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Biomedical subjects

F L Belloni

Publications and source records attributed to F L Belloni.

30 records · Page 2Linked to original sources
PubMed1985

Absence of a role for superoxide anion, hydrogen peroxide and hydroxyl radical in endothelium-mediated relaxation of rabbit aorta.

We tested the hypothesis that the endothelium-dependent relaxation of rabbit thoracic aorta in vitro is mediated by reduced metabolites of oxygen. Helical vascular strips were contracted with either norepinephrine or phenylephrine. Oxygen metabolites, generated by the xanthine oxidase reaction, completely relaxed norepinephrine-induced contractile tone but not tone induced by phenylephrine. A mixture of oxygen metabolite scavengers (superoxide dismutase, catalase and mannitol) eliminated the relaxation induced by the xanthine oxidase products. Acetylcholine caused a dose-dependent and endothelium-dependent relaxation of the strips; this was not inhibited by the presence of the scavengers. We conclude that reduced oxygen metabolites have little direct effect on rabbit aortic smooth muscle in vitro, although they indirectly but specifically relax norepinephrine-induced tone, presumably by oxidation of norepinephrine. Oxygen metabolites do not appear to mediate the endothelium-dependent relaxation response of this tissue to acetylcholine.

Acetylcholine↗
PubMed1984

Intracellular adenosine in isolated rat liver cells.

Our objective was to determine whether a non-extracellular pool of adenosine exists in mammalian cells. Rat liver cells were dispersed by a collagenase perfusion technique and suspended in buffered salt solution. The adenosine content of these suspensions rose during hypoxia. Exogenous adenosine deaminase prevented or reversed the hypoxic increment but failed to reduce suspension adenosine levels to zero. This residual adenosine pool (average size = 85 +/- 10 pmol/mg protein) was not located in the extracellular medium, on surface adenosine receptors or in solution in the cytoplasm. A likely locus is the adenine-analog binding protein which has been described for liver and other tissues. Thus, our study supports the existence of an intracellular adenosine pool in isolated rat liver cells which is a large fraction of the total tissue adenosine. This situation may exist in other cell types as well, based on the ubiquity of the adenosine binding protein. Tissue adenosine content may not, therefore, accurately reflect interstitial adenosine concentration; thus, such measurements must be interpreted cautiously. It is not clear what, if any, functional role this putative, intracellular, bound adenosine pool plays in local vasoregulation.

Adenosine↗
PubMed1980

Atrioventricular conduction disturbances during hypoxia. Possible role of adenosine in rabbit and guinea pig heart.

Adenosine and related compounds can produce atrioventricular (A-V) conduction block. Similar conduction disturbances are observed in myocardial hypoxia. To investigate the possibility that adenosine might be causally involved in hypoxic conduction disturbances, we measured A-V conduction times, subdivided into atrial-to-His bundle (A-H) and His bundle-to-ventricular (H-V) intervals, with extracellular electrodes in isolated rabbit and guinea pig hearts perfused with modified Krebs-Henseleit solution. Adenosine produced dose-dependent prolongation of A-V conduction time in both species, although guinea pig hearts responded to lower doses (10(-7) M) and showed a steeper dose-response relationship than rabbit hearts. Higher adenosine doses produced second-degree heart block in both species. Conduction delay was confined to the A-H interval, implicating action on A-V node cells. Further investigation of guinea pig hearts revealed a specific antagonism towards adenosine's effects by 10(-5) M aminophylline. Conduction disturbances produced by acetylcholine or MnCl2 were unaffected by aminophylline as were adenosine's effects by atropine. Perfusion with hypoxic perfusate caused A-V conduction delays and second-degree block in guinea pigs hearts. This effect was dramatically attenuated by aminophylline. We conclude that endogenously released adenosine may cause at least some of the A-V conduction disturbances associated with acute myocardial hypoxia. Furthermore, methylxanthines may prove to be of therapeutic value in combatting such disturbances in a clinical setting.

Adenosine↗
PubMed1979

The role of adenosine in prolonged vasodilation following flow-restricted exercise of canine skeletal muscle.

A period of prolonged vasodilation follows flow-restricted exercise of skeletal muscle. We tested the hypothesis that adenosine participates in mediating this vascular response. Vascularly isolated, anterior calf muscles of anesthetized dogs were stimulated to contract at a rate of 4 twitches/sec. Blood flow was held constant at 12.5 +/- 1.3 ml/min per 100 g which was about 14% of the expected free flow for this exercise level. Skeletal muscle tissue adenosine was measured with the an enzymatic, spectophotometric assay of trichloroacetic acid extracts of congruent to 50 mg biopsy samples. Tissue adenosine rose from 2.30 +/- 0.90 nmol/g in resting muscle to 22.5 +/- 5.8 nmol/g by the end of the 22-minute exercise. Following exercise, tissue adenosine fell toward its baseline value with a time course very similar to the early portion of the return of skeletal muscle vascular resistance to its control level. Thus, skeletal muscle adenosine content (1) increases to a sufficient magnitude and (2) falls with an appropriate time course to be at least partly responsible for the early portion of prolonged vasodilation seen after flow-restricted exercise of skeletal muscle.

Adenosine↗
PubMed1979

The role of potassium in the metabolic control of coronary vascular resistance of the dog.

We tested the hypothesis that potassium ion (K+) is involved in the local control of the coronary circulation. The left coronary artery was perfused at constant flow in closed-chest, anesthetized dogs. Step increases in heart rate caused transient (six dogs) or sustained (three dogs) increases in coronary sinus plasma [K+] averaging 0.53 mEq/liter. When the effects of vascular transit delay were accounted for, we found that [K+] changes preceded the vasodilation seen with increased heart rate. We used a mathematical model to calculate changes in interstitial [K+] from arterial and venous [K+] and K+ release rate. The magnitude of the changes in interstitial [K+] appeared to be sufficient to account for a considerable portion but not all of the initial changes in coronary vascular resistance associated with increased heart rate. Thus potassium seems to be involved at least transiently, and, in three of nine dogs, for a more sustained period, in heart rate-induced coronary vasodilation. Cessations (for 15 seconds) of coronary blood flow resulted in transient postischemic increases of coronary sinus [K+] averaging 0.55 mEq/liter. In this case, correction for vascular transit disclosed that the recovery of [K+] preceded the return of vascular tone to baseline for only the second half of the recovery, implying only a limited role for potassium in this response. Potassium appears to play a significant but transient role in the local control of the coronary circulation.

Animals↗
PubMed1978

Coronary vascular resistance and myocardial oxygen consumption dynamics in response to catecholamine infusion.

These experiments were performed in order to ascertain whether activation of coronary vascular adrenergic receptors could change the time course of the coronary vasodilatation accompanying increases in myocardial metabolic activity. The left common coronary arteries of dog hearts were perfused in situ with blood at constant flow. Coronary perfusion pressure and coronary sinus blood 02 content were continuously monitored. Norepinephrine was infused into the coronary artery at 0.5 to 5 microgram.min-1. and isoprenaline at 0.5 to 2 microgram.min-1. The amplitude of the vascular resistance change was less with norepinephrine than with isoprenaline infusion for a similar change in oxygen consumption. The time course of coronary vascular resistance, after correction for the effects of vascular transit, lagged significantly behind the time course of coronary sinus 02 content in the case of norepinephrine infusion. On the average, no lag was observed with isoprenaline infusion. It is concluded that stimulation of coronary vascular adrenergic receptors can alter the time course and the magnitude of the coronary vascular response to increases in myocardial metabolic activity resulting from myocardial beta-receptor stimulation.

Animals↗
PubMed1978

Effect of indomethacin on coronary vascular response to increased myocardial oxygen consumption.

We tested the hypothesis that arachidonic acid metabolites mediate the coronary vascular response to changes in cardiac activity. Isoproterenol was administered intravenously to five chloralose-anesthetized, open-chest dogs. Left anterior descending coronary artery blood flow, systemic arterial blood pressure, and great cardiac vein O2 content were continuously measured, and blood gas determination (including O2 content) were made before and after infusions. From these data, coronary vascular conductance, coronary O2 delivery, and myocardial O2 consumption were calculated. Isoproterenol increased conductance, O2 delivery, and O2 consumption. Indomethacin, a blocker of prostaglandin synthesis, was administered, and the isoproterenol infusions were repeated. The changes in conductance, O2 delivery, and O2 consumption associated with isoproterenol were not different after indomethacin was administered than before indomethacin was administered. Neither were the relations between conductance or O2 delivery and O2 consumption affected by indomethacin. We conclude that, in this preparation and with this stimulus, prostaglandins do not appear to mediate or modulate the coronary vascular response to changes in cardiac activity.

Animals↗
PubMed1977

Dynamics of myocardial oxygen consumption and coronary vascular resistance.

Coronary vascular resistance may be regulated in part by substances whose concentrations are determined by or reflect the rate of myocardial oxygen consumption (e.g., adenosine, vessel wall PO2). We tested this hypothesis by comparing the time course of changes in myocardial oxygen consumption and coronary vascular resistance following 20 beat/min changes in heart rate. Main left coronary arteries of in situ dog hearts were perfused with blood at constant flow. Coronary sinus O2 content was monitored continuously with a densitometer and reflected the time course of changes in oxygen consumption and also the effects of vascular transit between tissue and the coronary sinus. These transit effects were estimated from dye transit curves and added to the time course of changes in coronary perfusion pressure which was proportional to coronary vascular resistance at constant flow. Coronary sinus O2 content changes preceded the adjusted time course of vascular resistance. This supports the hypothesis that coronary vascular resistance is regulated in part by factors closely linked to oxidative metabolism.

Animals↗
PubMed1975

Simultaneous counting of 85Kr in lung and myocardium during measurement of coronary blood flow.

Coronary blood flow rate (ml-min-1-100 g-1) was estimated by a) measuring pump flow into the cannulated circumflex branch of the left coronary artery and dividing by the weight of perfused myocardium and b) measuring the clearance of 85Kr following intra-arterial injection (detection with a 2-in. crystal with cylindrical collimation). Although the correlation between the two measurements was relatively high (r equals 0.90), the line best fitting the data was 85Kr flow equals 0.55 pump flow + 25.6. We tested the possibility that the discrepancy between the two methods was primarily due to the counting of 85Kr removed from myocardium and delivered to lung. Relative efficiency of lung counting versus myocardial counting was determined as well as clearance pattern of 85Kr from lung in each dog. A simple mathematical model which assumes no recirculation of 85Kr to heart allowed correction of coronary clearance curves using this information. When corrected 85Kr flow equals 1.00 pump flow + 4.1 (r equals 0.90). Thus, the major systematic cause for the discrepancy between the two measurements under the conditions of this experiment appears to be simultaneous counting of 85Kr in lung and in myocardium.

Adenosine↗