Sarcolemmal permeability changes during early myocardial anoxia

Author(s):  
M. Ashraf ◽  
L. Landa ◽  
L. Nimmo ◽  
C. M. Bloor

Following coronary artery occlusion, the myocardial cells lose intracellular enzymes that appear in the serum 3 hrs later. By this time the cells in the ischemic zone have already undergone irreversible changes, and the cell membrane permeability is variably altered in the ischemic cells. At certain stages or intervals the cell membrane changes, allowing release of cytoplasmic enzymes. To correlate the changes in cell membrane permeability with the enzyme release, we used colloidal lanthanum (La+++) as a histological permeability marker in the isolated perfused hearts. The hearts removed from sprague-Dawley rats were perfused with standard Krebs-Henseleit medium gassed with 95% O2 + 5% CO2. The hypoxic medium contained mannitol instead of dextrose and was bubbled with 95% N2 + 5% CO2. The final osmolarity of the medium was 295 M osmol, pH 7. 4.

2015 ◽  
Vol 25 (17) ◽  
pp. 3610-3615 ◽  
Author(s):  
Junsuke Hayashi ◽  
Tomoko Hamada ◽  
Ikumi Sasaki ◽  
Osamu Nakagawa ◽  
Shun-ichi Wada ◽  
...  

1974 ◽  
Vol 64 (6) ◽  
pp. 706-729 ◽  
Author(s):  
W. R. Redwood ◽  
E. Rall ◽  
W. Perl

The permeability coefficients of dog red cell membrane to tritiated water and to a series of[14C]amides have been deduced from bulk diffusion measurements through a "tissue" composed of packed red cells. Red cells were packed by centrifugation inside polyethylene tubing. The red cell column was pulsed at one end with radiolabeled solute and diffusion was allowed to proceed for several hours. The distribution of radioactivity along the red cell column was measured by sequential slicing and counting, and the diffusion coefficient was determined by a simple plotting technique, assuming a one-dimensional diffusional model. In order to derive the red cell membrane permeability coefficient from the bulk diffusion coefficient, the red cells were assumed to be packed in a regular manner approximating closely spaced parallelopipeds. The local steady-state diffusional flux was idealized as a one-dimensional intracellular pathway in parallel with a one-dimensional extracellular pathway with solute exchange occurring within the series pathway and between the pathways. The diffusion coefficients in the intracellular and extracellular pathways were estimated from bulk diffusion measurements through concentrated hemoglobin solutions and plasma, respectively; while the volume of the extracellular pathway was determined using radiolabeled sucrose. The membrane permeability coefficients were in satisfactory agreement with the data of Sha'afi, R. I., C. M. Gary-Bobo, and A. K. Solomon (1971. J. Gen. Physiol. 58:238) obtained by a rapid-reaction technique. The method is simple and particularly well suited for rapidly permeating solutes.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jun-ichi Suzuki ◽  
Shin Wakatsuki ◽  
Masahito Ogawa ◽  
Susumu Muto ◽  
Akiko Itai ◽  
...  

Amplification of inflammatory response in the non-infarct area plays an important role in the pathogenesis of ventricular remodeling after myocardial ischemia. Activation of nuclear factor-kappa B (NF-kB) is involved in this amplification through a positive feedback loop of proinflammatory cytokines. We investigated the efficiency of IKK blockade with IMD-0560, a novel inhibitor of IKK, in a rat myocardial ischemia model. Left coronary artery occlusion (28 days) was carried out in Sprague-Dawley rats. The rats were assigned randomly to the two groups: IMD-0560 injection (5mg/kg i.p.) daily for 28 days (MI + IMD group, n=10); vehicle injection (i.p.) daily for 28 days (MI + vehicle group, n=10); and thoracotomy with LAD isolation without ligation (Sham group, n=5). Treatment with IMD-0560 significantly improved cardiac function, as indicated by the preservation of % fractional shortening (vehicle-treated, 20.2±1.5; IMD-0560-treated, 26.7±2.4; P < 0.05), and lower serum brain natriuretic peptide level (vehicle, 0.079±0.040; IMD-0560, 0.033±0.016; P < 0.05). Histological analysis showed that hypertrophy of myocardium was suppressed in the peri-infarct area (vehicle, 756.71±48.57mm2; IMD-0560, 633.35±29.83mm2; P < 0.05), and the thickness of infarct area was maintained (vehicle, 0.890±0.027mm; IMD-0560, 1.136±0.087mm; P < 0.05). The sham group showed no effect. Moreover, in situ zymography showed that matrix metalloproteinase-9 activity was inhibited in the infarct area. We revealed that IMD-0560 is potent in the suppression of chronic ventricular remodeling after myocardial ischemia.


Lab on a Chip ◽  
2021 ◽  
Author(s):  
Hsiu-Yang Tseng ◽  
Chiu-Jen Chen ◽  
Zong-Lin Wu ◽  
Yong-Ming Ye ◽  
Guo-Zhen Huang

Cell-membrane permeability to water (Lp) and cryoprotective agents (Ps) of a cell type is a crucial cellular information for achieving optimal cryopreservation in the biobanking industry. In this work, a...


1991 ◽  
Vol 96 (2) ◽  
pp. 644-649 ◽  
Author(s):  
Junping Chen ◽  
Edward I. Sucoff ◽  
Eduard J. Stadelmann

2012 ◽  
Vol 48 (2) ◽  
pp. 293-302 ◽  
Author(s):  
Michel Lavoie ◽  
Séverine Le Faucheur ◽  
Amiel Boullemant ◽  
Claude Fortin ◽  
Peter G. C. Campbell

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