Progressive cardiac dysfunction with repeated pacing-induced ischemia: protection by AICA-riboside

1991 ◽  
Vol 261 (5) ◽  
pp. H1570-H1577 ◽  
Author(s):  
M. A. Young ◽  
K. M. Mullane
Keyword(s):  
Blood Flow ◽  
Regional Wall Motion ◽  
Posterior Wall ◽  
Saline Group ◽  
Left Ventricular ◽  
Saline Control ◽  
Regional Myocardial Blood Flow ◽  
Control Group ◽  
Wall Thickening ◽  
Progressive Decline

The effects of repeated episodes of demand-induced ischemia on regional myocardial wall thickening, endocardial electrogram, and regional myocardial blood flow are not well delineated. We studied the cumulative effects of six periods of pacing-induced ischemia in 35 chloralose-anesthetized dogs with circumflex coronary stenosis. Repetitive ischemia of the posterior left ventricular free wall was induced with six 5-min pacing periods separated by 15-min recovery periods. The three groups of dogs studied were 1) saline control, 2) the purine precursor 5-aminoimidazole 4-carboxamide riboside (AICA-r), and 3) nitroglycerin (NTG). During the initial pacing period (before treatment), thickening of the posterior wall declined in the saline group (43 +/- 5% of control), the AICA-r group (47 +/- 8% of control), and the NTG group (55 +/- 3% of control), associated with endocardial S-T segment elevation and a decrease in subendocardial blood flow. Wall thickening continued to decrease in each group with each successive pacing episode. However, during the sixth pacing period wall thickening was significantly (P less than 0.05) less in the saline group (2 +/- 5% of control) than in the AICA-r (31 +/- 7% of control) or NTG (61 +/- 7% of control) group. The progressive decline in wall thickening was accompanied by a further decrease in subendocardial blood flow and a rise in S-T segment in the saline group but not in the AICA-r or NTG group (P less than 0.05). These results demonstrate that sequential periods of ischemia and reperfusion cause a progressive decline in regional wall motion, coincident with a progressive decrease in subendocardial blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Depression of regional blood flow and wall thickening after brief coronary occlusions

1978 ◽  
Vol 234 (6) ◽  
pp. H653-H659 ◽  
Author(s):  
G. R. Heyndrickx ◽  
H. Baig ◽  
P. Nellens ◽  
I. Leusen ◽  
M. C. Fishbein ◽  
...  
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Coronary Occlusion ◽  
Reactive Hyperemia ◽  
Left Ventricular ◽  
Regional Myocardial Blood Flow ◽  
Wall Thickening ◽  
Flow Ratio ◽  
Systolic Wall Thickening ◽  
Regional Myocardial Blood

The effects of a 15-min coronary occlusion and subsequent reperfusion were investigated in conscious dogs previously instrumented for measurement of left ventricular pressure, dP/dt, regional wall thickening, electrograms, and myocardial blood flow. Coronary occlussion reduced overall left ventricular function only slightly but eliminated systolic wall thickening in the ischemic zone and reduced regional myocardial blood flow in the ischemic zone from 1.04 +/- 0.04 to 0.27 +/- 0.02 ml/min per g and the endo/epi flow ratio from 1.23 +/- 0.04 to 0.44 +/- 0.04, while S-T segment elevation increased from 1.1 +/- 0.3 to 8.2 +/- 0.9 mV. After release of the occlusion, S-T segment elevation disappeared within 1 min while reactive hyperemia in the previously occluded artery and a transient increase in cardiac diastolic wall thickness occurred and then subsided by 15 min. In contrast, systolic wall thickening and the endo/epi flow ratio remained significantly depressed for more than 3 h. Thus reperfusion after a 15 minute coronary occlusion results in a prolonged period of reduced regional myocardial blood flow, particularly in the endocardial layers, which correlates with the prolonged depression of regional myocardial shortening and wall thickening.

Heart rate reduction improves myocardial ischemia in swine: role of interventricular blood flow redistribution

1991 ◽  
Vol 261 (3) ◽  
pp. H910-H917 ◽  
Author(s):  
C. Indolfi ◽  
B. D. Guth ◽  
S. Miyazaki ◽  
T. Miura ◽  
R. Schulz ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Left Ventricular ◽  
Regional Myocardial Blood Flow ◽  
Lv Function ◽  
Wall Thickening ◽  
Regional Dysfunction ◽  
Electrical Pacing ◽  
And Function

Regional myocardial blood flow (MBF) distribution and function upon slowing the heart rate (HR) during ischemia were studied in anesthetized swine, a species without coronary collaterals. Perfusion of the left anterior descending artery by a pump allowed controlled production of regional ischemia. Slowing tachycardia by electrical pacing (127 to 87 beats/min) caused marked improvement of regional dysfunction [% wall thickening (WTh) from 9 to 27%] and increased subendocardial MBF [from 0.31 to 0.55 ml.min-1.g-1 (P less than 0.001)] without change of subepicardial MBF. Total left ventricular (LV) MBF increased, whereas right ventricular (RV) MBF fell by 18% (P less than 0.02). The mechanism of MBF changes during slowed HR was assessed by surgically excluding the RV and comparing findings with previous experiments with RV intact when HR was slowed from 96 to 60 beats/min. A similar improvement of regional LV function occurred (8% vs. 30% WTh) with the RV excluded, but without a change in total flow to the LV bed, whereas subendocardial MBF increased and subepicardial MBF fell, indicating transmural redistribution only. These findings show that the RV vascular bed can contribute to LV perfusion in swine during ischemia, and they document the potential for “reverse RV steal” during slowed heart rate in this setting.

Alpha-adrenergic vasoconstriction in normal and hypoperfused myocardium during sympathetic nerve stimulation

1992 ◽  
Vol 263 (6) ◽  
pp. H1682-H1688 ◽  
Author(s):  
J. Westby ◽  
S. Birkeland ◽  
S. E. Rynning ◽  
O. L. Myking ◽  
J. Lekven ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Adrenergic Receptors ◽  
Left Ventricular ◽  
Regional Myocardial Blood Flow ◽  
Control Group ◽  
Coronary Perfusion ◽  
Sympathetic Nerve Stimulation

Coronary vasoconstriction mediated by postjunctional alpha 1- and alpha 2-adrenergic receptors was studied in normally perfused (control group) and left coronary hypoperfused (stenosis group) hearts of vagotomized, beta-blocked (propranolol) cats. Cardiac sympathetic nerve stimulation was combined with alpha 1- and subsequent alpha 2-adrenergic antagonism (doxazosin and SK &F 104078). Coronary perfusion pressure and heart rate were kept constant within groups; regional myocardial blood flow and cardiac output were obtained by means of microspheres with concomitant measurement of left ventricular myocardial oxygen consumption (MVO2). alpha 1-Adrenergic antagonism alone did not significantly alter blood flow in any wall layer in either group. Subsequent alpha 2-adrenergic antagonism increased epicardial as well as composite transmural flow in the stenosis group (P < 0.025). The inverse correlation between coronary resistance and MVO2 vanished in the stenosis group following alpha 1- and alpha 2-adrenergic antagonism. Maximal first derivative of the left ventricular pressure-time relation (dP/dt) and cardiac output were reduced simultaneously (P < 0.001). Hence, the significance of alpha 1- and alpha 2-adrenergic stimulation of inotropy and cardiac performance are augmented by myocardial hypoperfusion. Furthermore, alpha 2-adrenergic receptors are responsible for epicardial vasoconstriction in hypoperfused myocardium.

Beneficial actions of superoxide dismutase and catalase in stunned myocardium of dogs

1986 ◽  
Vol 250 (3) ◽  
pp. H372-H377 ◽  
Author(s):  
G. J. Gross ◽  
N. E. Farber ◽  
H. F. Hardman ◽  
D. C. Warltier
Keyword(s):  
Blood Flow ◽  
Superoxide Dismutase ◽  
Free Radicals ◽  
Oxygen Free Radicals ◽  
Ischemia Reperfusion ◽  
Free Radical Scavengers ◽  
Stunned Myocardium ◽  
Regional Myocardial Blood Flow ◽  
Control Group ◽  
Myocardial Segment

Recent evidence suggests that oxygen free radicals may partially mediate irreversible ischemia-reperfusion injury in the myocardium. In the present study, the effect of a combination of two oxygen free radical scavengers, superoxide dismutase plus catalase (SOD + CAT), on the recovery of subendocardial segment function following 15 min of coronary artery occlusion followed by 3 h of reperfusion ("stunned" myocardium) was compared with a control group in barbital-anesthetized dogs. Myocardial segment shortening (%SS) in the subendocardium of nonischemic and ischemic areas was measured by sonomicrometry and regional blood flow by radioactive microspheres. SOD and CAT were infused into the left atrium 30 min before and throughout the occlusion period. Compared with the control group, %SS in the subendocardium of the ischemic region was significantly (P less than 0.05) greater in the SOD plus CAT-treated group during occlusion and throughout reperfusion. Since there were no significant differences in hemodynamics or regional myocardial blood flow between the SOD plus CAT and the control groups, these results suggest that toxic oxygen free radicals may be partially involved in the reversible ischemic injury that occurs during short periods of coronary occlusion followed by reperfusion.

Cardiac vasculature and flow during pressure-overload hypertrophy

1986 ◽  
Vol 251 (5) ◽  
pp. H1031-H1037 ◽  
Author(s):  
E. A. Breisch ◽  
F. C. White ◽  
L. E. Nimmo ◽  
C. M. Bloor
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Weight Ratio ◽  
Pressure Overload ◽  
Capillary Density ◽  
Left Ventricular ◽  
Control Group ◽  
Cross Sectional ◽  
Ventricle Hypertrophy ◽  
Aortic Cuff

The effects of pressure-overload hypertrophy (H) on myocardial blood flow and microvasculature were studied in the porcine left ventricle. Hypertrophy was produced in nine adult pigs by an aortic cuff constriction of the ascending aorta. Eight pigs served as controls. After 30 days the aortic cuff was released, and the hypertrophy group was studied 1 day postrelease. The degree of hypertrophy, determined by left ventricular-to-body weight ratio, was 45%. With hypertrophy, left ventricular blood flows were normal at rest. During exercise with adenosine infusion, myocardial blood flow to the endomyocardium was reduced compared with the control (C) group (H = 4.02 +/- 0.35, P less than 0.05; C = 5.33 +/- 0.41 ml X min-1 X g-1). Minimal coronary vascular resistance in the endomyocardium was increased during exercise with adenosine in the hypertrophy group compared with the control group. Anatomic studies revealed that hypertrophy causes a reduction in the endomyocardial capillary density (H = 1,654 +/- 168, P less than 0.025; C = 2,168 +/- 106, no./mm2) with a similar trend noted for the transmural arteriolar density. Arteriolar media wall cross-sectional area was unaffected by the pressure overload. These results indicate that changes in the vascular bed do not parallel myocyte growth during pressure-overload hypertrophy. The resultant anatomic imbalance compromises endomyocardial flow, making this region vulnerable to ischemia.

scholarly journals Myocardial involvement in diabetes mellitus: echocardiography data

1996 ◽  
Vol 42 (2) ◽  
pp. 15-17
Author(s):  
Ye. I. Sokolov ◽  
A. P. Zayev ◽  
R. P. Olkha ◽  
T. P. Morozova ◽  
S. A. Zhizhina ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Peripheral Resistance ◽  
Posterior Wall ◽  
Minute Volume ◽  
Left Ventricular ◽  
Specific Power ◽  
Control Group ◽  
End Diastolic Volume ◽  
Myocardial Fibers ◽  
Hyperdynamic Syndrome

Echocardiographic parameters of the central and intracardiac hemodynamics were analyzed in 67 patients with compensated diabetes mellitus of types I and II of 2 to 6 years standing. The control group consisted of 30 subjects. The increase of the minute volume, stroke volume, specific power of the left ventricle, and reduction of total peripheral resistance were revealed in both groups of patients. These shifts are characteristic of a hyperkinetic type of central hemodynamics. The hyperdynamic syndrome was due to left-ventricular hypertrophy in patients with noninsulin-dependent diabetes and due to increased heart rate and the rate of circulatory shortening of myocardial fibers in patients with the insulin-dependent condition. Impaired diastolic function presenting as an increase of the end diastolic volume and a reduced rate of relaxation of the left-ventricular posterior wall myocardium were observed in all the patients, no matter what the type of the condition. The above shifts are predictors of a reduction of myocardial contractility, responsible for the grave and atypical course of coronary disease in diabetics.

scholarly journals Effects of Long-term Nonylphenol Exposure on Myocardial Fibrosis and Cardiac Function in Rats

2021 ◽  
Author(s):  
Chao Liu ◽  
Chengyu Ni ◽  
Weichu Liu ◽  
Xiaolian Yang ◽  
Renyi Zhang ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Myocardial Fibrosis ◽  
Posterior Wall ◽  
Anterior Wall ◽  
Left Ventricular ◽  
Environmental Estrogens ◽  
Control Group ◽  
Cardiac Structure ◽  
Collagen Iii

Abstract Background: Myocardial fibrosis is a critical pathological basis for the poor prognosis of cardiovascular diseases. Studies have found that myocardial fibrosis is closely associated with exposure to environmental estrogens such as nonylphenol (NP), as a representative of environmental estrogens. The aim of this study was to examine the effects of NP chronic exposure on myocardial fibrosis as well as cardiac structure and function. Forty Sprague Dawley rats were randomly divided into four groups (n = 10): control group (C), low NP dose (0.4 mg/kg, L), medium NP dose (4 mg/kg, M), and high NP dose (40 mg/kg, H) groups. The NP dose groups were gavaged with NP for 180 days. Results: The NP level in the heart of the NP groups was significantly higher than those in the control group (F = 43.658, P < 0.001). Serum aspartate aminotransferase (AST), creatine kinase (CK), creatine kinase isozyme (CK-MB), lactate dehydrogenase (LDH) and α-hydroxybutyrate dehydrogenase (α-HBDH) significantly increased in the NP groups compared with the control group (). Histopathological examination of the heart biopsy illustrates that in the medium and high NP groups, the fibrous connective tissue had a disordered and loose gridding shape, muscle fibers had fractured, and muscle fibers were loose with a widened gap. Extensive inflammatory cell infiltration and fibroblast proliferation in the myocardial interstitium were also found. With increasing NP dose, the degree of muscle fiber loosing and disorder became more significant in the NP treatment groups, and the collagen volume fraction (CVF) was higher than that in the control group (P < 0.01). Compared with the control group, the expression of collagen I and collagen III increased significantly in the medium and high NP groups (P < 0.05). The values of the systolic thickness of the left ventricular anterior wall (LVAWs), the diastolic thickness of the left ventricular posterior wall (LVPWd), the systolic thickness of the left ventricular posterior wall (LVPWs), and the left ventricular anterior wall (LVAWd) in the NP groups are were slightly lower than those in of the control group. The values of left ventricular end systolic dimensions (LVIDs) in the NP groups increased compared with the control group. Conclusions: Long-term NP exposure could lead to fibrosis in the rat myocardium, which is characterized by increased expressions of myocardial collagen I and collagen III, as well as elevated cardiac enzymes. In addition, the cardiac structure was affected and changes were observed in the thinner ventricular wall and as an enlarged ventricular cavity.

Abstract P028: The Effect of Cotransplantation of Human Embryonic Stem Cell--Derived Cardiomyocytes and Mesenchymal Stem Cells on Ventricular Function and Remodeling After Myocardial Infarction in Nude Rats

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Wangde Dai ◽  
Mary Kearns-Jonker ◽  
Paul Gerczuk ◽  
Mirja Gunthart ◽  
Nandini Girish ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Human Embryonic Stem Cell ◽  
Embryonic Stem ◽  
Saline Group ◽  
Left Ventricular ◽  
Control Group ◽  
Lv Function ◽  
Left Ventriculography ◽  
Nude Rats

We determined whether co-transplantation of human embryonic stem cell-derived cardiomyocytes (hESC-CMs) and mesenchymal stem cells (MSCs) had additive effects on left ventricular (LV) function and remodeling compared with hESC-CMs treatment alone in a rat myocardial infarction model. One week after myocardial infarction induced by left coronary ligation, nude rats received hESC-CMs (n=15), hESC-CMs + MSCs (n=16), hESC-CMs + MSCs transduced to over-express hemeoxygenase 1(HO-1) (n=14), or saline (n=19). At 4 weeks after treatment, LV function was assessed by left ventriculography, echocardiography and Millar catheter. Some hearts were processed for histology. The LV ejection fraction (LVEF) in sham noninfarcted hearts was 78.1±1.8% (n=5) in the nude rat model. LVEF in the 3 cell treated groups (hESC-CMs: 67.6±1.4%; hESC-CMs + MSCs: 67.2±1.6%; and hESC-CMs + MSCs with HO-1: 66.3±1.7%) were comparable, and significantly higher than in the saline group (60.6±1.2%, n=19; p=0.0022). There was a trend for less left ventricular akinesis and dyskinesis (expressed as % of LV circumference) assessed by left ventriculography at 8.96±1.9% in hESC-CMs group, 8.37±1.67% in hESC-CMs + MSCs group and 4.57±1% in hESC-CMs + MSCs with HO-1 group compared to 10.73±1.76% in the control group (p=0.056). There was a nonsignificant trend for LV fractional shortening assessed by echocardiography to be greater in the 3 cell groups (32.1±3.9% in hESC-CMs; 30.2±2% in hESC-CMs + MSCs; 31.0±1.9% in hESC-CMs + MSCs with HO-1) compared to 24.8±2.2% in the saline group (p=0.18). Expansion index reflecting thinning and dilatation of the infarct was significantly worse in the control group at 0.71±0.05 versus the other 3 groups at 0.32±0.05 (p=0.0039). Thus, cell therapy by hESC-CMs alone or combination transplantation of hESC-CMs and MSCs (with or without HO-1) significantly improved LV function assessed by left ventriculography and reduced expansion index. However, co-transplantation of hESC-CMs and MSCs did not provide better functional improvement compared with hESC-CMs treatment alone after left coronary artery occlusion in nude rats over a period of 4 weeks, suggesting that there may be a ceiling effect above which LV function can not further improve after cell therapy.

Steady-state catecholamine stimulation does not increase cytosolic adenosine in canine hearts

1994 ◽  
Vol 266 (2) ◽  
pp. H503-H510
Author(s):  
K. Kroll ◽  
G. V. Martin
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Myocardial Blood Flow ◽  
Left Ventricular ◽  
Control Group ◽  
Atrial Pacing ◽  
Homocysteine Thiolactone ◽  
Rate Dependent ◽  
Unstimulated Control ◽  
Metabolic Stimulation

Myocardial adenosine production increases transiently during the onset of catecholamine stimulation; however, there is conflicting evidence regarding whether cytosolic adenosine concentrations are increased during sustained steady-state stimulation. If cytosolic adenosine is not elevated during steady-state stimulation, then adenosine produced in the cytosol does not play a role in mediating the sustained increase in myocardial blood flow. The purpose of the present study was to determine whether cytosolic adenosine concentrations in the anesthetized dog heart are increased during steady-state stimulation with norepinephrine, epinephrine, and atrial pacing. Regional cytosolic adenosine concentrations were assessed by measuring myocardial content of S-adenosyl-L-homocysteine (SAH) after 20 min of intravenous administration of L-homocysteine thiolactone. Excess homocysteine causes myocardial accumulation of SAH at a rate dependent on the cytosolic concentration of adenosine. Steady-state metabolic stimulation caused more than twofold increases in myocardial blood flow and oxygen consumption, but there was no increase in left ventricular content of SAH in the stimulation group [6.3 +/- 0.9 nmol/g (SE); n = 6] relative to a parallel unstimulated control group (6.4 +/- 0.9 nmol/g; n = 6). The transmural distribution of SAH was nearly uniform, and there was no correlation between regional measurements of blood flow and myocardial content of SAH or ATP either during metabolic stimulation or under control conditions. In separate experiments, myocardial ischemia caused fivefold increases in SAH content, confirming the sensitivity of the SAH method for increased cytosolic adenosine.(ABSTRACT TRUNCATED AT 250 WORDS)

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