Influence of subendocardial ischemia on transmural myocardial function

1992 ◽  
Vol 262 (2) ◽  
pp. H568-H576 ◽  
Author(s):  
N. C. Edwards ◽  
A. J. Sinusas ◽  
J. D. Bergin ◽  
D. D. Watson ◽  
M. Ruiz ◽  
...  

The relationship between regional myocardial perfusion and function under ischemic conditions was examined by using a nontraumatic single-crystal pulsed Doppler system that permits complete transmural assessment of myocardial thickening. Sixteen open-chest dogs underwent either 50 (n = 4) or 180 (n = 12) min of partial coronary artery occlusion. Simultaneous measurements of myocardial thickening fraction (TF) and microsphere-determined blood flow (BF) were taken in the subepicardial, midwall, and subendocardial thirds of the left ventricular wall. During ischemia, there was an excellent correlation between BF and TF in the subendocardium. Mean subendocardial BF was reduced to 0.45 +/- 0.3 ml.min-1.g-1, resulting in a subendocardial TF of 0.8 +/- 19%. Although subepicardial BF was relatively preserved at 1.03 +/- 0.4 ml.min-1.g-1, subepicardial TF was diminished markedly and not significantly different from subendocardial TF. Subepicardial and midwall TF were highly dependent on subendocardial flow rather than on the actual flow in these areas. Hence these studies show a marked dependence of transmural myocardial function on subendocardial blood flow. Outer wall function is more dependent on subendocardial than subepicardial blood flow.

2002 ◽  
Vol 96 (3) ◽  
pp. 675-680 ◽  
Author(s):  
Franz Kehl ◽  
John G. Krolikowski ◽  
Boris Mraovic ◽  
Paul S. Pagel ◽  
David C. Warltier ◽  
...  

Background Volatile anesthetics precondition against myocardial infarction, but it is unknown whether this beneficial action is threshold- or dose-dependent. The authors tested the hypothesis that isoflurane decreases myocardial infarct size in a dose-dependent fashion in vivo. Methods Barbiturate-anesthetized dogs (n = 40) were instrumented for measurement of systemic hemodynamics including aortic and left ventricular pressures and rate of increase of left ventricular pressure. Dogs were subjected to a 60-min left anterior descending coronary artery occlusion followed by 3 h of reperfusion and were randomly assigned to receive either 0.0, 0.25, 0.5, 1.0, or 1.25 minimum alveolar concentration (MAC) isoflurane in separate groups. Isoflurane was administered for 30 min and discontinued 30 min before left anterior descending coronary artery occlusion. Results Infarct size (triphenyltetrazolium staining) was 29 +/- 2% of the area at risk in control experiments (0.0 MAC). Isoflurane produced significant (P < 0.05) reductions of infarct size (17 +/- 3, 13 +/- 1, 14 +/- 2, and 11 +/- 1% of the area at risk during 0.25, 0.5, 1.0, and 1.25 MAC, respectively). Infarct size was inversely related to coronary collateral blood flow (radioactive microspheres) in control experiments and during low (0.25 or 0.5 MAC) but not higher concentrations of isoflurane. Isoflurane shifted the linear regression relation between infarct size and collateral perfusion downward (indicating cardioprotection) in a dose-dependent fashion. Conclusions Concentrations of isoflurane as low as 0.25 MAC are sufficient to precondition myocardium against infarction. High concentrations of isoflurane may have greater efficacy to protect myocardium during conditions of low coronary collateral blood flow.


1986 ◽  
Vol 64 (3) ◽  
pp. 254-262 ◽  
Author(s):  
Bodh I. Jugdutt

The relationship between myocardial infarct size (IS) and occluded bed size (OBS) in pentobarbital-anesthetized (A, n = 16) and conscious (C, n = 20) dog models were compared. IS and OBS (postmortem coronary arteriography) were measured by computerized planimetry of weighed left ventricular (LV) rings 7 days after permanent left anterior descending (LAD, n = 19) or circumflex (LC, n = 17) coronary artery occlusion. For both A and C groups, IS was directly related to OBS (p < 0.001) and no infarcts developed for small occluded beds. For either LAD or LC subgroups, infarcts were larger in A than C dogs (49 ± 18 vs. 30 ± 19% OBS, p < 0.025), with greater slope of the linear regression between IS and OBS (p < 0.001) and less epicardial sparing on topographic mapping (p < 0.05). Although postocclusion mean arterial and left atrial pressures were similar in A and C groups, heart rates were greater in the A dogs, both pre- (125 vs. 88 beats/min, p < 0.001) and post-occlusion (151 vs. 108 beats/min, p < 0.001). Endocardial flows (radioactive microspheres) in infarct centers and margins were less in A than C dogs. Also, endocardial/epicardial (endo/epi) flow ratios in all regions were less in A than C dogs, both pre- and post-occlusion. Increasing heart rate in 10 other C dogs with LAD occlusion to that of the A group (151 beats/min) by right ventricular pacing resulted in larger infarcts with greater slope of the linear regression and less endo/epi flow ratios, as in the A group. Thus, infarcts are larger in A than C dog models. The effect appears to be related to increased myocardial oxygen demands and transmural maldistribution of flow associated with tachycardia.


1985 ◽  
Vol 249 (4) ◽  
pp. H783-H791 ◽  
Author(s):  
R. H. Murdock ◽  
A. Chu ◽  
M. Grubb ◽  
F. R. Cobb

The effects of permanent circumflex coronary artery occlusion (PO) compared with reestablishing blood flow (OR) at 2 and 6 h after occlusion on the final extent of histological infarction (HI) was assessed in chronically instrumented awake dogs. The relationships between the extent of left ventricular ischemia measured by microsphere techniques and HI in the PO group were used as models to predict the expected infarction in the 2- and 6-h OR groups. Mean HI (+/-SD) in the PO and 6- and 2-h OR groups was 21 +/- 13, 19 +/- 10, and 13 +/- 12% of left ventricular weight, respectively; values were not significantly different. The extent of HI in samples grouped according to epicardial and endocardial layers and ischemic blood flow ranges (0-15, 16-30, 31-50, 51-75% of control region blood flow) was reduced in the 2-h but not 6-h OR group. Analysis of individual animals using total ischemic region blood flow to epicardial and endocardial layers demonstrated that OR at 2 h but not 6 h reduced infarction in most animals but not in certain animals with the largest ischemic regions.


1984 ◽  
Vol 246 (4) ◽  
pp. H601-H607
Author(s):  
K. H. McDonough ◽  
R. B. Dunn ◽  
D. M. Griggs

The distribution of the coronary collateral circulation is an important determinant of the myocardial response to acute coronary artery occlusion. The dog shows an unequal response across the ventricular wall, whereas the pig seems to have more uniform transmural changes. This study was undertaken to compare the metabolic and blood flow response in pigs and dogs to acute occlusion of the circumflex artery. Microspheres (8-10 micron) were used to determine control blood flow and flow 5 min after occlusion. A transmural tissue sample from the center of the ischemic zone was taken at 8 min after occlusion, and inner, middle, and outer layers were analyzed for high-energy phosphates and lactate. The remainder of the heart was analyzed for microsphere distribution. The epicardium in the dog showed less severe damage than the subendocardium. High-energy phosphates were higher and lactate lower in this region. In the pig high-energy phosphates and lactate were the same in the subepicardium and subendocardium. Blood flow to regions surrounding the central ischemic zone in pigs was generally uniform across the ventricular wall or greater in the inner wall than in the outer wall. These results verify that dogs as a group have a greater subepicardial protection during coronary artery occlusion. Pigs, however, demonstrate uniform ischemia or even slightly less severe ischemia in the subendocardium in regions of restricted blood flow.


1996 ◽  
Vol 270 (5) ◽  
pp. H1812-H1818 ◽  
Author(s):  
Y. T. Shen ◽  
J. T. Fallon ◽  
M. Iwase ◽  
S. F. Vatner

To determine whether the extent of myocardial infarction differs in conscious baboons and pigs, both devoid of performed collaterals, the effects of 40 and 90 min of coronary artery (CA) occlusion (O) both followed by 4-7 days of CA reperfusion (R) were examined in both species. CAO reduced subendocardial and subepicardial blood flows similarly, almost to zero, in baboons and pigs for the entire CAO period. At 24 h of CAR, subendocardial blood flow had almost returned to pre-CAO control levels in baboons but remained significantly depressed in pigs. The major difference in hemodynamics during CAO and CAR was in left ventricular end-diastolic pressure, which rose by 6 +/- 1 mmHg in pigs over the initial 24-h reperfusion period but did not change significantly in baboons. These data on recovery of subendocardial blood flow and left ventricular end-diastolic pressure suggest larger infarcts in pigs than in baboons. Indeed, infarct size expressed as a function of area at risk (IF/AAR) was significantly greater (P <0.05) in pigs (53 +/- 4.9%) than in baboons (17 +/- 2.9%) with 90 min of CAO and 4-7 days of CAR. With 40 min of CAO and 4-7 days of CAR, IF/AAR was 46 +/- 3.6% in pigs, whereas in baboons the IF/AAR was minimal, i.e., 2 +/- 0.6%. Thus pigs and baboons were characterized by minimal coronary collateral circulation, but infarct size was significantly less in conscious baboons than in conscious pigs. Potentially, these differences could be explained, in part, by natural protective mechanisms and/or less reperfusion injury in primates. These results in primates may also help explain the salutary effects of CAR in patients at intervals longer than have been demonstrated to be beneficial in other experimental animals.


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