Splenic blood-flow response following myocardial infarction in rat

2018 ◽  
Vol 96 (11) ◽  
pp. 1060-1068
Author(s):  
Sara A. Ruggiero ◽  
Jason S. Huber ◽  
Coral L. Murrant ◽  
Keith R. Brunt ◽  
Jeremy A. Simpson
Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jyun-Ei Obata ◽  
Yoshinobu Kitta ◽  
Yasushi Kodama ◽  
Takamitsu Nakamura ◽  
Ken-ichi Kawabata ◽  
...  

Myocardial ischemia-reperfusion causes endothelial injury in the infarct-related coronary artery. We have previously shown that sirolimus-eluting stent (SES) implantation can aggravate endothelium-dependent vasomotor dysfunction in infarct-related coronary arteries. This study examined effects of SES implantation on duration of reperfusion-induced endothelial dysfunction in infarct-related coronary arteries. This study enrolled 44 patients with a first acute myocardial infarction (AMI) due to occlusion of the left anterior descending coronary artery (LAD) and successful reperfusion therapy using SESs (n = 22) or bare metal stents (BMS, n = 22). Vasomotor function of LAD in response to acetylcholine (ACh) was repeated 2 weeks, 6 months, and 9 months after AMI. Patients with either residual stenosis or in-stent restenosis in LAD were not included in this study. The vasomotor function was also assessed in 20 control subjects for comparison with that in AMI patients. The SES and BMS groups were similar in terms of AMI-related variables including peak CK levels and 2 week LVEF. At 2 weeks after AMI, SES-treated LAD had greater impairment of epicardial dilation and less blood flow increase in response to ACh than BMS-treated LAD (diameter response; 12% vs. 34% of controls, blood flow response; 23% vs. 76% of controls, at 10 μg/min of ACh, respectively). In BMS-treated LAD, the responses of epicardial diameter and blood flow to ACh had recovered to levels similar to those of controls at 6 months (diameter response; 94% of controls, blood flow response; 92% of controls), and the responses showed no further improvement from 6 to 9 months. In SES-treated LAD, the responses were improved but remained lowered compared with BMS-treated LAD at 6 months (diameter response; 58% of controls, blood flow response; 74% of controls). However, the responses in SES-treated LAD at 9 months showed further improvement to levels near to those of BMS-treated LAD or controls (diameter response; 79% of controls, blood flow response; 88% of controls). Although incomplete, the adverse effects of SES on endothelium-dependent vasomotor function in infarct-related coronary arteries were restored through late catch-up recovery after stent implantation.


2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S198-S198
Author(s):  
Joseph R Meno ◽  
Thien-son K Nguyen ◽  
Elise M Jensen ◽  
G Alexander West ◽  
Leonid Groysman ◽  
...  

Circulation ◽  
1995 ◽  
Vol 92 (4) ◽  
pp. 796-804 ◽  
Author(s):  
Danilo Neglia ◽  
Oberdan Parodi ◽  
Michela Gallopin ◽  
Gianmario Sambuceti ◽  
Assuero Giorgetti ◽  
...  

Hypertension ◽  
1995 ◽  
Vol 26 (3) ◽  
pp. 497-502 ◽  
Author(s):  
Daniel Hayoz ◽  
Roger Weber ◽  
Blaise Rutschmann ◽  
Roger Darioli ◽  
Michel Burnier ◽  
...  

2008 ◽  
Vol 28 (7) ◽  
pp. 1369-1376 ◽  
Author(s):  
Inna Sukhotinsky ◽  
Ergin Dilekoz ◽  
Michael A Moskowitz ◽  
Cenk Ayata

Cortical spreading depression (CSD) evokes a large cerebral blood flow (CBF) increase in normal rat brain. In contrast, in focal ischemic penumbra, CSD-like periinfarct depolarizations (PID) are mainly associated with hypoperfusion. Because PIDs electrophysiologically closely resemble CSD, we tested whether conditions present in ischemic penumbra, such as tissue hypoxia or reduced perfusion pressure, transform the CSD-induced CBF response in nonischemic rat cortex. Cerebral blood flow changes were recorded using laser Doppler flowmetry in rats subjected to hypoxia, hypotension, or both. Under normoxic normotensive conditions, CSD caused a characteristic transient CBF increase (74 ± 7%) occasionally preceded by a small hypoperfusion (−4 ± 2%). Both hypoxia ( pO2 45 ± 3 mm Hg) and hypotension (blood pressure 42 ± 2 mm Hg) independently augmented this initial hypoperfusion (−14 ± 2% normoxic hypotension; −16 ± 6% hypoxic normotension; −21 ± 5% hypoxic hypotension) and diminished the magnitude of hyperemia (44 ± 10% normoxic hypotension; 43 ± 9% hypoxic normotension; 27 ± 6% hypoxic hypotension). Hypotension and, to a much lesser extent, hypoxia increased the duration of hypoperfusion and the DC shift, whereas CSD amplitude remained unchanged. These results suggest that hypoxia and/or hypotension unmask a vasoconstrictive response during CSD in the rat such that, under nonphysiologic conditions (i.e., mimicking ischemic penumbra), the hyperemic response to CSD becomes attenuated resembling the blood flow response during PIDs.


1988 ◽  
Vol 95 (3) ◽  
pp. 642-650 ◽  
Author(s):  
Josep M. Pique ◽  
Felix W. Leung ◽  
Heck W. Tan ◽  
Edward Livingston ◽  
Oscar U. Scremin ◽  
...  

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