d-Propranolol prevents adenosine formation associated with myocardial hypoperfusion

1989 ◽  
Vol 256 (3) ◽  
pp. H772-H778 ◽  
Author(s):  
R. D. Wangler ◽  
W. P. Peterson ◽  
H. V. Sparks
Keyword(s):  
Coronary Flow ◽  
Oxygen Supply ◽  
Perfusion Pressure ◽  
Oxygen Demand ◽  
Myocardial Tissue ◽  
Adenosine Release ◽  
Consumption Ratio ◽  
Similar Decrease ◽  
Myocardial Hypoperfusion ◽  
Vascular Compartment

d-Propranolol eliminates the increased adenine nucleoside release from hypoperfused hearts [R. D. Wangler, D. F. DeWitt, and H. V. Sparks, Am. J. Physiol. 247 (Heart Circ. Physiol. 16): H330-H336, 1984]. To determine whether d-propranolol reduces adenosine formation or adenosine release into the vascular compartment, we measured myocardial tissue adenosine (TADO). Decreased formation would lower TADO, whereas decreased release would elevate TADO. Reduction of perfusion pressure by 50% reduced coronary flow (CF), venous oxygen tension (PVO2), and myocardial oxygen consumption (MVO2) by approximately 40, 25, and 35%, respectively. Total adenosine and inosine released during 30 min of hypoperfusion increased 10- and 5-fold, respectively. Also, TADO increased from 2.68 +/- 0.37 to 5.17 +/- 0.67 nmol/g (P less than 0.05). In the presence of d-propranolol, the same reduction in perfusion pressure caused a similar decrease in CF and MVO2. d-Propranolol eliminated the release of adenosine and inosine associated with hypoperfusion. TADO after 30 min of hypoperfusion plus d-propranolol was not significantly increased (3.27 +/- 0.40 nmol/g) and was significantly less than hypoperfused hearts. When severe hypoperfusion was created by reducing perfusion pressure 75%, adenosine release still did not increase if d-propranolol was present. When adenosine release was plotted as a function of oxygen supply-consumption, they were related in a hyperbolic fashion. Despite the severity of hypoperfusion, in the presence of d-propranolol the supply-to-consumption ratio was similar to that of the control perfusion group (no drug). We conclude that d-propranolol blocks nucleoside formation during hypoperfusion by reducing oxygen demand such that a reduction of oxygen supply no longer stimulates adenosine formation.

Modeling pressure-flow relations in cardiac muscle in diastole and systole

1997 ◽  
Vol 272 (3) ◽  
pp. H1516-H1526 ◽  
Author(s):  
M. A. Vis ◽  
P. Sipkema ◽  
N. Westerhof
Keyword(s):  
Mechanical Properties ◽  
Cardiac Muscle ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Muscle Length ◽  
Cardiac Contraction ◽  
Myocardial Tissue ◽  
Time Varying ◽  
Pressure Flow ◽  
Slack Length

Pressure-flow relations were calculated for a symmetrical, maximally dilated, crystalloid-perfused coronary vascular network embedded in cardiac muscle in (static) diastole and (static) systole at two muscle lengths: slack length and 90% of maximal muscle length (Lmax). The calculations are based on the "time-varying elastance concept." That is, the calculations include the mechanical properties of the vascular wall and the (varying) mechanical properties of the myocardial tissue (in cross-fiber direction). We found that, at any given perfusion pressure, coronary flow is smaller in systole than in diastole. Relative reduction in vascular cross-sectional area, which forms the basis of flow impediment, was largest for the smallest arterioles. At a constant perfusion pressure of 62.5 mmHg, the transition from (static) diastole to (static) systole at constant muscle length ("isometric contraction") was calculated to reduce flow by 74% (from 18.9 to 5.0 ml x min(-1) x g(-1)) and by 64% (from 12.6 to 4.6 ml x min(-1) x g(-1)) for the muscle fixed at slack length and 90% of Lmax, respectively. At this perfusion pressure, contraction with 14% shortening (from 90% of Lmax in diastole to slack length in systole) was calculated to reduce flow by 61% (from 12.6 to 5.0 ml x min(-1) x g(-1)). Increasing muscle length from slack length to 90% of Lmax decreases coronary flow by 34% in diastole and by 8% in systole. We conclude that modeling cardiac contraction on the basis of the time-varying elastic properties of the myocardial tissue can explain coronary flow impediment and that contractions, with or without shortening, have a larger effect on coronary flow than changes in muscle length.

Contribution of extravascular compression to reduction of maximal coronary blood flow

1992 ◽  
Vol 262 (1) ◽  
pp. H68-H77
Author(s):  
F. L. Abel ◽  
R. R. Zhao ◽  
R. F. Bond
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Storage Site

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

scholarly journals Serum enzymes markers in myocardial infarction: A study of rural area

2017 ◽  
Vol 8 (2) ◽  
pp. 34-37 ◽  
Author(s):  
Mamata Pochhi ◽  
MG Muddeshwar
Keyword(s):  
Myocardial Infarction ◽  
Coronary Flow ◽  
Oxygen Demand ◽  
Serum Enzymes ◽  
Marker Enzymes ◽  
Medical Sciences ◽  
Significant Elevation ◽  
Cardiac Enzymes ◽  
Cardiac Marker ◽  
Present Thesis

Background: Acute Myocardial Infarction is the reduction of coronary flow to such an extent that supply of oxygen to the myocardium do not need the oxygen demand of myocardial tissues. The diagnosis of AMI cannot be fulfilled unless the elevated levels of serum cardiac enzymes particularly CK-MB iso-enzyme activity. The rate of release of cardiac enzymes is highly diagnostic.Aims and Objectives: Therefore, the present thesis aim is-in evaluating, whether the elevated levels of cardiac marker enzymes can be compared to the extent of the Myocardial infarction.Material and Methods: Therefore the present study was undertaken on 50 patients of MI and 50 patients of control. They were group according to the age and sex. The activity of different cardiac enzymes were studied.Result: The AMI patients had significantly elevated levels of 90% patients of high LDH values and 86% patients have elevated levels of AST. The significant elevation of serum enzymes as compared to the control.Conclusion: The magnitude of the elevated levels of enzymes can be compared to the extent of the myocardial infarction. Serum GGT can also be useful marker of oxidative stress in myocardial infarction.Asian Journal of Medical Sciences Vol.8(2) 2017 34-37

Relationship between coronary flow and adenosine release in reactive hyperemia

Life Sciences ◽  
1985 ◽  
Vol 36 (2) ◽  
pp. 105-112 ◽  
Author(s):  
Michael O. Onwochei ◽  
S. Jamal Mustafa
Keyword(s):  
Coronary Flow ◽  
Reactive Hyperemia ◽  
Adenosine Release

Oxygen partial pressure and free intracellular adenosine of isolated cardiomyocytes

1991 ◽  
Vol 260 (4) ◽  
pp. C708-C714 ◽  
Author(s):  
R. T. Smolenski ◽  
J. Schrader ◽  
H. de Groot ◽  
A. Deussen
Keyword(s):  
Oxygen Consumption ◽  
Extracellular Space ◽  
Oxygen Supply ◽  
Oxygen Demand ◽  
Nucleoside Transport ◽  
Isolated Cardiomyocytes ◽  
Homocysteine Thiolactone ◽  
Rat Cardiomyocytes ◽  
Extracellular Adenosine ◽  
Adenosine Concentration

Adenosine formation by the heart is known to critically depend on the ratio of oxygen supply to oxygen demand, but the sensitivity of cardiomyocytes to defined changes in PO2 is not known. Isolated metabolically stable rat cardiomyocytes were incubated up to 45 min at constant PO2 values ranging from 0.1 to 100 mmHg using a feedback-controlled incubation system (oxystat system). Changes of the free intracellular adenosine concentration were measured after trapping of adenosine by cytosolic S-adenosylhomocysteine (SAH) hydrolase in the presence of 200 microM L-homocysteine thiolactone. Rate of SAH formation was constant at a PO2 between 3 and 100 mmHg and gradually increased at PO2 less than 3 mmHg. Cellular ATP decreased only at PO2 less than 1 mmHg, and this was accompanied by a decline of oxygen consumption. Treatment of cells with 5.5 mM deoxyglucose and 4 micrograms/ml oligomycin increased SAH formation 60-fold and was associated with elevated intra- and to a lesser extent extracellular adenosine levels. Inhibition of nucleoside transport with 20 microM S-(p-nitrobenzyl)-6-thioinosine steepened the transmembrane adenosine gradient. Our findings suggest that the cardiomyocyte responds to metabolic poisoning and oxygen deprivation with an enhanced formation of adenosine. This adenosine is mainly formed intracellularly and reaches the extracellular space by diffusion. Threshold for adenosine formation is as low as 3 mmHg.

AICA riboside improves myocardial ischemia in coronary microembolization in dogs

1994 ◽  
Vol 267 (4) ◽  
pp. H1483-H1495 ◽  
Author(s):  
M. Hori ◽  
M. Kitakaze ◽  
S. Takashima ◽  
T. Morioka ◽  
H. Sato ◽  
...  
Keyword(s):  
Extraction Ratio ◽  
Control Group ◽  
Myocardial Tissue ◽  
Metabolic Dysfunction ◽  
Left Carotid Artery ◽  
Adenosine Release ◽  
Coronary Microembolization ◽  
Beneficial Effects ◽  
Coronary Embolization ◽  
Fractional Shortening

This study was undertaken to examine whether 5-amino-4-imidazolecarboxamide (AICA) riboside (acadesine), which augments adenosine release in ischemic myocardium, further attenuates ischemic injury after acute coronary microembolization. The left anterior descending coronary artery was cannulated and perfused with blood from the left carotid artery in 46 dogs, and coronary blood flow (CBF) of the perfused area was measured. In 12 dogs, 15-microns microspheres (5.0 x 10(4)/ml) were injected repeatedly until CBF approached zero. Changes in CBF, fractional shortening, lactate extraction ratio, and adenosine release were measured with and without administration of AICA riboside. In the control group (n = 7), CBF increased to 154 +/- 11 ml.100 g-1.min-1 at 16-30% of total coronary embolization, and adenosine release was 6.1 +/- 1.0 nmol.100 g-1.min-1. Administration of AICA riboside (n = 5) enhanced coronary hyperemia (187 +/- 8 ml.100 g-1.min-1, P < 0.05), adenosine release (11.9 +/- 0.9 nmol.100 g-1.min-1, P < 0.001), and myocardial adenosine content (0.434 +/- 0.069 vs. 0.118 +/- 0.019 nmol/mg wet wt, P < 0.01) and attenuated decreases in fractional shortening and lactate extraction ratio. AICA riboside preserved myocardial tissue ATP content of the embolized area. The administrations of 8-phenyltheophylline (n = 12) and alpha,beta-methyleneadenosine 5'-diphosphate (n = 10) abolished the beneficial effects of AICA riboside. Furthermore, AICA riboside increased ectosolic and cytosolic 5'-nucleotidase activity of the embolized myocardium (n = 12). Thus we conclude that AICA riboside attenuates contractile and metabolic dysfunction by enhancing adenosine release via activation of ectosolic 5'-nucleotidase and inducing local hyperemia in acute coronary microembolization.

Right ventricular oxygen supply/demand balance in exercising dogs

2001 ◽  
Vol 281 (2) ◽  
pp. H823-H830 ◽  
Author(s):  
Bradley J. Hart ◽  
Xiaoming Bian ◽  
Patricia A. Gwirtz ◽  
Srinath Setty ◽  
H. Fred Downey
Keyword(s):  
Right Ventricular ◽  
Oxygen Supply ◽  
Venous Blood ◽  
Oxygen Demand ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Strenuous Exercise ◽  
Conscious Animal ◽  
Flow Reserve ◽  
Exercise Induced

This is the first investigation of right ventricular (RV) myocardial oxygen supply/demand balance in a conscious animal. A novel technique developed in our laboratory was used to collect right coronary (RC) venous blood samples from seven instrumented, conscious dogs at rest and during graded treadmill exercise. Contributions of the RV oxygen extraction reserve and the RC flow reserve to exercise-induced increases in RV oxygen demand were measured. Strenuous exercise caused a 269% increase in RV oxygen consumption. Expanded arteriovenous oxygen content difference (A-VΔO2) provided 58% of this increase in oxygen demand, and increased RC blood flow (RCBF) provided 42%. At less strenuous exercise, expanded A-VΔO2 provided 60–80% of the required oxygen, and increases in RCBF were small and driven by increased aortic pressure. RC resistance fell only at strenuous exercise after the extraction reserve had been mobilized. Thus RC resistance was unaffected by large decreases in RC venous Po 2 until an apparent threshold at 20 mmHg was reached. Comparisons of RV findings with published left ventricular data from exercising dogs demonstrated that increased O2 demand of the left ventricle is met primarily by increasing coronary flow, whereas increased O2extraction makes a greater contribution to RV O2 supply.

Myocardial tissue oxygen supply and utilization during coronary artery bypass surgery: evidence of microvascular no-reflow

2000 ◽  
Vol 98 (3) ◽  
pp. 321 ◽  
Author(s):  
Mohamed K. AL-OBAIDI ◽  
Philip J. ETHERINGTON ◽  
David J. BARRON ◽  
C. Peter WINLOVE ◽  
John R. PEPPER
Keyword(s):  
Coronary Artery ◽  
Coronary Artery Bypass ◽  
Coronary Artery Bypass Surgery ◽  
Oxygen Supply ◽  
Bypass Surgery ◽  
Artery Bypass ◽  
Myocardial Tissue ◽  
Tissue Oxygen ◽  
No Reflow ◽  
Tissue Oxygen Supply

Design and Analysis of the Oxygen Regulator in the Aircraft

2015 ◽  
Vol 752-753 ◽  
pp. 1073-1077
Author(s):  
Ying Jie Zhao ◽  
Hui Xiang Wu
Keyword(s):  
Oxygen Supply ◽  
Oxygen Demand ◽  
Oxygen Flow ◽  
Design Calculation ◽  
Structure Parameters ◽  
Peak Demand ◽  
Valve Opening ◽  
Opening Width

Based on the analysis of the aircrafts oxygen supply performance, an new electronic oxygen supply regulator is designed. Meanwhile, the design calculation work is conducted and the structure parameters is obtained. From the results we can see that the designed oxygen regulator can satisfy the pilot’s oxygen demand under designed heights and that oxygen flow rise under different outlet pressures is not boundless as the valve opening width is increasing .Furthermore, when the valve opens to the half of its radius, the oxygen flow no longer changes as the opening width is increasing. Also, when it opens to the maximum, the peak demand under emergency can be satisfied.

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