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R Rubio

Publications and source records attributed to R Rubio.

At least 199 records · Page 11Linked to original sources
PubMed1976

Adenosine and active hyperemia in dog skeletal muscle.

Adenosine as a possible mediator of active hyperemia in skeletal muscle was studied in hindlimbs of dogs. Sciatic nerve stimulation decreased vascular resistance to 55 +/- 5% (mean +/- SE) of the control value in hindlimbs perfused at a constant flow rate (61 +/- 6 ml/min). Venous plasma K+ concentrations were elevated after 2 min (from 4.0 +/- 0.2 to 4.8 +/- 0.2 meq/liter; P is less than 0.005) and 20 min (4.7 +/- 0.2 meq/liter; P is less than 0.001) of contraction, but the arteriovenous difference in plasma osmolality was changed only after 2 min of contraction (from -3.0 +/- 0.6 to -7.2 +/- 0.8 mosmol/kg H2O; P is less than 0.001). The muscle adenosine contents were not significantly elevated after 5 min of contraction, but were increased after 10 min (from 1.97 +/- 0.33 to 8.35 +/- 0.97 nmol/g; P is less than 0.05) and 25 min (from 1.64 +/- 0.22 to 7.57 +/- 2.20 nmol/g; P is less than 0.05) of contraction. Thirty minutes after contraction had ceased, the adenosine contents were significantly below control values (from 2.22 +/- 0.59 to 1.51 +/- 0.40 nmol/g; P is less than 0.005). Venous plasma adenosine concentrations did not increase during muscle contraction. No relationship was found between the increase in the plasma inorganic phosphate level and the activity of the muscles. These data indicate that the adenosine content of skeletal muscle is increased by contraction, and support the concept that adenosine may be a mediator of sustained active hyperemia.

Adenosine↗
PubMed1975

Release of adenosine and lack of release of ATP from contracting skeletal muscle.

Adenosine triphosphate (ATP) has been suggested as a mediator of active hyperemia and its levels have been reported to increase in the venous plasma from contracting skeletal muscle. However, the source of the ATP is unknown. The present study indicates that a large portion of the plasma ATP is released from the formed elements of blood when the blood is collected in the presence of EDTA. When EDTA was added to blood that was previously incubated at 37 degrees C for 5 min to destroy all free ATP, the ATP level was 0.57 plus or minus 0.12 (plus or minus S.E.) nmoles/ml. However, it was possible to detect exogenously added ATP only when blood samples were collected into EDTA; collection into saline or citrate afforded no protection against ATP degradation by the ATPases of the blood. In dog hindlimb preparations perfused at constant flow or constant pressure, the venous plasma ATP of blood collected in the presence of EDTA exhibited no consistent increase during or following tetanic contraction of the muscles. In isolated, perfused rat hindlimbs, no ATP was detectable in the venous effluents from resting or contracting muscles (ATP smaller than 0.08 nmoles/ml). However, the levels of adenosine in the venous effluents were greater in contracting than in resting hindlimbs. The data indicate that it is not possible to make valid determinations of plasma ATP levels and thus, one cannot determine the role of ATP in active hyperemia based on these data. However, the currently available data from isolated muscle preparations do not support the concept that ATP is released from contracting skeletal muscle, and therefore, it is unlikely that ATP is a mediator of the metabolically-linked local regulation of skeletal muscle blood flow. The enhanced release of adenosine from contracting rat hindlimb muscles may indicate a role for this nucleoside in the regulation of blood flow in skeletal muscle.

Adenosine↗
PubMed1975

Uptake of adenosine by dispersed chich embryonic cardiac cells.

Adenosine is involved in the regulation of coronary blood flow, but its mechanism of action is not clear. The present investigation is an attempt to understand the mechanism(s) of uptake of adenosine in dispersed chick embryonic cardiac cells and its relationship to the adenosine hypothesis. Adenosine is readily taken up by these cardiac cells, and a small fraction is incorporated into adenine nucleotides, whereas a major fraction is deaminated to inosine. The mechanism of uptake is different in 12- to 15-day-old chick embryos compared to 16- to 22-day-old embryos. The younger embryo heart cells show the incorporation of adenosine into adenine mononucleotides of the incubation medium as well as all the adenine nucleotides of the cells, whereas the older embryo heart cells show incorporation of adenosine only into the adenine nucleotides of the cells. The isolated cells used in the present study do not leak any significant amounts of adenosine kinase and/or nucleotides, and free adenosine was not found in the cells, even with extracellular concentrations as high as 1 mM. The absence of free adenosine in isolated dispersed cells reflects the activities of adenosine kinase and adenosine deaminase and is compatible with the adenosine hypothesis for the regulation of coronary blood flow.

Adenosine↗
PubMed1975

Adenosine metabolism in cultured chick-embryo heart cells.

Adenosine, a coronary vasodilator, in involved in the regulation of coronary blood flow, but the mechanism (s) of vasodilation especially with respect to the influence of dipyridamole and aminophylline are not clearly understood. Cultured cardiac cells of 16-day-old chick embryos were used as a model for the mammalian heart. Hypoxia produced a twofold increase in the production of adenosine and its metabolic products in this preparation, indicating that the source of adenosine in the hypoxic heart is the myocardial cell. Neither dipyridamole (1 times 10-minus 6M) nor aminophylline (1 times 10-minus 5M) blocked the release of adenosine from the myocardial cells, but dipyridamole aminophylline was without effect. These data suggest that dipyridamole exerts its vasodilator effect by blocking the uptake of adenosine into the cells, thereby increasing its extracellular levels and the concentration of adenosine in the vicinity of coronary resistance vessels. The mechanism whereby aminophylline attenuates the vasodilation produced by adenosine is not known. However, aminophylline does not interfere with the release or uptake of adenosine.

Adenosine↗
PubMed1975

Relationship between adenosine concentration and oxygen supply in rat brain.

Since adenosine is present in normal brain tissue and cerebrosipinal fluid and since it dilates the pial vessels, it is possible that adenosine, in addition to H-+, is also a mediator of the metabolic regulation of cerebral blood flow. Evidence supporting this hypothesis was obtained under various experimental conditions characterized by achange in brain oxygen supply. The brain was frozen in situ by means of a small bonerongeur precooled in liquid N2 and the tissue was processed for adenosine determination (nmol/g of tissue). Electrical stimulation of the cortex at 0, 15, 30, and 45 Hz yielded adenosine levels of 5.4 plus or minus 0.7, 10.5 plus or minus 1.7, 13.0 plusor minus 1.2, and 9.0 plus or minus 2.1 nmol/g. Arterial pressures of 87, 60, and 40mmHg gave adenosine levels of 7.5 plus or minus 0.76, 13 plus or minus 2.6, and 26.6plus or minus 3.3, respectively. Ventilation with 29.7, 20, 10.7, and5.5% O2 significantly increased the adenosine levels to 9.4 plus or minus 3.0, 6.4 plus or minus 1.2, 30.0 plus or minus 9.3, and 63.3 plus or minus 18.2 nmol/g, respectively. Hyperventilation significantly increased adenosine form 6.7 plus or minus 1.0 to 11.8 plus or minus 1.4 nmol/g. This increased adenosine level was reduced by additionof CO2 to the ventilating gas mixture. Lactate, the main H-+ donor, pyruvate, and cAMP changed in a fashion parallel to adenosine. However, cAMP showedonly a small increase in adenosine. These findings are in accordance with the concept that adenosine and H-+ may act synergistally to regulate cerebral blood flow and that endogenous adenosine may exert a small effect on cAMP formation.

Adenosine↗
PubMed1975

Release of adenosine by hypoxic canine lung tissue and its possible role in pulmonary circulation.

Adenosine is a possible mediator of myocardial and skeletal muscle blood flow regulation. Whether adenosine plays a similar role in modulating the pulmonary pressor response to acute alveolar hypoxia is not known. Adenosine levels (nmol/g tissue) in lung in six dogs ventilated with 95% N2, and 5% CO2 for a period of 3 min increased nearly 10-fold. Inosine and hypoxanthine, adenosine enzymatic degradation products, sustained a 10- and 7-fold increase, respectively. These degradative products are mainly formed in the capillary endothelial cells that contain the degradative enzyme nucleoside phosphorylase as demonstrated by histochemical techniques. To determine the effect of ATP, ADP, AMP, and adenosine on the pulmonary circulation, the in situ left lower lobe of 10 dogs was perfused at either free flow or constant flow via its pulmonary artery. ATP and ADP increased lobar vascular resistance; AMP and adenosine decreased the resistance. During hypoxic ventilation, adenosine infusions (100 nmol/ml blood) entirely abolished the increase in vascular resistance that was due solely to hypoxia. Dipyridamole produced similar responses. These data indicate that adenosine is a pulmonary vasodilator and that it may modulate the pulmonary pressor response to acute alveolar hypoxia. The findings suggest that the use of adenosine or dipyridamole may be beneficial in patients with pathologic elevations of the pulmonary vascular resistance which are a result of an exaggerated pulmonary pressor response to hypoxia, as seen in high-altitude pulmonary edema or that following cerebral injury.

Adenosine↗