 tenting (DS) approach (24-48 hours) improves myocardial reperfusion, versus immediate stenting, in pa

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