Hyaluronidase reversal of increased coronary vascular resistance in ischemic rat hearts

1983 ◽  
Vol 245 (2) ◽  
pp. H183-H188 ◽  
Author(s):  
K. P. Sunnergren ◽  
M. J. Rovetto
Keyword(s):  
Myocardial Ischemia ◽  
Vascular Resistance ◽  
Coronary Flow ◽  
Low Flow ◽  
Coronary Vascular Resistance ◽  
Tissue Water ◽  
Atp Levels ◽  
Tissue Edema ◽  
Rat Hearts ◽  
Testicular Hyaluronidase

Testicular hyaluronidase prevents increased coronary vascular resistance (CVR) during prolonged myocardial ischemia. The mechanism is unknown, but edema and contracture both have been suggested to increase CVR. Additionally, the extent of contracture has been inversely related to ATP levels. Therefore, isolated perfused ischemic rat hearts were treated with hyaluronidase, following a 25% increase in CVR, to determine whether 1) increased CVR was reversed, 2) edema or contracture was reduced, and 3) tissue ATP levels were increased. Three hours of low-flow ischemia decreased coronary flow (CF) from 17.4 +/- 0.13 to 12.6 +/- 0.2 ml X min-1 X g dry tissue-1. During the subsequent 2 h of ischemia, CF of vehicle-treated hearts continued to decline to 8.0 +/- 0.76 ml X min-1 X g dry tissue-1, whereas CF of hyaluronidase-treated hearts increased to 15.6 +/- 1.17 ml X min-1 X g dry tissue-1. These changes in CF persisted during postischemic perfusion. Furthermore, restoration of coronary vascular resistance by hyaluronidase was associated with a 19% reduction in tissue water compared with control ischemic hearts but not with a reduction in cardiac contracture or an increase in tissue ATP. These results suggest that treatment of ischemic hearts with hyaluronidase reverses increased CVR through a reduction in tissue edema.

scholarly journals Reduced myocardial reflow and increased coronary vascular resistance following prolonged myocardial ischemia in the dog.

1975 ◽  
Vol 36 (6) ◽  
pp. 771-781 ◽  
Author(s):  
J T Willerson ◽  
J T Watson ◽  
I Hutton ◽  
G H Templeton ◽  
D E Fixler
Keyword(s):  
Myocardial Ischemia ◽  
Vascular Resistance ◽  
Coronary Vascular Resistance

scholarly journals Hypothermic preservation of rat hearts using antifreeze glycoprotein

2020 ◽  
pp. 1029-1038
Author(s):  
Shintaro Takago ◽  
Isao Matsumoto ◽  
Hiroki Kato ◽  
Naoki Saito ◽  
Hideyasu Ueda ◽  
...  
Keyword(s):  
Control Group ◽  
Tissue Water ◽  
Uw Solution ◽  
Antifreeze Glycoprotein ◽  
University Of Wisconsin ◽  
Metabolic Functions ◽  
Cardiac Contractile ◽  
Hypothermic Preservation ◽  
Atp Levels ◽  
Rat Hearts

Antifreeze proteins are an effective additive for low-temperature preservation of solid organs. Here, we compared static hypothermic preservation with and without antifreeze glycoprotein (AFGP), followed by nonfreezing cryopreservation of rat hearts. The heart was surgically extracted and immersed in one of the cardioplegia solutions after cardiac arrest. Control rat hearts (n=6) were immersed in University of Wisconsin (UW) solution whereas AFGP-treated hearts (AFGP group) (n=6) were immersed in UW solution containing 500 μg/ml AFGP. After static hypothermic preservation, a Langendorff apparatus was used to reperfuse the coronary arteries with oxygenated Krebs-Henseleit solution. After 30, 60, 90, and 120 min, the heart rate (HR), coronary flow (CF), cardiac contractile force (max dP/dt), and cardiac diastolic force (min dP/dt) were measured. Tissue water content (TWC) and tissue adenosine triphosphate (ATP) levels in the reperfused preserved hearts were also assessed. All the parameters were compared between the control and AFGP groups. Compared with the control group, the AFGP group had significantly (p<0.05) higher values of the following parameters: HR at 60, 90, and 120 min; CF at all four time points; max dP/dt at 90 min; min dP/dt at 90 and 120 min; and tissue ATP levels at 120 min. TWC did not differ significantly between the groups. The higher HR, CF, max dP/dt, min dP/dt, and tissue ATP levels in the AFGP compared with those in control hearts suggested that AFGP conferred superior hemodynamic and metabolic functions. Thus, AFGP might be a useful additive for the static/nonfreezing hypothermic preservation of hearts.

Effects of hypermagnesemia on general and coronary hemodynamics of the dog

1965 ◽  
Vol 208 (1) ◽  
pp. 158-161 ◽  
Author(s):  
George M. Maxwell ◽  
Robert B. Elliott ◽  
Richard H. Burnell
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Coronary Flow ◽  
Coronary Vascular Resistance ◽  
Before And After

Vascular pressures, cardiac output (Fick), and coronary flow (N2O Fick) were measured before and after the induction of hypermagnesemia with MgCl2. A significant tachycardia and hypotension resulted. There was no effect upon coronary flow, coronary vascular resistance, or myocardial O2 and CO2 metabolism.

Effect of estrogen on global myocardial ischemia-reperfusion injury in female rats

2000 ◽  
Vol 279 (6) ◽  
pp. H2766-H2775 ◽  
Author(s):  
Peiyong Zhai ◽  
Thomas E. Eurell ◽  
Robert Cotthaus ◽  
Elizabeth H. Jeffery ◽  
Janice M. Bahr ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Coronary Flow ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
The Other ◽  
Female Rats ◽  
Rat Hearts ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

We investigated the effects of estrogen on global myocardial ischemia-reperfusion injury in rats that were ovariectomized (Ovx), sham-operated, or ovariectomized and then given 17β-estradiol (E2β) supplementation (Ovx+E2β). Hearts were excised, cannulated, perfused with and then immersed in chilled (4°C) cardioplegia solution for 30 min, and then retrogradely perfused with warm (37°C), oxygenated Krebs-Henseleit bicarbonate buffer for 120 min. The coronary flow rate, first derivative of left ventricular pressure, and nitrite production were all significantly lower in Ovx than in sham-operated or Ovx+E2β hearts. However, coronary flow rates or nitrate production were not consistently different throughout the entire reperfusion period. Ca2+accumulated more in Ovx rat hearts than in sham-operated or Ovx+E2β hearts, and mitochondrial respiratory function was lower in Ovx hearts than in hearts from the other two groups. Marked interstitial edema and contraction bands were seen in hematoxylin-eosin-stained sections of Ovx rat hearts but not in hearts from either of the other groups. Hematoxylin-basic fuchsin-picric acid-stained sections revealed fewer viable myocytes in hearts from the Ovx group than from the sham or Ovx+E2β group. Transmission electron microscopy demonstrated more severely damaged mitochondria and ultrastructural damage to myocytes in Ovx rat hearts. Our results indicate that estrogen plays a cardioprotective role in global myocardial ischemia-reperfusion injury in female rats.

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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