Activity profile in elite Italian soccer team.

The purpose of this study was to analyse the activity profile of players in a top-class team in the Italian national football league over the course of a season (n=388). The effect of playing position and the two halves on the number and duration of short, intense bursts of effort and recovery phases was studied. The main results show that midfielders cover significantly more distance than players in other positions (p<0.001). For midfielders, the number of displacements of 2-40 m and the number of sprints covering between 2 and 9 m and between 30 and 40 m are considerably greater than for other positions (p<0.05). The distances covered in the second half compared to the first half are significantly lower for all categories of run (p<0.05). In the second half, the distance covered at very high intensity is significantly lower (p<0.01), whilst the number of recovery times greater than 120 s increases significantly compared to the first half (p<0.01). This study provides data which could be used as a basis for the work of scientists as well as football professionals.

The homologous rat chromogranin A1-64 (rCGA1-64) modulates myocardial and coronary function in rat heart to counteract adrenergic stimulation indirectly via endothelium-derived nitric oxide.

Chromogranin A (CGA), produced by human and rat myocardium, generates several biologically active peptides processed at specific proteolytic cleavage sites. A highly conserved cleavage N-terminal site is the bond 64-65 that reproduces the native rat CGA sequence (rCGA1-64), corresponding to human N-terminal CGA-derived vasostatin-1. rCGA1-64 cardiotropic activity has been explored in rat cardiac preparations. In Langendorff perfused rat heart, rCGA1-64 (from 33 nM) induced negative inotropism and lusitropism as well as coronary dilation, counteracting isoproterenol (Iso) - and endothelin-1 (ET-1) -induced positive inotropic effects and ET-1-dependent coronary constriction. rCGA1-64 also depressed basal and Iso-induced contractility on rat papillary muscles, without affecting calcium transients on isolated ventricular cells. Structure-function analysis using three modified peptides on both rat heart and papillary muscles revealed the disulfide bridge requirement for the cardiotropic action. A decline in Iso intrinsic activity in the presence of the peptides indicates a noncompetitive antagonistic action. Experiments on rat isolated cardiomyocytes and bovine aortic endothelial cells indicate that the negative inotropism observed in rat papillary muscle is probably due to an endothelial phosphatidylinositol 3-kinase-dependent nitric oxide release, rather than to a direct action on cardiomyocytes. Taken together, our data strongly suggest that in the rat heart the homologous rCGA1-64 fragment exerts an autocrine/paracrine modulation of myocardial and coronary performance acting as stabilizer against intense excitatory stimuli.

Role of nitric oxide and platelet-activating factor in cardiac alterations induced by tumor necrosis factor-alpha in the guinea-pig papillary muscle.

OBJECTIVE: Tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine with negative inotropic properties, is implicated in several pathophysiological events. To clarify the mechanism of action of TNF-alpha on myocardium, we investigated the possible role of platelet-activating factor (PAF) and nitric oxide (NO) as secondary mediators of the depressant effect of this cytokine. METHODS: Isometric twitches and intracellular action potentials were recorded from guinea pig papillary muscles. The effects of TNF-alpha (1-10 ng/ml) were studied in controlled conditions and after treatment with 0.5% Triton X-100, to destroy the endocardial endothelium NG-nitro-L-arginine methyl ester (L-NAME), D-NAME (1 mM) and the two different PAF-receptor antagonists WEB 2170 (3 microM) and CV 3988 (5 microM) were used to study the role of NO and PAF in cardiac depression induced by TNF-alpha. To study the role of NO in cardiac alterations induced by PAF, papillary muscles were pretreated with L-NAME or D-NAME and then challenged with PAF (0.1-1 microM). Nitrite production by papillary muscles challenged with TNF-alpha alone. TNF-alpha in the presence of WEB 2170 or CV 3988, or PAF was studied with the Greiss reagent method. PAF production by papillary muscles stimulated by TNF-alpha was studied by a bioassay method. RESULTS: TNF-alpha induced an initial, transient positive inotropic effect, then reduced the contractility and the action potential duration in a concentration-dependent manner. Treatment of papillary muscle with Triton X-100 did not modify the response to TNF-alpha, suggesting that the effect of TNF-alpha is not mediated by endocardial endothelial cells. Pretreatment with indomethacin reduced the negative effect of TNF-alpha, while propranolol abolished the initial increase of contractility. The role of PAF and NO as mediators of TNF-alpha was suggested by: (1) the protective effect of L-NAME, but not of D-NAME, on electrical and mechanical alterations; (2) the stimulatory effect of TNF-alpha on nitrite production; (3) the inhibitory effect of WEB 2170 and CV 3988, on both the electromechanical alterations and the nitrite production; (4) the synthesis of PAF induced by TNF-alpha. L-NAME blocked the negative effect of PAF and PAF enhanced nitrite production by papillary muscle. CONCLUSIONS: The present results suggest that in cardiac muscle: (1) the release of PAF triggered by TNF-alpha may account for the stimulation of NO production; (2) both PAF and NO contribute to the development of the electrical and mechanical alterations induced by TNF-alpha; (3) NO production was down-stream to the synthesis of PAF.

The effects of Gaboon viper (Bitis gabonica) venom on the electrical and mechanical activity of the guinea-pig myocardium.

The effects of Bitis gabonica venom were tested on guinea-pig heart, using both Langendorff preparations and isolated atrial strips or papillary muscles. In the self-paced whole heart, a single passage of 50 micrograms of venom per ml produced in sequence: irregularities of the A-V conduction and decrease of the contractile strength, progressive failure to relax and systolic arrest of the heart. Pretreatment with atropine reduced but did not abolish these effects. Venom recycled through the heart was effective at a much lower dose. The relationship between resting membrane potential and [K+]o was unaffected by envenomation, suggesting that the action of the venom cannot be ascribed to a loss of ionic selectivity of the cell membrane. The peak amplitude of action potentials declined in papillary muscle exposed to venom at physiological [K+]o, while in atrial cells it was affected only at higher [K+]o. Maximum upstroke rate of the action potential vs. resting potential at different [K+]o gave a sigmoid relationship, characterized by a higher upper asymptote as compared to controls, and by a shift of the curve towards more negative voltage values. A marked shortening of the action potential duration, paralleled by a decrease in time to peak tension, was recorded as well. 'Slow' action potentials, elicited in 20 mM K+ solution, were completely abolished within 10 min of perfusion with venom. These results are consistent with the hypothesis that the venom interacts with both transmembrane Ca2+ inflow and Ca2+ binding at the external side of the cell membrane. A transient positive inotropic effect induced by the venom was observed in papillary muscle and in atropinized atrium. This effect was abolished by previous administration of reserpine to the animal or by addition of propranolol to the perfusing solution, suggesting a venom-induced release of both adrenergic and cholinergic transmitters from nerve endings within the cardiac tissue.

The mechanical and electrical effects of rhinoceros viper (Bitis nasicornis) venom on the isolated perfused guinea pig heart and atrial preparations.

The mechanical and electrical effects of the venom of Bitis nasicornis were studied on the guinea-pig Langendorff and left atrial myocardium preparations. While Langendorff preparations were treated with individual doses of 0.1, 0.6 and 1.4 mg, isolated left atria were treated using concentrations of 2.0, 20 and 200 micrograms/ml of venom in the perfusion solution. In the Langendorff preparation, transient increases in left ventricular systolic pressure (LVSP) and heart rate (HR) were seen after 0.1 mg of venom. When 0.6 mg of venom was given, the increases were followed by decreases, while 1.4 mg doses simply induced decreases in LVSP and HR. After both 0.6 and 1.4 mg doses the decreases were accompanied by increases in left ventricular diastolic pressure. In addition to these mechanical effects, transient increases in HR with atrio-ventricular blocks, ventricular extrasystoles and tachycardia were observed after each dose. In the left atrium the 2 micrograms/ml venom concentration produced an increase, followed by a decrease, in the maximum tension developed, which was only seen to decrease with higher concentrations of 20 and 200 micrograms/ml of venom. A dose dependent significant reduction in the action potential duration was observed for the doses of 0.6 and 1.4 mg in the ventricle and for all three concentrations in the atrium.

Role of endothelial cells in modulation of contractility induced by hexarelin in rat ventricle.

The synthetic growth hormone (GH) secretagogue hexarelin has important cardiac effects, that include a reduction of dysfunction in ischemic-reperfused hearts from GH-deficient rats after a chronic treatment and an increase of ejection fraction in acutely treated men. To investigate the mechanisms of its cardiac activity, we studied the effects of hexarelin (1-10 microM) on contractility of rat papillary muscles. We observed, in hexarelin treated papillary muscles, an improved recovery of contractility after anoxia. Hexarelin induced time- and frequency-dependent inotropic effects on papillary muscle. These effects were a transient increase in contractile force, abolished by propranolol (0.2 microM), followed by a reduction at low (60-240/min), but not at high (400-600/min) beating frequencies. The typical negative force-frequency relationship present in rat papillary muscles was therefore modified, and a minor increase in diastolic tension occurred after a sudden increase in stimulus frequency. Blockade of NO synthesis with 1 mM L-NAME, partially altered the response to hexarelin. MK-677 (1 microM), a non peptidyl GH secretagogue, reduced contractility, but did not alter the force-frequency relationship. The remaining effects of hexarelin were absent in papillary muscles pre-treated with indomethacin (1 microM), or after removal of endocardial endothelium with 0.5% triton X-100. The release of the prostacyclin metabolite 6-keto-PGF1alpha was increased during reoxygenation after a period of anoxia in hexarelin treated papillary muscles. Hexarelin had no significant effect on calcium transients and on I(Ca) measured in isolated ventricular cells. These findings suggest that the effects of hexarelin are mainly due to endothelium-released PGI2.

Effects of yew alkaloids and related compounds on guinea-pig isolated perfused heart and papillary muscle.

The mechanical and electrical effects of selected yew alkaloids were studied on two different cardiac preparations: the isolated coronary perfused heart and the isolated papillary muscle of the guinea-pig. In the isolated heart, the Winterstein acid type alkaloids 1, 2 and 3 induced electrical and mechanical effects similar to those reported after yew intoxication (negative inotropic effect, block of atrio-ventricular conduction), but the coronary flow was unchanged. Taxine B (1), the most potent compound of this group, reduced cardiac contractility and the maximum rate of depolarisation of the action potential in the isolated papillary muscle, acting as a class I antiarrhythmic drug. In the isolated heart, the cinnamates 4 and 5, corresponding to the degradation products of 1 and 3, exerted arrhythmogenic effect due to a reduction of coronary flow. No alterations in electrical and contractile activities were in fact recorded after perfusion of the isolated papillary muscle with 4. Taxine A (6) and the taxane alcohol 7, corresponding to the terpenoid core of 3 had no significant cardiac effect. Our results suggest that the poisonous properties of the yew tree are probably due to the combined activity of alkaloids of the Winterstein acid type and their corresponding cinnamtes, which can reduce both the excitability and the coronary flow of the heart.

Cardiovascular alterations in the rabbit infused with platelet activating factor (PAF): effect of kadsurenone, a PAF-receptor antagonist.

The ECG and haemodynamic alterations caused by the i.v. infusion of platelet-activating factor (PAF) in the rabbit were studied after pretreatment with Kadsurenone, a specific PAF-receptor antagonist. Infusion of PAF at 0.8 microgram/kg in the rabbit caused important ECG changes, such as ST-segment depression and conduction arrhythmias, concomitantly with a marked reduction in left ventricular systolic pressure, mean arterial pressure and cardiac output, with a rise in total peripheral resistances and mean right atrial pressure. These physiological parameters became maximal at 75-120 seconds after PAF challenge, and returned to near prechallenge values within 25-60 minutes. Pretreatment with Kadsurenone, administered either intravenously (0.014 M, 1 ml/kg) or intraperitoneally (0.14 M, 1 ml/kg), exerted a quite complete protective effect in regard to the ECG changes and caused a significant reduction in the magnitude of all the haemodynamic alterations observed after intravenous infusion of PAF (0.8 microgram/kg). These results suggest that Kadsurenone is an effective inhibitor of PAF-induced cardiovascular changes in the rabbit, probably due to its competitive antagonism against PAF binding to specific receptors.

Endothelium dependent cardiovascular effects of the Chromogranin A-derived peptides Vasostatin-1 and Catestatin.

The involvement of Chromogranin A (CgA) in the cardiovascular function regulation is attributed to its function as a prohormone. Several studies indicated that CgA-derived peptides, particularly Vasostatin-1 (VS-1) and Catestatin (CST), exert signaling effects in numerous organs/systems, including the cardiovascular system. This review focuses on the recently described signaling pathways activated by VS-1 and CST, giving insights into the mechanisms at the basis of their cardiac negative inotropic action, their vasodilator effects and their cardioprotective role observed in different experimental conditions. Accumulated evidences provided convincing support for VS-1 and CST as vasoactive peptides indirectly acting on cardiomyocytes through a Ca(2+)-independent/PI3-K-dependent NO release from endothelial cells. This pathway is supposed to be triggered by the interaction of these peptides with the plasma membrane. The premise of these studies grounds on the biochemical features of VS-1 and CST, which are structurally characterized by amphipathic properties and the ability to interact with mammalian and microbial membranes. On the other hand, recent data obtained in both isolated heart and isolated cardiomyocytes suggest that the VS-1 and CST-mediated cardioprotective effects are primarily direct on the myocardium, rather than endothelium-dependent. Anyway, both direct and indirect pathways seem to be characterized by the absence of specific membrane receptors on target cells, highlighting intriguing novelties in the topic of cell signaling, in particular respect to an hypothetical receptor-independent eNOS activation.

Post-ischaemic activation of kinases in the pre-conditioning-like cardioprotective effect of the platelet-activating factor.

AIM: Platelet-activating factor (PAF) triggers cardiac pre-conditioning against ischemia/reperfusion injury. The actual protection of ischaemic pre-conditioning occurs in the reperfusion phase. Therefore, we studied in this phase the kinases involved in PAF-induced pre-conditioning. METHODS: Langendorff-perfused rat hearts underwent 30 min of ischaemia and 2 h of reperfusion (group 1, control). Before ischaemia, group 2 hearts were perfused for 19 min with PAF (2 x 10(-11) M); groups 3-5 hearts were co-infused during the initial 20 min of reperfusion, with the protein kinase C (PKC) inhibitor chelerythrine (5 x 10(-6) M) or the phosphoinositide 3-kinase (PI3K) inhibitor LY294002 (5 x 10(-5) M) and atractyloside (2 x 10(-5) M), a mitochondrial permeability transition pore (mPTP) opener respectively. Phosphorylation of PKCepsilon, PKB/Akappat, GSK-3beta and ERK1/2 at the beginning of reperfusion was also checked. Left ventricular pressure and infarct size were determined. RESULTS: PAF pre-treatment reduced infarct size (33 +/- 4% vs. 64 +/- 5% of the area at risk of control hearts) and improved pressure recovery. PAF pre-treatment enhanced the phosphorylation/activation of PKCepsilon, PKB/Akappat and the phosphorylation/inactivation of GSK-3beta at reperfusion. Effects on ERK1/2 phosphorylation were not consistent. Infarct-sparing effect and post-ischaemic functional improvement induced by PAF pre-treatment were abolished by post-ischaemic infusion of either chelerythrine, LY294002 or atractyloside. CONCLUSIONS: The cardioprotective effect exerted by PAF pre-treatment involves activation of PKC and PI3K in post-ischaemic phases and might be mediated by the prevention of mPTP opening in reperfusion via GSK-3beta inactivation.

Cardiac impairment in rabbits fed a high-fat diet is counteracted by dehydroepiandrosterone supplementation.

AIMS: The biochemical and structural cardiac oxidative-dependent damage induced by high-fat (HF) diet was examined in a rabbit model, together with the role of dehydroepiandrosterone (DHEA) in contrasting tissue damage. MAIN METHODS: New Zealand white rabbits fed a HF diet supplemented or not with DHEA (0.02%) were utilized for 12 weeks. Oxidative stress, inflammatory and necrosis parameters, fatty deposition, heavy-chain myosin isoforms (MHC) expression and papillary muscle functionality were examined in the left ventricle of rabbits. KEY FINDINGS: Rabbits fed a HF diet that showed hyperglycemia, insulin resistance and dyslipidemia together with increase of oxidative stress and of advanced end-glycation product levels have been observed. Concerning pro-inflammatory insults, there was increased p65-NFkB activation and increased tumor necrosis factor-alpha and C-reactive protein expressions. Cellular damage induced by the HF diet was detected through the switch of expression of MHC isoforms, indicating impairment of cardiac contractility, confirmed by altered of basal parameters of papillary muscle functionality. Rabbits fed the HF diet supplemented with DHEA showed a partial reduction of oxidative stress and the inflammatory state. Cardiac necrosis, the shift of MHC isoforms, and cardiac functionality, were also partially counteracted. SIGNIFICANCE: Rabbits fed with a HF diet showed a beneficial effect when low-dose DHEA was added to the diet. The steroid, without affecting high plasma glucose level or insulin resistance, restored oxidative balance, lowered lipid levels and inflammation insults, preventing cellular and functional alterations of cardiac tissue and thus delaying the onset of cardiac damage.

The platelet activating factor triggers preconditioning-like cardioprotective effect via mitochondrial K-ATP channels and redox-sensible signaling.

Endogenous platelet activating factor (PAF) is involved in heart ischemic preconditioning. PAF can also afford pharmacological preconditioning. We studied whether mitochondrial-ATP-sensitive K(+) (mK(ATP)) channels and reactive oxygen species (ROS) are involved in PAF-induced cardioprotection. In Group 1 control hearts, Langendorff-perfused rat hearts underwent 30 min ischemia and 2 hours of reperfusion. Group 2 hearts, before ischemia, were perfused for 19 min with PAF (2x10(-11) M); Groups 3 and 4 hearts were co-infused with PAF and N-acetyl-L-cysteine or 5-hydroxydecanoate to scavenge ROS or to block mK(ATP) channels, respectively. Left ventricular pressure and infarct size were determined. PAF-pretreatment reduced infarct size (33 +/- 4% vs 64 +/- 4.6 % of the area at risk of control hearts) and improved pressure recovery. Infarct-sparing effect of PAF was abolished by N-acetyl-L-cysteine and 5-hydroxydecanoate. Thus, the cardioprotective effect exerted by PAF-pretreatment involves activation of mK(ATP) channels and redox signaling in pre-ischemic phase.

Staircase in lizard ventricle. I. Time-course analysis in the normal inotropic state.

The staircases drawn by the isometric twitches up to the attainment of the steady-state at frequencies in the range of 1 to 60 min-1 have been studied in superfused half-ventricles of lizard, showing a normal inotropic state. The differences between the instantaneous twitch tension and the steady-state value has proved to be fitted by the algebraic sum of 3 or 4 exponential phases. The analysis of the electrical and mechanical activity of the preparation suggests a correlation between each exponential contribution to the staircase profile and the changes of the action potential duration as well as of the balance between the two sources (transmembrane influx and impulsive release from an intra or extracellular store) of calcium ions activating the contraction.

Staircase in lizard ventricle. II. Time-course analysis in the hypodynamic state.

The analysis of the staircases in lizard ventricle, that was the object of the preceding paper, has been extended to the hypodynamic condition, induced by the prolonged perfusion of the ventricular preparation at high flow rate. For comparison, the effects of lowered [Ca]0 on the normal ventricle as well as of raised [Ca]0 on the hypodynamic ventricle have been also investigated. The results show that the low rate (less than or equal to 2 min-1) staircase in hypodynamic condition is formally described by the same algebraic sum of exponentials as in normal hearts: Pt - Ps - - phi 1 - phi 2 + phi 5, although with altered values of both their extrapolations P' at the time t0 and their time constants tau. On the contrary, t high beat rates the staircase profiles obey to the the eqn.: Pt - Ps = - phi 2 + phi 3 - phi 4 + phi 5, which is characterized by the absence of the phi 1 component, as well as by the occurrence of the phi 4 component, that fits to an early phase of rapid build-up of the isometric twitch tension from the reduced values of the hypodynamic "rested state contraction'. A two-fold increase of the [Ca]0 approaches the time-course of the hypodynamic staircases, whether at low or at high beat rate, to that displayed by the ventricles in normal inotropic state. The results are discussed on the assumption of the double-source hypothesis for the Ca that activates the contraction in the lizard ventricular cells.

On the reversal of the heart hypodynamia by means of a prolonged cooling.

Lizard ventricles induced to hypodynamia by the high flow rate of the perfusing solution were submitted either to brief periods of cooling (from 20 to 25 degrees C), or to a prolonged hypothermic incubation (35 h at 4 degrees C) followed by a recovery at room (20 degrees C) or reduced (15 degrees C) temperature. Isometric rested state contractions as well as staircases and steady-state twitches at 20 or 4 min-1 were recorded. While a brief exposure to reduced temperature proved to increase the peak tension of the twitches, without altering the peculiar tension-frequency relation and the pattern of the staircases which characterize the hypodynamic condition, a transitory post-effect of the prolonged hypothermic incubation was noticed, that causes the reappearance of the contractility features which characterize the normal inotropic state. The results are discussed in the light of the double-component hypothesis for the twitch in lizard ventricular cells, and interpreted as evidences that a brief exposure to low temperatures enhances the transmembrane Ca++ influx during the AP, that causes an augmentation of the late, slow rising component of the twitch; while the prolonged hypothermic incubation would cause also an increase of the Ca++ content in a cellular store, and consequently a potentiation of the early, impulsive component of the twitch.

Acetylcholine's inhibitory effect on the calcium-dependent depolarization in the heart cells of a reptile (Lacerta sicula campestris). Preliminary notes.

The results of experiments performed with high - K+ solutions suggest that in the lizard atrial cells Ach normally displays its negative inotropic effects by a double mechanism = an "indirect" inhibition, mediated by the increase of the membrane permeability to K+ ions; and a "direct" inhibition of the Ca- carried slow inward current. In the ventricular fibres there isn't a direct-effect of this drug, under normal conditions.

Effect of temperature on the electrical and mechanical activity of lizard ventricular myocardium.

Intracellular action potentials and isometric twitches were recorded from lizard ventricles electrically driven at 20 and 4 beats/min and submitted to temperatures changes between 10.5 and 21 degrees C. It was found that cooling induced a depolarization of the diastolic membrane potential ER, which below 15 degrees C exceeded that predictable for a diffusion potential; on the contrary, during the recovery from hypothermia ER underwent a transitory hyperpolarization. Other effects of the low temperature were a decrease of the maximum rate of depolarization, a lengthening of both the action potential duration and the time to peak contraction, an increase of the strength of contraction, in the hearts driven at 20/min it became apparent also an increase of the action potential overshoot. The hypothesis is discussed that the positive inotropic effect of low temperatures may be due not only to a slowing down of the repolarization of the action potential, but also to an increase of the slow inward current intensity.

Calcium-dependent action potentials elicited in the lizard ventricle by a prolonged hypothermic incubation.

After a prolonged hypothermic incubation (48 h at 4 degrees C), lizard ventricles perfused with a solution containing 15 mM k+ and 1 mM Ca2+ exhibit slow responses, which are similar (prescinding from their noticeable greater duration) to the responses which can be elicited, in the same depolarizing solution, by increasing the external calcium concentration or by adding catecholamines to the perfusing medium. The phenomenon is transient, and vanishes within 90 min from the end of the hypothermia.

Effect of Bitis gabonica venom on the action potentials of guinea-pig heart. Preliminary results.

The effect exerted by different doses (50 to 500 mg/kg body weight, or 1 or perfusing solution) of the lyophilised secretion of B. gabonica venom glands has been studied -by intracellular electrodes- on the electrical activity of atrial and ventricular cells from guinea-pigs hearts, by using both open-chested animals and isolated preparations. Noticeable changes in the features and duration of the repolarization phase of the action potentials precede the abolition (reversible, after washing) of the contractile activity. No significant changes of the diastolic potentials have been evidenced in the preparations perfused in vitro.

Prostacyclin inhibits the platelet-dependent effects of platelet-activating factor in the rabbit isolated heart.

In a previous study we showed that platelet-activating factor (PAF) is released in the coronary effluent early after reperfusion of ischemic, isolated rabbit heart. The amounts released were sufficient to induce intracoronary platelet activation and release of secondary mediators, suggesting a relevant contribution of this mediator to the cardiac dysfunction during reperfusion. We examined the modulatory effect of prostaglandin I2 (PGI2) on the cardiac alterations caused by infusion of PAF and autologous platelets in rabbit isolated heart. The intra-coronary infusion of PAF (10 ng-1 microgram) in the presence of autologous platelets induced marked alterations in the electrical and mechanical activities in rabbit heart, characterized by a transient positive inotropic effect (mean +/- SD = 113 +/- 6.1% of the control at 10 ng, 116 +/- 11.6% at 1 microgram), followed by a decrease in coronary flow (76 +/- 6.5 and 57 +/- 8.1%), contractile force (88 +/- 2.5 and 56 +/- 10.6%), and action potential duration (APD, 87 +/- 2.5 and 83 +/- 4.9%), and by conduction arrhythmias (75 and 100% of cases). The infusion of adenosine (1 x 10(-5) M) to increase coronary flow maximally abolished PAF and platelet-dependent reduction in coronary flow (CF) and contractile force, as well as conduction arrhythmias, but not the early transient positive inotropic effect. The alterations induced by platelets and PAF infusion were not affected by treatment of hearts with aspirin (3 x 10(-4) M), indicating that endogenous PGI2 generation did not affect the platelet-dependent response of the rabbit heart to PAF.(ABSTRACT TRUNCATED AT 250 WORDS)