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J Pesquero

Publications and source records attributed to J Pesquero.

12 recordsLinked to original sources
PubMed2001

CO2 in static mesenteric venous blood during intestinal ischemia and ischemic preconditioning in rats.

During intestinal ischemia, CO2 accumulates in tissue as a result of bicarbonate buffering of anaerobic acid generation. Previous studies have shown that nitric oxide (NO) generated during ischemic preconditioning acts as a glycolytic modulator, thus decreasing tissue lactate production. We studied if ischemic preconditioning induces NO-dependent changes in static mesenteric venous blood Pco2 values and CO2 accumulation during intestinal ischemia. Superior mesenteric venous (smv) acid base variables were studied in 4 groups of rats: a control group (C), an ischemic (90-min period of flow arrest) group (I), an ischemic group subjected to previous ischemic preconditioning (P), and an ischemic group subjected to previous ischemic preconditioning in which nitric oxide synthase (NOS) was inhibited by N-nitro-L-arginine methyl ester (L-NAME) administration (P+N). Preconditioning induced acidosis in smv blood during reperfusion before ischemia, but this effect was counteracted by L-NAME. Group P showed the lowest values of end-ischemic tissue lactate, smv blood CO2 accumulation, and LDH in perfusate, whereas group P+N showed the highest level of LDH in perfusate but the lowest end-ischemic smv blood Pco2 and acidity. We conclude that lower ischemic CO2 accumulation in static smv blood, but not lower end-ischemic Pco2, was related with the protective effect of ischemic preconditioning in our rat model. Thus, the use of stagnant smv blood Pco2 as an indicative of intestinal dysoxia can lead to misinterpretations if a broader acid-base picture is not considered.

Anaerobiosis↗
PubMed2000

Acid-base analysis during experimental anemia in rats.

The present study evaluated the acid-base status of anemic rats by using two approaches of acid-base analysis: one based on the base excess (BE) calculation and the other based on Stewart's physicochemical analysis. Two sets of experimental data, derived from two different methods of inducing anemia, were used: repetitive doses of phenylhydrazine (PHZ) and bleeding (BL). A significant uncompensated respiratory alkalosis was found in both groups of anemic rats. BE increased slightly, whereas strong ion difference ([SID]) and weak acid buffers ([A(TOT)]) remained unchanged in anemic rats. The reasons for the absence of compensation for hypocapnia and the differences in the behaviour of acid-base variables are discussed. BE increase was considered paradoxical; its calculation was affected by the experimental conditions and BE had little physiological relevance during anemia. The absence of metabolic renal compensation in anemic rats could be due to a lower pH in the kidney due to anemic hypoxia. Finally, the changes in buffer strength related to low Hb and low P(CO2) might influence plasma [SID] through counteracted shifts of strong ions between erythrocytes and plasma, finally resulting in unchanged [SID] during anemia.

Acid-Base Imbalance↗
PubMed1999

Modification of glyceraldehyde-3-phosphate dehydrogenase in response to nitric oxide in intestinal preconditioning.

BACKGROUND: Previous studies have demonstrated that intestinal preconditioning is triggered by an initial increase in nitric oxide synthesis. This confers resistance to the organ in face of a subsequently sustained period of ischemia-reperfusion. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a key enzyme in the glycolytic cascade that could be modulated by nitric oxide. The purpose of the present study is to evaluate a possible inhibitory effect on intestinal GAPDH by the nitric oxide generated during preconditioning. This could lead to a reduction of lactate accumulation during subsequent ischemia. METHODS: GAPDH activity was measured after intestinal preconditioning, and the effect of nitric oxide synthase inhibition was evaluated. RESULTS: Preconditioning induced a significant, but transient, decrease in GAPDH activity. This effect appears to be correlated with a reduced amount of lactate accumulation during ischemia. Inhibition of nitric oxide synthesis reversed these changes. In addition, increased synthesis of nitric oxide was detected after preconditioning. CONCLUSIONS: In summary, this study indicates that nitric oxide generated during ischemic preconditioning could act as a glycolytic modulator during subsequent ischemia, through its effect on GAPDH activity.

Animals↗
PubMed1999

Na(+)-K(+) pump and metabolic activities of trout erythrocytes during anoxia.

Metabolic activity in the red blood cells of brown trout was monitored under conditions of oxygen depletion and chemically induced anoxia. Although metabolic activity was reduced during anoxia to one-third of the normoxic value, these cells maintained their ATP contents stable and were viable for hours in the absence of oxygen. In addition, Na(+)-K(+) pump activity was not down-regulated when metabolic activity was reduced during anoxia. The compatibility of this finding with energy equilibrium and ion homeostasis was investigated.

Adenosine Triphosphate↗
PubMed1999

Acid-base disturbance during hemorrhage in rats: significant role of strong inorganic ions.

The present study tests the hypothesis that changes in the strong inorganic ion concentrations contribute significantly to the acid-base disturbance that develops during hemorrhage in the arterial plasma of rats in addition to lactate concentration ([Lac-]) increase. The physicochemical origins for this acid-base disorder were studied during acute, graded hemorrhage (10, 20, and 30% loss of blood volume) in three groups of rats: conscious, anesthetized with ketamine, and anesthetized with urethan. The results support the hypothesis examined: strong-ion difference (SID) decreased in the arterial plasma of all groups studied because of an early imbalance in the main strong inorganic ions during initial hemorrhagic phase. Moreover, changes in plasma [Lac-] contributed to SID decrease in a later hemorrhagic phase (after 10% hemorrhage in urethan-anesthetized, after 20% hemorrhage in ketamine-anesthetized, and after 30% hemorrhage in conscious group). Inorganic ion changes were due to both dilution of the vascular compartment and ion exchange with extravascular space and red blood cells, as compensation for blood volume depletion and hypocapnia. Nevertheless, anesthetized rats were less able than conscious rats to preserve normal arterial pH during hemorrhage, mainly because of an impaired peripheral tissue condition and incomplete ventilatory compensation.

Acid-Base Equilibrium↗
PubMed1997

Seasonal variation in uptake of short-chain neutral amino acid by red blood cells and hepatocytes in trout (Salmo trutta).

The present study shows that the capacity of trout (Salmo trutta) red blood cells (RBCs) and freshly isolated hepatocytes to take up short-chain neutral amino acids changes according to a seasonal pattern. Maximal amino acid uptake rates in RBCs were obtained in winter and spring, while minima were seen in summer and autumn. In contrast, the maximal rates for the freshly isolated hepatocytes were obtained in autumn and winter, and the minima were seen in spring and summer. In addition, by studying the uptake of glycine, evidence was found that the activities of the amino acids carriers ASC, asc and Gly in RBCs varied according to a seasonal rhythm. The activity of the ASC and asc systems changed in parallel with the global uptake of amino acids. Moreover, the RBC:plasma concentration ratio for certain substrates of these carriers (alanine, serine and glycine) varied accordingly. In contrast, the activity of the Gly system was modified inversely with respect to the overall amino acid uptake. The activity of the ASC system in freshly isolated hepatocytes was also seasonally modified, reaching a maximum in autumn, shortly before the reproductive period.

Amino Acids↗
PubMed1996

Factors influencing the acid-base changes in the air-pouch exudate following carrageenan induced inflammation in rats.

The interactions between the acid-base variables that contribute to exudate acidosis were studied in the subcutaneous air-pouch after carrageenan injection in rats. We studied the concurrent changes of exudate gases (PCO2 and PO2), main ions ([Na+], [K+], [Ca2+], [Mg2+], [Cl-] and [Lac-]), inorganic phosphate (P(i)) and albumin in acutely inflamed rats (4, 8, 12, 24 and 48 h of inflammation). A notable hypercapnia was found in the exudate after only 8 h (exudate PCO2 = 64.3 +/- 2.9 mm Hg) but this hypercapnia decreased after 48 h (32.9 +/- 12.7 mm Hg), coincident with the greatest increase in exudate cells. With respect to the metabolic acid-base variables, the most important changes found were a parallel decrease in the strong ion difference ([SID]) and exudate pH, as well as increases in the exudate weak acid buffers ([ATOT]) due to albumin and inorganic phosphate (P(i)) increases. However, after 12 h, the exudate acidosis was stable at around pH 7. A similar acid pH was obtained after 24 h of inflammation when the carrageenan solution injected was previously adjusted to a physiological pH (7.4). This pH, analogous to that of the exudate, was the result of compensation by the acid-base independent variables, a fact which suggests that acid pH may be a beneficial condition for cells taking part in inflammatory processes.

Acid-Base Equilibrium↗
PubMed1996

Regulation of the ASC system and Na+/K + pump activities in brown trout (Salmo trutta) hepatocytes

The present study investigates the regulation of Na+/K+ pump activity and alanine uptake in trout hepatocytes. Pump activity increased when cells were incubated in an amino-acid-free medium, while it was reduced in cells from fasted animals. Short-term exposure (3 h) to glucagon modified the activity of the pump in a complex seasonally dependent pattern: in experiments carried out in autumn and winter there was some inhibition, while in spring the pump was activated by this hormone. Pharmacological modification of levels of two intracellular signal transducers, namely cyclic AMP and Ca2+, always led to a reduction in pump activity. These experiments were conducted in May, when activation of the pump by glucagon exposure occurred. There is no apparent explanation for the mechanism by which this hormone modifies the activity of the pump. Glucagon also regulates the activity of system ASC (a Na+-dependent amino acid carrier with short-chain neutral amino acids as preferred substrates). This regulation also showed a seasonally dependent pattern, although the pattern was opposite to that found for the regulation of Na+/K+ pump activity.

Journal Article↗
PubMed1994

ENERGY METABOLISM BY TROUT RED BLOOD CELLS: SUBSTRATE UTILISATION

The present study investigates energy metabolism by trout red blood cells. It is shown that they are able to use pyruvate at physiological concentrations as an aerobic source of energy. Moreover, microcalorimetric data suggest that trout erythrocytes are also able to use internal substrates, at least when maintained in vitro. Although the actual nature of these substrates has not been elucidated, glycogen appears to be the most probable. The relationship between heat dissipation and oxygen consumption suggests that most of the oxygen is used to oxidize substrates, and the inhibition of respiratory activity by antimycin A indicates that there is no substantial utilisation of non-respiratory oxygen. However, the oxygen uptake by these cells does not appear to be related to substrate utilisation, measured from transformation of labelled molecules (either pyruvate or glucose); this may be due to mixing of labelled compounds with non-labelled molecules in the intracellular pools, because of the low metabolic rate of these cells.

Journal Article↗
PubMed1992

Glucose metabolism by trout (Salmo trutta) red blood cells.

Glucose metabolism has been studied in Salmo trutta red blood cells. From non-metabolizable analogue (3-O-methyl glucose and L-glucose) uptake experiments it is concluded that there is no counterpart to the membrane transport system for glucose found in mammalian red blood cells. Once within the cells, glucose is directed to CO2 and lactate formation through both the Embden-Meyerhoff and hexose monophosphate shunts; lactate appears as the most important end-product of glucose metabolism in these cells. From experiments under anaerobic conditions, and in the presence of an inhibitor of pyruvate transfer to mitochondria, most of the CO2 formed appears to derive from the hexose monophosphate pathway. Appreciable O2 consumption has been detected, but there is no clear relationship between this and substrate metabolism. Key enzymes of glucose metabolism, hexokinase, fructose-6-phosphate kinase and, probably, pyruvate kinase are out of equilibrium, confirming their regulatory activity in Salmo trutta red blood cells. The presence of isoproterenol, a catecholamine analogue, induces important changes in glucose metabolism under both aerobic and anaerobic conditions, and increases the production of both CO2 and lactate. From the data presented, glucose appears to be the major fuel for Salmo trutta red blood cells, showing a slightly different pattern of glucose metabolism from rainbow trout red blood cells.

3-O-Methylglucose↗
PubMed1988

Converting enzyme activity and angiotensin metabolism in the dog brainstem.

The concentrations of angiotensin converting enzyme (ACE) activity, norepinephrine, and serotonin were measured in microdissected regions of the dog's brainstem and spinal cord. In addition, we determined the in vitro metabolism of 125I-angiotensin I (Ang I) in homogenates of the same brain punch regions. High ACE-specific activity was found in the monoamine-containing regions of the brainstem and in the intermediolateral column of the spinal cord. In brainstem homogenates 125I-Ang I was metabolized to angiotensin II (Ang-[1-8]) and the N-terminal heptapeptide Ang-(1-7). In the presence of MK 422 (50 microM), Ang-(1-7) was still generated, while the production of Ang-(1-8) was inhibited. This study revealed the presence of high ACE activity in monoamine regions of dog brainstem and spinal cord, and showed that the metabolite Ang-(1-7) is the major product generated from Ang I in the presence and absence of ACE inhibition.

Angiotensin I↗