scholarly journals Effects of nifedipine on diastolic abnormalities in low-flow and pacing-induced ischemia in isolated rat hearts.

1991 ◽  
Vol 55 (6) ◽  
pp. 623-633 ◽  
Author(s):  
SHIN-ICHI MOMOMURA ◽  
TAKASHI SERIZAWA ◽  
HIROSHI IKENOUCHI ◽  
TSUNEAKI SUGIMOTO ◽  
MASAHIKO IIZUKA
Keyword(s):  
Low Flow ◽  
Rat Hearts ◽  
Isolated Rat

Independent dual perfusion of left and right coronary arteries in isolated rat hearts

1991 ◽  
Vol 261 (6) ◽  
pp. H2082-H2090 ◽  
Author(s):  
M. Avkiran ◽  
M. J. Curtis
Keyword(s):  
High Energy ◽  
Low Flow ◽  
Blue Dye ◽  
Ischemia And Reperfusion ◽  
Langendorff Preparation ◽  
Rat Hearts ◽  
Left And Right ◽  
Conventional Models ◽  
Aortic Cannula ◽  
Isolated Rat

A novel dual lumen aortic cannula was designed and constructed to permit independent perfusion of left and right coronary beds in isolated rat hearts without necessitating the cannulation of individual arteries. Stability of the dual-perfusion preparation was shown to be similar to that of the conventional Langendorff preparation, in terms of coronary flow, heart rate, and high-energy phosphate content. The independence of left and right perfusion beds was confirmed by unilateral infusion of disulfine blue dye and spectrophotometric detection of the dye in ventricular homogenates. Transient cessation of flow to the left coronary bed resulted in severe ventricular arrhythmias upon reperfusion, as in conventional models of regional ischemia and reperfusion. The dual-perfusion model is technically undemanding, reproducible, inexpensive, and can be used in several species. It enables studies with 1) regional low flow ischemia, 2) regional zero-flow ischemia without coronary ligation (with attendant damage to vasculature), 3) selective application of drugs or interventions to the ischemic-reperfused zone, and 4) selective application of components of ischemia and reperfusion to a site anatomically relevant to ischemic heart disease.

The Effects of Low-Flow Ischemia on K+Fluxes in Isolated Rat Hearts Assessed by87Rb NMR

1999 ◽  
Vol 31 (4) ◽  
pp. 817-826 ◽  
Author(s):  
V.V. Kupriyanov ◽  
B. Xiang ◽  
B. Kuzio ◽  
R. Deslauriers
Keyword(s):  
Low Flow ◽  
Rat Hearts ◽  
Isolated Rat

scholarly journals Dynamics of myocardial adaptation to low-flow ischemia and hypoxemia

1996 ◽  
Vol 271 (6) ◽  
pp. H2300-H2305
Author(s):  
G. Merati ◽  
S. Allibardi ◽  
L. D. Monti ◽  
J. W. de Jong ◽  
M. Samaja
Keyword(s):  
Low Flow ◽  
Control Performance ◽  
Perfusion Medium ◽  
Atp Production ◽  
Lactate Release ◽  
Rat Hearts ◽  
O2 Supply ◽  
Developed Pressure ◽  
Myocardial Adaptation ◽  
Isolated Rat

We investigated whether one or more factors control performance in O2-limited hearts. For this purpose, we measured the dynamics of myocardial adaptation to reduced O2 supply with a specially designed setup, analyzing early changes after reduction in either flow of the perfusion medium or its PO2. For 10 min, 38 isolated rat hearts underwent low-flow ischemia or hypoxemia, matched for O2 supply. Early during ischemia, developed pressure declined at a rate of 311 +/- 25 mmHg/s; lactate release increased and then leveled off to 3.4 +/- 0.7 mumol/min within 2 min. During hypoxemia, pressure dropped initially, as observed during ischemia. However, it then increased before slowly decreasing. Lactate release during hypoxemia peaked at 13.0 +/- 2.3 mumol/min after 2 min, leveling off to 3.5 +/- 1.3 mumol/min. Glycogen decreased by 52 and 81% in ischemic and hypoxemic hearts, respectively (P < 0.05). Reexposure to ischemia or hypoxemia induced comparable changes in both groups. We conclude that, at the beginning of ischemia, a single factor does limit myocardial performance. This variable, which remains undisturbed for 10 min, is presumably O2 availability. In contrast, approximately 20 s after induction of hypoxemia, glycolytic ATP production can partially override low O2 availability by providing most of the energy needed. During repeated restriction of O2 supply, O2 availability alone limits performance during both ischemia and hypoxemia.

Diastolic Abnormalities in Low-Flow and Pacing Tachycardia-Induced Ischemia in Isolated Rat Hearts—Modification by Calcium Antagonists

1994 ◽  
pp. 265-274
Author(s):  
Takashi Serizawa ◽  
Shin-Ichi Momomura ◽  
Yasushi Nagai ◽  
Toshiaki Ogawa ◽  
Tadashi Sato ◽  
...  
Keyword(s):  
Calcium Antagonists ◽  
Low Flow ◽  
Rat Hearts ◽  
Isolated Rat

Low-flow reperfusion after myocardial ischemia enhances leukocyte accumulation in coronary microcirculation

1997 ◽  
Vol 273 (3) ◽  
pp. H1154-H1165 ◽  
Author(s):  
L. S. Ritter ◽  
P. F. McDonagh
Keyword(s):  
Shear Rate ◽  
Myocardial Ischemia ◽  
Leukocyte Adhesion ◽  
Low Flow ◽  
Early Reperfusion ◽  
Leukocyte Accumulation ◽  
Cell Velocity ◽  
Rat Hearts ◽  
Labeled Leukocytes ◽  
Isolated Rat

During early reperfusion after myocardial ischemia, the mechanisms responsible for leukocyte accumulation in the heart are unclear. We examined the effects of reducing coronary blood flow during reperfusion on leukocyte accumulation in coronary capillaries and postcapillary venules. Isolated rat hearts were perfused for 30 min and then subjected to 30 min of 37 degrees C, no-flow ischemia. The deposition of fluorescently labeled leukocytes was observed directly in coronary capillaries and venules using intravital microscopy after 5, 20, and 35 min of reperfusion. Blood cell velocity was measured in venules after 5 min of reperfusion (R5), and shear rate (s-1) was calculated. Four groups were studied: nonischemic control (NIC) hearts and postischemic hearts reperfused at full flow (I/R100) and at 50 and 10% of full flow (I/R50 and I/R10, respectively). In I/R100 hearts, there was a significant increase in leukocyte trapping in capillaries compared with the NIC group (R5: 5.7 +/- 0.6 vs. 2.0 +/- 0.4 leukocytes/capillary field, respectively; P < 0.05). However, the increase in leukocyte adhesion to venules was not statistically significant compared with NIC (R5: 3.2 +/- 0.4 vs. 1.5 +/- 0.6 leukocytes/100-micron venule, respectively; P < 0.2). In I/R50 hearts, a further increase in leukocyte accumulation occurred in the capillaries but not in the venules. However, in I/R10 hearts, there was a statistically significant increase in both capillaries (R5: 9.2 +/- 0.8; P < 0.05) and venules (R5: 4.4 +/- 0.5; P < 0.05). When leukocyte margination in coronary venules was examined as a function of venular shear rate, a significant correlation (r = 0.99, P < 0.05) was found. These results suggest that, after ischemia, a reduction in reflow enhances leukocyte trapping in capillaries and that leukocyte adhesion in venules is inversely related to shear rate. Enhanced leukocyte accumulation may in turn increase the leukocyte contribution to early reperfusion injury in the heart.

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