PubMed Health⌕ Search

Biomedical subjects

R Rubio

Publications and source records attributed to R Rubio.

At least 181 records · Page 10Linked to original sources
PubMed1979

Transmural distribution of myocardial adenosine content during coronary constriction.

The transmural distribution of tissue adenosine content was determined in samples of the left ventricle of anesthetized open-chest dogs. Transmural tissue samples were obtained and quickly freeze-clamped during either normal coronary perfusion or partial constriction of the inflow tubing to the left common coronary artery. Inner, middle, and outer segments of the samples were assayed for adenosine, inosine, ATP, creatine phosphate, and lactate. In control experiments, there were no significant differences among the tissue contents of the substances in the three segments. However, during a 50.2 +/- 4.7% reduction of coronary inflow, adenosine content of inner, middle, and outer segments was 0.41 +/- 0.007, 0.030 +/- 0.006, and 0.016 +/- 0.003 nmol/mg protein, respectively. Outer segment content was significantly less than either middle or inner content. Lactate distribution was similar to that of adenosine, whereas ATP and creatine phosphate were lowest in the inner segment. Increases of the inner/outer adenosine ratio occurred when the coronary-ventricular pressure index was lower than 1.2. Thus, selective underperfusion of the subendocardium during reduced coronary inflow can result in greater accumulation of adenosine in that region.

Adenosine↗
PubMed1979

Brain adenosine production in the rat during 60 seconds of ischemia.

In rats, cerebral perfusion pressure were altered abruptly by aortic transection to determine the production by ischemic brain of adenosine and its metabolites, inosine and hypoxanthine. Brain samples were obtained after 0, 5, 10, 15, 30, and 60 seconds of ischemia. Also measured were ATP, ADP, AMP, phosphocreatine (PCr), lactate, and pyruvate. Blood pressure was monitored continuously, and arterial PO2, PCO2, and pH were measured just prior to induction of ischemia. Adenosine was elevated t 2.30 +/- 0.31 (SE) nmol/g at 5 seconds from a control value of 0.96 +/- 0.07. A significant elevation of adenosine continued to 60 seconds (5.50 +/- 1.24). Furthermore, inosine showed a progressive upward trend during the entire 60 seconds of ischemia, whereas no change in hypoxanthine occurred between the moment of transection (31.81 +/- 2.01 nmol/g) and 60 seconds of ischemia (34.72 +/- 2.93). PCr decreased by 1.24 mumol/g within the first 5 seconds. After the onset of hypotension, significant changes did not occur in AMP and ADP until 30 seconds, and in ATP and pyruvate until 60 seconds after aortic transection; lactate was elevated by 10 seconds. The rapid rise of cerebral adenosine within 5 seconds after the onset of ischemia supports a role for adenosine in the regulation of cerebral blood flow.

Adenosine↗
PubMed1978

Production, metabolism and possible functions of adenosine in brain tissue in situ.

Adenosine and H+ may act synergistically to regulate cerebral blood flow because adenosine production is enhanced under various experimental conditions associated with an imbalance between oxygen supply and oxygen need. Direct application of adenosine dilates the pial vessels, but changes in cerebral vascular resistance are not observed when adenosine is infused intraarterially. This is because adenosine does not readily cross the blood-brain barrier. The studies reported here show that in dogs the adenosine released into the interstitium is partly reincorporated into adenine nucleotides via an adenosine kinase (EC 2.7.1.20) reaction (salvage pathway) and partly degraded to inosine and hypoxanthine. However, in contrast to other tissues, the accumulation of iosine and hypoxanthine in brain tissue proceeds at a rate slower than that of adenosine because one of the degradative enzymes, namely purine-nucleoside phosphorylase (EC 2.4.2.1) is located only in the vessel wall, which is not readily permeable to adenosine. Thus, the slow access of adenosine to its degradative enzymes delays the appearance of its products, inosine and hypoxanthine.

Adenine Nucleotides↗
PubMed1978

Adenosine production in the ischemic kidney.

We conducted experiments to determine (1) tissue, blood, and urine levels of adenosine produced by the ischemic kidney under conditions of renal artery occlusion, and (2) the site(s) of production and release of adenosine by the kidney. Concentrations of adenosine, inosine, and hypoxanthine in the dog urine were found to increase after 2 minutes of renal artery occlusion as were concentrations of these metabolites in renal tissue after 10 minutes of renal artery occlusion. Renal venous plasma levels of inosine and hypoxanthine also were elevated after 3 minutes of arterial occlusion. In modified stop-flow experiments, adenosine appeared in the urine in a peak that corresponded most closely with proximal tubule fluid. 5'-Nucleotidase, the enzyme which catalyzes the dephosphorylation of 5'-AMP or 5'-IMP to adenosine or inosine, respectively, was found to be located primarily on the external membranes and mitochondria of proximal tubule cells, but not in distal tubule or collecting duct cells. Since adenosine has been demonstrated to elicit renal vasoconstriction and is produced by the ischemic kidney, it is suggested that adenosine may be involved in the mediation of postocclusion renal ischemia.

Adenosine↗
PubMed1977

Formation of adenosine nucleotide derivatives in isolated hog carotid artery strips.

Media strips of hog carotid artery formed hypoxanthine and inosine during incubation under conditions of normoxia (95% O2, 5% CO2). During anoxia (95% N2, 5% CO2), hypoxanthine increased fivefold and inosine twofold. Stimulation with 124 mM K+ resulted in a twofold increase in hypoxanthine and a threefold increase in inosine. Concurrent with the increase in the concentrations of purine derivatives was a decrease in tissue ATP. Although significant amounts of adenosine were not detected in the medium of incubating artery strips, the following evidence suggests adenosine was formed and rapidly deaminated to inosine: 1) Exogenous adenosine added to the medium of incubating strips was rapidly deaminated to inosine. 2) Exogenous 5'-AMP concentration decreased, whereas adenosine and, subsequently, inosine levels increased during incubation of artery strips. The reaction was specific for 5'-AMP and the data suggest that AMP is dephosphorylated to adenosine. 3) The specific activity of exogenous [U-14C]adenosine added to the medium of incubated strips decreased after 15 min. It is concluded that adenosine is formed in isolated artery strips but is rapidly deaminated to inosine.

Adenosine↗
PubMed1976

Adenosine relaxation of isolated vascular smooth muscle.

Adenosine relaxed hog carotid media strips contracted with norepinephrine (NE) and potassium (K+). Adenosine (3 X 10(-6)M) was more effective in relaxing the NE contractures than those produced by K+. In both cases, adenosine's efficacy decreased with increasing concentrations of the stimulating agent. A high adenosine concentration (1 X 10(-3)M) was necessary to elicit relaxation of completely depolarized (124 mM K+) media strips and equimolar concentrations of aminophylline caused greater relaxation than did adenosine. Adenosine inhibited the Ca2+ dose-response curves of strips stimulated with 20 mM and 30 mM K+ and its effect was dependent on the Ca2+ concentration. Neither 1 X 10(-6)M nor 1 X 10(-4)M adenosine produced any change in the cAMP content of vascular strips. Only at high concentrations did adenosine increase the cAMP content of vascular strips, but the increase was signficantly more than that observed with the same dose of aminophylline. The present results are consistent with the possibility that adenosine relaxes vascular smooth muscle by directly altering Ca2+ permeability and/or membrane potential; they do not support a role for cAMP in the adenosine-induced relaxation of vascular smooth muscle.

Adenosine↗