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Biomedical subjects

R Rubio

Publications and source records attributed to R Rubio.

At least 145 records · Page 8Linked to original sources
PubMed1986

Uptake and release of adenosine by cultured rat aortic smooth muscle.

We wanted to determine whether CO2, H+ and K+ affect the adenosine metabolism of vascular smooth muscle in a way that could account for the effects of these substances on vascular reactivity and their ability to modulate adenosine-induced vascular relaxation. Accordingly, 1-week-old cultures of rat aortic smooth muscle were incubated in phosphate-buffered saline with various [K+]'s and pH's and aerated in an incubation chamber with gases containing various proportions of CO2. Uptake was measured as 14C incorporation into cellular constituents during exposure to 2 microM [14C]adenosine. Release was measured as net extracellular adenosine accumulation. Uptake of adenosine was not significantly affected by any of the experimental maneuvers, except that it was greatly attenuated by dipyridamole (10(-5) and 10(-4) M) and transiently enhanced by the low CO2 levels. Adenosine release, however, was depressed by lowering atmospheric CO2 (0% vs 5%) and also by normocapnic acidosis (pH 6.8 vs pH 7.4). We conclude that vascular smooth muscle in culture releases adenosine at a rate that might have vasoactive significance in vivo. Furthermore, some of the vascular actions of CO2 and H+, but not those of K+, may be partially explained by their effects on vascular smooth muscle's adenosine metabolism.

Adenosine↗
PubMed1986

Increases in cerebral interstitial fluid adenosine concentration during hypoxia, local potassium infusion, and ischemia.

This study used the brain dialysis technique to test the hypothesis that the adenosine concentration of cerebral interstitial fluid increases during situations in which cerebral oxygen supply is inadequate for oxygen demand. Sealed 300-micron hollow dialysis fibers were implanted in the caudate nucleus of pentobarbital-anesthetized rats and perfused at 2 microliter/min with artificial cerebrospinal fluid. In vitro tests indicated the recovery of adenosine, inosine, and hypoxanthine from the external medium to be approximately 20% at 2 microliter/min and close to 100% at 0.1 microliter/min. Three in vivo interventions were tested: hypoxia/hypotension (PaO2 = 41.9 mm Hg; MABP = 42.8 mm Hg; n = 9), local potassium infusion (n = 4), and cerebral anoxia/ischemia (n = 10). These interventions produced 10-, 4-, and 30-fold increases in perfusate adenosine concentration, respectively, as well as increases in perfusate concentrations of inosine and hypoxanthine. A separate group of rats (n = 9) perfused at 0.1 microliter/min yielded estimates of cerebral interstitial fluid adenosine, inosine, and hypoxanthine concentrations of 1.26, 3.30, and 7.19 microM, respectively. These results are consistent with the adenosine hypothesis for the regulation of CBF.

Adenosine↗
PubMed1986

Control of rectal gland secretion in the dogfish (Squalus acanthias): steps in the sequence of activation.

We measured the venous and arterial pressure, as well as the rate of secretion and content of cyclic AMP and high energy phosphate compounds, of the rectal gland of the anaesthetized dogfish, Squalus acanthias (L.). Intravenous infusion of isotonic solutions produced a very large increase in the rate of secretion by the rectal gland. The increase in secretion was preceded by an increase in venous blood pressure, but arterial blood pressure was not modified. Injections of small doses of veratridine stimulated gland secretion when given in the vicinity of the heart but not when given in the dorsal aorta. During volume expansion the creatine phosphate and ATP content of the gland were markedly reduced, while ADP and AMP as well as cyclic AMP content were increased. We conclude that: volume expansion leads to the release of a message that activates adenyl cyclase in the gland; the increased venous pressure may be the initial signal in the sequence that leads to the release of the activating messenger; there is a receptor mechanism in the atrial and cardiac region that triggers the sequence that activates glandular secretion; the reduction in the content of high energy phosphate compounds during volume expansion is caused by an increase in energy expenditure, probably due to gland secretion.

Adenine Nucleotides↗
PubMed1985

Effect of chronic denervation on pharmacological responsiveness of coronary vessels.

We have hypothesized that the well-established regional heterogeneity of the properties of the vascular smooth muscle results from peculiarities of the microenvironment in every region. In particular, the coronary vasculature has well-established differences between large and small coronary arteries in their responsiveness to alpha and beta agonists, nitroglycerin and adenosine. To test our hypothesis, we altered the micro-environment of coronary vessels by chronic surgical sympathectomy in dogs. Our in vitro studies on vessels from normally innervated hearts confirmed previous studies and showed that in large vessels, alpha and beta epinephrine or norepinephrine responses can be demonstrated; the alpha effect is dominant and epinephrine is a more potent alpha agonist than is norepinephrine. In small vessels only a beta catecholamine effect can be demonstrated. Chronically sympathectomized blood vessels show an alpha norepinephrine effect in small vessels. Denervation caused a reduction in the sensitivity to K+-induced contraction in both large and small vessels. In large vessels the responses to nitroglycerin were not affected by denervation, whereas in small vessels the sensitivity to adenosine was reduced. These results indicate that chronic denervation alters the pharmacological responsiveness of the vasculature to various agonists indicating that vascular smooth muscle possesses the ability to respond to long-term modulatory influences arising in the immediate environment.

Adenosine↗
PubMed1985

Application of the combustion method in a closed flask to the lead determination in atmospheric aerosols.

The destruction of the filter for metal determination in atmospheric aerosols is an important step in the analysis. Nowadays the decomposition of this kind of sample has not been completely solved, so it is interesting to study new methods for filter sample attack. In the present work the application of the combustion method in a closed flask for mixed cellulose esters filter decomposition for lead determination is proposed. For this purpose optimum operating conditions as stopper flask design, sample size, flask volume, shaking time and volume and concentration of absorbing solution are established, and accuracy and precision of the proposed method using AAS for the measurements is given. The results obtained by the closed flask combustion are compared with those found by wet attack with HNO3. The method proposed is rapid, has low reagent contamination and no loss of lead by volatilization or by amalgamation occurs. This method shows an accuracy and a precision in good agreement with the standard method.

Air Pollutants, Occupational↗
PubMed1985

The role of adenosine in the regulation of coronary blood flow in newborn lambs.

Adenosine is a metabolic vasodilator of the coronary vessels in the adult. Whether it plays a similar role in the regulation of coronary blood flow (CBF) in the newborn is not known. We evaluated changes in adenosine release during periods of decreased oxygen supply (hypoxia) and increased oxygen demand (dobutamine infusions). In anesthetized open-chest lambs (age 1 to 8 days), aortic and coronary sinus adenosine concentrations, circumflex CBF, and myocardial oxygen consumption (MVO2) were measured. Adenosine was assayed by high-performance liquid chromatography, and the release of adenosine was calculated as the product of the aortic-coronary sinus plasma level difference and CBF in milliliters per minute per 100 gm myocardial tissue. Control values were obtained when the lambs were ventilated with 60% oxygen. In the first series of experiments, hypoxemia resulted in an increase in CBF from 120 +/- 5 to 171 +/- 8 ml/min/100 gm (p less than 0.01). This was associated with sixfold increase in adenosine release. In a second set of experiments the intravenous infusion of dobutamine resulted in parallel increases in MVO2 and CBF. Concomitantly, adenosine release increased by fivefold. There were significant linear relationships between MVO2 and CBF (r = 0.96; p less than 0.01), MVO2 and adenosine release (r = 0.69; p less than 0.002), and adenosine release and CBF (r = 0.71; p less than 0.002). These data support the hypothesis that adenosine may play an important role in the regulation of CBF in the newborn lamb.

Adenosine↗
PubMed1984

Calcium-dependent atrial slow action potentials generated with phosphatidic acid or phospholipase D.

Phosphatidic acid (PA) formed following phosphatidylinositol hydrolysis has been proposed as a necessary step in receptor-mediated Ca2+ flux. This study demonstrates that PA generates Ca2+-dependent slow action potentials (APs) in rat atrium partially depolarized with 22 mM K+. The slow response was not due to release of endogenous catecholamines or prostaglandin formation since propranolol and indomethacin failed to attenuate the PA-induced slow AP in normal and reserpinized rats. PA-induced slow APs demonstrated Ca2+-dependence such that increasing [Ca2+]o from 0.5 to 5.0 mM caused the amplitude of the slow AP to rise linearly with the logarithm of [Ca2+]o. Phospholipase D (PLD) but not phospholipase C, was able to induce a slow AP, possibly through PA formation. Adenosine attenuated the PA and PLD-induced slow response and aminophylline reversed these effects. The observation that PA and PLD generate Ca2+-dependent slow APs in depolarized rat atrium supports a role for PA mediating Ca2+ influx.

Action Potentials↗
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↗
PubMed1984

Effects of dipyridamole on myocardial adenosine and active hyperemia.

Dipyridamole, a vasodilator that potentiates the actions of exogenous adenosine, is known to inhibit cellular uptake of adenosine, but its effects on cellular adenosine release, and thus interstitial adenosine levels, are disputed. We used the accumulation of adenosine in pericardial infusates (PCI) as an index of interstitial adenosine concentration and observed the effects of dipyridamole on relationships among coronary blood flow (CBF), myocardial oxygen consumption (MVO2), and PCI adenosine concentrations during steady-state alterations of cardiac work. Dipyridamole increased CBF and PCI adenosine concentration without altering MVO2. The relationship between PCI adenosine and CBF was unaltered, supporting a cause and effect relationship between interstitial adenosine concentration and CBF. In addition, we determined that unlike previous studies in isolated perfused hearts the washout of adenosine by coronary plasma was unaffected by dipyridamole. The results support previous suggestions that, whereas dipyridamole inhibits adenosine uptake, it does not alter cellular adenosine release, and therefore interstitial adenosine levels are increased. The constant relationship between PCI adenosine and CBF supports hypotheses that attribute the hyperemias associated with increased cardiac work or with dipyridamole to increased interstitial adenosine.

Adenosine↗
PubMed1984

Pharmacological differentiation between large and small coronary vessels.

It has been reported that there are striking differences between large and small coronary arteries in their responsiveness to adenosine, nitroglycerin and catecholamines. The differential pharmacological responsiveness indicates differences in their excitation-contraction coupling mechanisms. Therefore, agents such as lyotropic anions (SCN-, NO3-, CH3SO4-) known to modulate these processes, and which by themselves do not have an inotropic effect, would be expected to differentially modulate the action of these substances on large and small coronary vessels. To test this hypothesis we studied the modulation by lyotropic anions of the effects of adenosine, nitroglycerin and verapamil on large and small intramural (0.5-0.6 mm diameter) dog coronary arteries. We have confirmed that small vessels are more sensitive to adenosine and verapamil and less sensitive to nitroglycerin than are large vessels. Replacement of Cl- by the lyotropic anions diminished the relaxing effects of adenosine in small vessels with the following order of potency, SCN- greater than NO3- greater than CH3SO4- greater than Cl-. NO3-. Replacement of Cl- resulted in almost total blockade of the adenosine response in small coronary arteries, whereas in large coronary vessels, the effects of nitroglycerin were reduced only 30%. The effects of verapamil in small vessels were slightly depressed whereas in large vessels its effects were unchanged. Our results further confirm that there are marked differences between the pharmacological responsiveness of large and small coronary vessels, indicating that these differences reside in the nature of their mechanisms controlling Ca++ translocation.

Adenosine↗
PubMed1983

Measurements of coronary plasma and pericardial infusate adenosine concentrations during exercise in conscious dog: relationship to myocardial oxygen consumption and coronary blood flow.

A conscious dog model was employed to evaluate the relationship among myocardial oxygen consumption (MVO2), myocardial adenosine release and coronary blood flow (CNF) during graded treadmill exercise. Two methods were utilized simultaneously as indexes of changes in interstitial adenosine concentrations, (1) a pericardial infusate technique and (2) to measurement of arterial-coronary sinus plasma adenosine concentration differences. Graded exercise was associated with graded increases in MVO2, CBF, pericardial infusate adenosine concentration (PI Ado) and adenosine washout in coronary plasma. Regression analysis demonstrated significant linear relationships for MVO2 v. CBF (r = 0.78, P less than 0.01), MVO2 v. PI Ado (r = 0.52, P less than 0.01), and PI Ado v. CBF (r = 0.76, P less than 0.01). Coronary plasma adenosine arterio-sinus differences, sinus plasma concentrations, and net washout of adenosine also increased with graded exercise, however, a significant inter-animal variance was noted. These data suggest that the plasma adenosine assay is capable of detecting directional (qualitative) changes associated with changes in cardiac metabolism, however, it may not be reliable as a quantitative indicator of interstitial adenosine concentrations due to multiple factors which may influence the plasma adenosine pool. The pericardial infusate technique, which presumably represents a model of diffusion, is relatively invariant by comparison. The results demonstrate a significant correlation among MVO2, PI Ado and CBF, and thereby provide support to the hypothesis that adenosine is a major factor in the coupling of myocardial oxygen demand to oxygen supply under physiological conditions.

Adenosine↗
PubMed1983

Prothrombin Habana: a new dysfunctional molecule of human prothrombin associated with a true prothrombin deficiency.

A Cuban family with a new congenital dysprothrombinaemia is described. The propositus was a 5-year-old female who presented with umbilical bleeding after birth followed by easy bruising and bleeding tendency throughout her life. The main laboratory features of the defect included prolongation of prothrombin time and partial thromboplastin time. Prothrombin activity was less than 10% in several one- and two-stage systems. However, the staphylocoagulase-complexed prothrombin level and immunologic methods yielded levels of about 50%. The migration of the abnormal prothrombin was more anodic in single and bidimensional immunoelectrophoresis system and did not change by the addition of calcium. Family studies revealed that the father had approximately 50% prothrombin activity and antigen, whereas the mother had 45% prothrombin activity but about 100% prothrombin antigen. We suggest that the propositus is heterozygous for an abnormal prothrombin and heterozygous for true prothrombin deficiency.

Child, Preschool↗
PubMed1983

Potentiation of slow action potentials with theophylline or "micro" adenosine deaminase.

The effects of endogenous adenosine on rat atrial and ventricular slow action potentials (AP) were studied using theophylline, an adenosine receptor antagonist, or "micro" adenosine deaminase (mADA), small polypeptides having adenosine deaminase activity. Exogenous adenosine (10(-6) M) depressed slow APs at low and high isoproterenol concentrations and shifted the isoproterenol dose-response curve to the right in the atrium. In the ventricle, exogenous adenosine inhibited slow APs at low isoproterenol doses and only shifted the bottom of the dose-response relationship to the right. mADA (0.84 U) or theophylline (5 X 10(-5) M) potentiated the response to threshold concentrations of isoproterenol and caused a parallel shift of the curve to the left in the atrium but only shifted the bottom portion of the curve in the ventricle. This potentiation of slow APs in the presence of mADA or theophylline suggests that endogenous adenosine attenuates the response to isoproterenol in cardiac muscle.

Action Potentials↗
PubMed1983

Consistent parallel relationships among myocardial oxygen consumption, coronary blood flow, and pericardial infusate adenosine concentration with various interventions and beta-blockade in the dog.

Coronary blood flow responds uniquely to changes in myocardial demand, regardless of the stimulus. If adenosine mediates this response, interstitial fluid adenosine concentration should also change in parallel with myocardial oxygen consumption and coronary blood flow during alterations of cardiac work. We tested this hypothesis by measuring coronary blood flow, myocardial oxygen consumption, and the concentration of adenosine in pericardial infusates, an index of interstitial fluid adenosine concentration, during six experimental conditions and control states in anesthetized, open-chest dogs. Significant alterations of myocardial oxygen consumption and coronary blood flow during aortic constriction, vagal stimulation, atrial pacing, or intravenous infusion of calcium chloride, norepinephrine, or isoproterenol were accompanied by significant alterations in pericardial infusate adenosine concentration. Significant linear relationships were determined among myocardial oxygen consumption, coronary blood flow, and pericardial infusate adenosine concentration for each of the experimental stimuli and their paired control values. There were no significant differences among the six different conditions for any of these relationships. In addition, these relationships were not altered by beta-blockade in five dogs subjected to aortic constriction and calcium infusion. Although beta-blockade may alter the effects of a stimulus, myocardial oxygen consumption, coronary blood flow, and adenosine all are affected proportionately. The results suggest that adenosine production responds to alterations of myocardial oxygen consumption independently of the stimulus which produces the change in oxygen demand, and the resultant change in interstitial fluid adenosine concentration may initiate the change in coronary blood flow to maintain the balance between oxygen supply and demand.

Adenosine↗
PubMed1983

Adenosine in the local regulation of blood flow: a brief overview.

Based on data from a variety of experiments from several laboratories, adenosine appears to play an important role in the adjustment of blood flow to the metabolic requirements of the tissue. This has been shown to be true for heart, brain, and skeletal muscle in several different species. A reduction in oxygen supply or an increase in oxygen demand results in vasodilation and adenosine release. However, adenosine is also coupled to blood flow increments with enhanced metabolic activity and in the presence of an adequate oxygen supply. To what extent other vasoactive agents participate with adenosine in producing vasodilation under a variety of conditions is not known.

Acetylcholine↗