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

1993 ◽  
Vol 264 (1) ◽  
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.

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.

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.

scholarly journals Regression Analysis of the Left-ventricular Isochoric Pressure Decay of the Heart: Four or Five Model Parameters?

2015 ◽  
Vol 4 ◽  
pp. 53
Author(s):  
John Langer
Keyword(s):  
Guinea Pig ◽  
Kinematic Model ◽  
Parametric Model ◽  
Left Ventricular ◽  
Model Parameters ◽  
Decay Data ◽  
Pressure Decay ◽  
Rat Hearts ◽  
Regression Error ◽  
Damped Oscillation

BACKGROUND: Isochoric (isovolumic) cardiac pressure decay data were previously described by a four-parametric logistic (tangens hyperbolicus) regression model (Langer model). However, a five-parametric kinematic model (Chung model), according to the differential equation of damped oscillation, was recently introduced to describe the isochoric pressure fall. The present study clarifies (a/) whether these five parameters can be reliably estimated from empirical pressure decay data and if the model excels the four-parametric one, and (b/) whether the kinematic Chung model validly describes these pressure decays. METHODS: High-fidelity intraventricular pressure decay data from 1203 isolated working guinea pig and rat hearts were analyzed by both models. RESULTS: Most cases present with a higher regression error in the five-parametric kinematic model, the median ratio (F value) of its regression variance by those of the four-parametric logistic model is 1.004 (95 per cent confidence interval: 1.002 to 1.006) in in the guinea pig as well as in the rat group. Additionally, the parameters of both models were estimated from the first and second half of the decay phase separately to check for the models' validity.  The five-parametric model yields significantly non-constant parameters more often than the four-parametric model. CONCLUSION: (a) the five parameters of the kinematic Chung model remain underdetermined by the empirical pressure data, and {b) this five-parametric model does not provide a valid description of the isochoric cardiac pressure decay.

Adenosine antagonism decreases metabolic but not functional recovery from ischemia

1991 ◽  
Vol 260 (1) ◽  
pp. H193-H200 ◽  
Author(s):  
D. A. Angello ◽  
J. P. Headrick ◽  
N. M. Coddington ◽  
R. M. Berne
Keyword(s):  
Functional Recovery ◽  
Left Ventricular ◽  
Low Flow ◽  
Ischemia And Reperfusion ◽  
Constant Flow ◽  
Hemodynamic Parameters ◽  
Isolated Hearts ◽  
Rat Hearts ◽  
Adenosine Antagonism ◽  
Developed Pressure

The effect of adenosine receptor antagonism on function and metabolism was examined in isolated hearts during low flow ischemia and reperfusion. Isovolumic rat hearts perfused at constant flow were subjected to 30 min of ischemia followed by 30 min of reperfusion. Infusion of vehicle or 10 microM 8-phenyltheophylline (8-PT) was initiated 10 min before ischemia and maintained throughout reperfusion. 8-PT infusion had no significant effects on hemodynamic parameters or metabolism preischemia. During ischemia, left ventricular developed pressure declined to approximately 15% of preischemic values in control and 8-PT hearts, and ATP and PCr decreased to approximately 73 and 60% of preischemic values. Inorganic phosphate (Pi) increased to 353 = 41 and 424 +/- 53% of preischemic values in control and 8-PT hearts, respectively. After reperfusion, function recovered to greater than 95% of preischemic levels in control and 8-PT hearts. Unlike control hearts, recovery of metabolites was significantly different during reperfusion in 8-PT hearts (P less than 0.05); ATP, phosphocreatine, and Pi recovered to 82 +/- 8, 71 +/- 8, and 281 +/- 27% of preischemic values, respectively. Venous purine washout was significantly greater (P less than 0.05) during reperfusion in 8-PT hearts (327 +/- 113 nmol) than in control hearts (127 +/- 28 nmol). Blockade of adenosine receptors appears to adversely affect metabolic but not functional recovery in the ischemic-reperfused myocardium.

Adenosine inhibition of beta-adrenergic induced responses in aged hearts

1993 ◽  
Vol 265 (2) ◽  
pp. H494-H503 ◽  
Author(s):  
J. G. Dobson ◽  
R. A. Fenton
Keyword(s):  
Adenosine Deaminase ◽  
Glycogen Phosphorylase ◽  
Cardiac Contractility ◽  
Sprague Dawley ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Fischer 344 ◽  
Rat Hearts ◽  
Fischer 344 Rat ◽  
Glycogen Phosphorylase Activity

Because adenosine has an antiadrenergic action in the heart, young (3-4 mo) and aged (18-20 mo) adult Sprague-Dawley and Fischer 344 rat hearts were perfused to determine whether interstitial adenosine plays a role in the reduced metabolic and mechanical responsiveness of the aged heart to beta-adrenergic stimulation. Interstitial adenosine was approximately twofold greater in aged hearts compared with young adult hearts, and 10(-8) M isoproterenol (ISO) further increased these levels. ISO increased myocardial adenosine 3',5'-cyclic monophosphate content, glycogen phosphorylase activity, and cardiac contractility by 83, 150, and 130%, respectively, in young hearts but only increased these variables by 45, 74, and 61%, respectively, in aged hearts. Sulfophenyl-theophylline prevented the reduced ISO-induced responsiveness of the above variables in aged hearts. Exogenously administered adenosine deaminase eliminated the reduced ISO-induced contractile responsiveness in aged hearts. The apparent activities of 5'-nucleotidase and adenosine deaminase were not significantly different in ventricular samples from young and aged hearts. These results suggest that the elevated interstitial level of adenosine exerts a greater antiadrenergic effect in the aged heart, rendering it less responsive to beta-adrenergic stimulation. The increased interstitial level of adenosine in the aged heart does not appear to be due to a difference in the activities of either 5'-nucleotidase or adenosine deaminase.

Reduced glutathione modulates the arachidonic acid induced coronary reactions

1984 ◽  
Vol 62 (10) ◽  
pp. 1261-1267 ◽  
Author(s):  
Jaime Talesnik ◽  
James N. Tsoporis
Keyword(s):  
Arachidonic Acid ◽  
Guinea Pig ◽  
Reduced Glutathione ◽  
Isolated Heart ◽  
Prostaglandin E ◽  
Guinea Pig Heart ◽  
Rat Hearts ◽  
Resistance Vessels ◽  
Vasodilator Action ◽  
Perfused Hearts

Coronary flow was recorded from spontaneously beating isolated perfused hearts of rats and guinea pigs. Arachidonic acid (AA), in single bolus doses, produced a fast short lasting coronary constriction followed by a slow developing but persisting vasodilation. These reactions (biphasic type) were characteristic of the guinea pig heart. In about 50% of the rat hearts the vasoconstrictor action predominated while the biphasic response was obtained in the rest of the experiments. Pretreatment of rats with aspirin prevented the responses to AA in the isolated heart. The administration of reduced glutathione (GSH) (about 1 mM to the rat or 0.5–0.75 mM to the guinea pig hearts) produced a marked development and (or) enhancement of the vasodilator action of AA. Repeated or single large doses of AA produced a change of pattern of responses from biphasic to constrictor type; the addition of GSH restored the vasodilator phase. Since GSH directs the endoperoxide metabolism towards the synthesis of prostaglandin E2 (PGE2), we postulate that the coronary dilatation of resistance vessels produced by AA would be due to a great extent to PGE2.

scholarly journals Adrenergic activation of electrogenic K+ secretion in guinea pig distal colonic epithelium: involvement of β1- and β2-adrenergic receptors

2009 ◽  
Vol 297 (2) ◽  
pp. G269-G277 ◽  
Author(s):  
Jin Zhang ◽  
Susan T. Halm ◽  
Dan R. Halm
Keyword(s):  
Epithelial Cells ◽  
Guinea Pig ◽  
Short Circuit ◽  
Surface Epithelium ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Bathing Solution ◽  
Adrenergic Stimulation ◽  
Ussing Chambers ◽  
Adrenergic Activation

Adrenergic stimulation of electrogenic K+ secretion in isolated mucosa from guinea pig distal colon required activation of two β-adrenergic receptor subtypes (β-AdrR). Addition of epinephrine (epi) or norepinephrine (norepi) to the bathing solution of mucosae in Ussing chambers increased short-circuit current ( Isc) and transepithelial conductance ( Gt), consistent with this cation secretion. A β-adrenergic classification was supported by propranolol antagonism of this secretory response and the lack of effect by the α-AdrR antagonists BE2254 (α1-AdrR) and yohimbine (α2-AdrR). Subtype-selective antagonists CGP20712A (β1-AdrR), ICI-118551 (β2-AdrR), and SR59320A (β3-AdrR) were relatively ineffective at inhibiting the epi-stimulated Isc response. In combination, CGP20712A and ICI-118551 inhibited the response, which supported a synergistic action by β1-AdrR and β2-AdrR. Expression of mRNA for both β1-AdrR and β2-AdrR was indicated by RT-PCR of RNA from colonic epithelial cells. Protein expression was indicated by immunoblot showing bands at molecular weights consistent with monomers and oligomers. Immunoreactivity (ir) for β1-AdrR and β2-AdrR was prominent in basolateral membranes of columnar epithelial cells in the crypts of Lieberkühn as well as intercrypt surface epithelium. Cells in the pericryptal sheath also had β1-AdrRir but did not have discernable β2-AdrRir. The adrenergic sensitivity of K+ secretion measured by Isc and Gt was relatively low as indicated by EC50s of 41 ± 7 nM for epi and 50 ± 14 nM for norepi. Adrenergic activation of electrogenic K+ secretion required the involvement of both β1-AdrR and β2-AdrR, occurring with an agonist sensitivity reduced compared with reported values for either receptor subtype.

Mechanisms of hypoxia-induced atrial natriuretic factor release from rat hearts

1989 ◽  
Vol 257 (1) ◽  
pp. H147-H156 ◽  
Author(s):  
R. A. Lew ◽  
A. J. Baertschi
Keyword(s):  
Atrial Natriuretic Factor ◽  
Isolated Heart ◽  
Inhibitory Effect ◽  
Atropine Sulfate ◽  
Base Line ◽  
Adrenergic Stimulation ◽  
Natriuretic Factor ◽  
Rat Hearts ◽  
6 Hydroxydopamine ◽  
Atrial Natriuretic

Potential mechanisms of hypoxia-induced atrial natriuretic factor (ANF) release [A.J. Baertschi, J.M. Adams, and M.P. Sullivan. Am. J. Physiol. 255 (Heart Circ. Physiol. 24): H295-H300, 1988] were investigated in Langendorff-perfused rat hearts. The ANF release was graded with stimulus intensity; 10 min of perfusion with Krebs-Henseleit solution equilibrated with 95, 20, 10, 5, and 0% oxygen led to peak ANF levels of 140 +/- 31 (SE), 202 +/- 20, 407 +/- 76, 659 +/- 119, and 516 +/- 83% of base-line ANF (159 +/- 14 pg/ml), respectively. Hypoxia-induced release of lactate dehydrogenase and creatine kinase did not correlate with ANF release; this finding, along with other experiments, rules out tissue damage as a significant factor. Phentolamine (1.3 microM) and propranolol (0.1 microM) each reduced peak hypoxia-induced (0% O2) ANF release to 333 and 310%, respectively, whereas atropine sulfate (15 microM) had no inhibitory effect. The three antagonists combined reduced the peak hypoxia-induced ANF release to the same extent (307%) as either phentolamine or propranolol alone. Earlier (24 h) catecholamine depletion of rats with 100 mg/kg 6-hydroxydopamine also significantly reduced peak hypoxia-induced ANF release to 330%. Neither the reduction of the ANF secretory responses by these interventions nor the remaining ANF response could be attributed to changes in atrial mechanics. Therefore, these studies demonstrate that alpha- and beta-adrenergic stimulation is responsible for approximately half the hypoxia-induced ANF release from the isolated heart, whereas an as yet undefined mechanism accounts for the remainder of the response.

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