Myocardial adenosine, flow, and metabolism during adenosine antagonism and adrenergic stimulation

1993 ◽  
Vol 264 (1) ◽  
pp. H61-H70 ◽  
Author(s):  
J. P. Headrick ◽  
S. W. Ely ◽  
G. P. Matherne ◽  
R. M. Berne
Keyword(s):  
Guinea Pig ◽  
Coronary Flow ◽  
Primary Role ◽  
Functional Hyperemia ◽  
Adrenergic Stimulation ◽  
Metabolic Disturbances ◽  
Guinea Pig Heart ◽  
Adenosine Release ◽  
Endogenous Adenosine ◽  
Adenosine Antagonism

Relationships between interstitial transudate adenosine and coronary flow and between global adenosine formation and cytosolic metabolism were examined in constant-pressure perfused guinea pig hearts during norepinephrine (NE) stimulation and adenosine antagonism with 10 microM 8-phenyltheophylline. Basal coronary flow was 5.7 ml.min-1 x g-1, and transudate and venous adenosine levels were approximately 0.26 and 0.06 microM, respectively. During 10 min of NE stimulation (15 nM), coronary flow and adenosine levels increased, the phosphocreatine-to-inorganic phosphate ratio ([PCr]/[Pi]) declined, and ATP and pH remained stable. Despite phasic release of adenosine, coronary flow correlated dose dependently with transudate adenosine, and adenosine release was inversely related to [PCr]/[Pi] under all conditions. 8-Phenyltheophylline infusion attenuated functional hyperemia by approximately 40%, enhanced the fall in [PCr]/[Pi], and potentiated elevations in transudate and venous adenosine. Similar results and correlations were obtained in hearts perfused at a constant-flow of 5.7 ml.min-1 x g-1, although stimulated adenosine levels and metabolic changes were greater and contractile responses smaller. These data indicate that: 1) endogenous adenosine plays a primary role in functional hyperemia in perfused guinea pig heart; 2) global adenosine formation appears related to phosphorylation status; and 3) adenosine receptor antagonism enhances metabolic disturbances during adrenergic stimulation and markedly potentiates adenosine release, indicating that the functional effects of antagonists may significantly underestimate the dilatory role of endogenous adenosine.

Hypoxia-induced activation of KATP channels limits energy depletion in the guinea pig heart

1995 ◽  
Vol 269 (2) ◽  
pp. H734-H742 ◽  
Author(s):  
U. K. Decking ◽  
T. Reffelmann ◽  
J. Schrader ◽  
H. Kammermeier
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Monophasic Action Potential ◽  
Resonance Spectroscopy ◽  
Energy Status ◽  
Guinea Pig Heart

The functional role of ATP-dependent potassium (KATP) in hypoxic cardiac failure was investigated in isolated guinea pig hearts with glibenclamide and rimalkalim as inhibitor and activator, respectively. Monophasic action potential duration at 90% of repolarization (MAP50), left ventricular function, and cardiac energy status (31P nuclear magnetic resonance spectroscopy) were measured during normotoxic (95% O2) and hypoxic (20% O2) perfusion. In normoxic hearts, 1 microM glibenclamide did not affect MAP50, left ventricular function, and coronary flow (n = 4). In contrast, rimalkalim rapidly shortened MAP50 and left ventricular pressure (LVP) in a dose-dependent fashion (e.g., by 60.2 +/- 3.5 and 80.8 +/- 8.2%, respectively, with 0.6 microM rimalkalim). This latter effect was reversed by 1 microM (glibenclamide (n = 4). With hypoxic perfusion, a reduction in LVP was observed, along with a shortening of the action potential (MAP90; 202 +/- 13 vs. 164 +/- 9 ms) and an increase in coronary flow. Glibenclamide (1 microM) reversed the MAP90 shortening and the increase in coronary flow. In addition, glibenclamide increased LVP transiently (n = 4). When coronary flow of hypoxic hearts was kept constant, however, glibenclamide elicited a sustained positive inotropic effect (n = 7). After glibenclamide, an increase in LVP from 54 +/- 4 to 64 +/- 3 mmHg was observed, along with a reduction in the free energy change of ATP hydrolysis from -54.5 +/- 1.9 to -52.9 +/- 0.2 nJ/mol and a further increase in the coronary venous adenosine from 269 +/- 48 to 1,680 +/- 670 nmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals ATP is involved in myocardial and vascular effects of exogenous bradykinin in ejecting guinea pig heart

1999 ◽  
Vol 277 (2) ◽  
pp. H818-H825 ◽  
Author(s):  
Peter B. Anning ◽  
Bernard D. Prendergast ◽  
Philip A. MacCarthy ◽  
Ajay M. Shah ◽  
Derek C. Buss ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Guinea Pig ◽  
Coronary Flow ◽  
Pyridoxal Phosphate ◽  
Left Ventricular ◽  
Luciferase Assay ◽  
Disulfonic Acid ◽  
Vascular Effects ◽  
Guinea Pig Heart ◽  
Nitric Oxide Release

It has recently been reported that bradykinin induces selective left ventricular (LV) relaxation in isolated guinea pig hearts via the release of nitric oxide. Exogenous bradykinin also induces vasodilation, which is only partly due to nitric oxide release. In the present study we investigated the role of adenyl purines on these bradykinin-induced effects. Isolated ejecting guinea pig hearts were studied. LV pressure was monitored by a 2-Fr micromanometer-tipped catheter. ATP concentrations were measured using a luciferin-luciferase assay. Bradykinin (1 and 100 nM) caused a progressive acceleration of LV relaxation together with a transient increase in coronary flow. These effects were inhibited by the nonselective P2 purinoceptor antagonist suramin (1 μM, n = 6) but were unaffected by the selective P2x purinoceptor antagonist pyridoxal phosphate 6-azophenyl-2′,4′-disulfonic acid (1 μM, n = 6). These myocardial and vascular effects of bradykinin were associated with increased ATP levels in coronary effluent. These data suggest that the selective enhancement of LV relaxation and rise in coronary flow induced by exogenous bradykinin involve endogenous ATP and the subsequent stimulation of P2 purinoceptors.

Effect of Acetaldehyde on the Isolated, Non-working Guinea-Pig Heart: Independence of the Coronary Flow Increase from Changes in Heart Rate and Oxygen Consumption

1974 ◽  
Vol 52 (3) ◽  
pp. 602-612 ◽  
Author(s):  
Minh-Hau Nguyen ◽  
L. Gailis
Keyword(s):  
Heart Rate ◽  
Oxygen Consumption ◽  
Guinea Pig ◽  
Gas Phase ◽  
Coronary Flow ◽  
Constant Pressure ◽  
Guinea Pig Heart ◽  
Bicarbonate Buffer

Guinea-pig hearts were perfused at constant pressure with Krehs–Henseleit bicarbonate buffer equilibrated with 95% O2 – 5% CO2. Acetaldehyde at 1 and 5 mM increased coronary flow, oxygen consumption, and heart rate. At 0.2 mM, it increased coronary flow and oxygen consumption only. In the rapidly paced heart, 1 mM acetaldehyde increased coronary flow, but not heart rate or oxygen consumption. Acetaldehyde increased coronary flow and oxygen consumption of the potassium-arrested heart. Acetaldehyde increased all parameters of the hypoxic heart (25% O2 gas phase), but the anoxic heart was not affected (coronary flow was already maximal).Reserpine (in vivo) and catecholamine β blockers (dichloroisoproterenol and propranolol) (in vitro) blocked the heart rate increases and moderated the rise in oxygen consumption. Dichloroisoproterenol plus phentolamine blocked the increases of both heart rate and oxygen consumption. None of the compounds affected the increase of coronary flow produced by acetaldehyde. Epinephrine, norepinephrine, and tyramine increased the heart rate and oxygen consumption, but not the coronary flow. Theophylline increased all three parameters. Neither tranylcypromine nor atropine modified the acetaldehyde effect. We conclude that the increase in heart rate is mediated by catecholamine β receptors. The increase in coronary flow is independent of the increase in heart rate or oxygen consumption and is not mediated by catecholamines.

scholarly journals EFFECTS OF ARACHIDONIC ACID AND BRADYKININ ON THE CORONARY FLOW, RELEASE OF PGI2 AND CARDIAC FUNCTIONS IN THE PERFUSED GUINEA-PIG HEART

1982 ◽  
Vol 32 (2) ◽  
pp. 351-358
Author(s):  
Zen-ichi TERASHITA ◽  
Hiroshi FUKUI ◽  
Kohei NISHIKAWA ◽  
Minoru HIRATA ◽  
Shintaro KIKUCH
Keyword(s):  
Arachidonic Acid ◽  
Guinea Pig ◽  
Coronary Flow ◽  
Guinea Pig Heart ◽  
Cardiac Functions

Endothelial control of coronary flow in perfused guinea pig heart

1995 ◽  
Vol 90 (2) ◽  
pp. 119-124 ◽  
Author(s):  
R. J. Gryglewski ◽  
S. Chlopicki ◽  
P. Niezabitowski
Keyword(s):  
Guinea Pig ◽  
Coronary Flow ◽  
Guinea Pig Heart ◽  
Endothelial Control

Interstitial transudate concentration of adenosine and inosine in rat and guinea pig hearts

1988 ◽  
Vol 254 (6) ◽  
pp. H1125-H1132 ◽  
Author(s):  
U. K. Decking ◽  
E. Juengling ◽  
H. Kammermeier
Keyword(s):  
Guinea Pig ◽  
Adenosine Deaminase ◽  
Coronary Flow ◽  
Close Correlation ◽  
Primary Role ◽  
Streptomyces Antibioticus ◽  
Flow Response ◽  
Rat Hearts ◽  
Heart Preparation ◽  
High Concentrations

Interstitial transudate (IT) was sampled from the surface of isolated constant pressure-perfused guinea pig and rat hearts. With endogenous adenosine (AR) formation, IT concentrations (Crr) of AR and inosine (IR) were 4- to 6.5-fold higher than those in the venous effluent. The AR-to-IR ratio varied between 0.5 and 0.1. During normoxic perfusion, CIT-AR reached a basal level of 0.18 microM. During maintained hypoxia, CIT-AR was elevated only initially up to 0.63 microM. Subsequently, it decreased to basal values, whereas coronary flow remained elevated. With repetitive hypoxia, CIT-AR decreased to basal values, with little alteration in the coronary flow response. Addition of 1,000 U/l adenosine deaminase reduced CIT-AR below 0.2 microM, with no change in coronary flow response to hypoxia. High concentrations of coformycin (Streptomyces antibioticus), an adenosine deaminase inhibitor (greater than 1 microM), were necessary to increase the AR-to-IR ratio to unity, indicating an intracellular site of action. During administration of 0.1 microM dipyridamole, no close correlation between CIT-AR and coronary flow was found. Administration of 1 microM AR did not induce a detectable change in Crr-AR despite a distinct coronary flow response. We conclude that at least in our heart preparation, interstitial adenosine seems to play no primary role in coronary flow regulation.

Myocardial adenosine, flow, and metabolism during adenosine antagonism and adrenergic stimulation

1993 ◽  
Vol 264 (6) ◽  
pp. 1-1
Author(s):  
J. P. Headrick ◽  
S. W. Ely ◽  
G. P. Matherne ◽  
R. M. Berne
Keyword(s):  
Guinea Pig ◽  
Adrenergic Stimulation ◽  
Rat Hearts ◽  
Adenosine Antagonism

Pages H61–H70: J. P. Headrick, S. W. Ely, G. P. Matherne, and R. M. Berne. “Myocardial adenosine, flow, and metabolism during adenosine antagonism and adrenergic stimulation.” The legends to Figs. 3, 4, and 7 incorrectly state that data were collected from rat hearts. All data in the study were in fact obtained from guinea pig hearts.

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