carmen acevedo - Academia.edu (original) (raw)

Papers by carmen acevedo

Research paper thumbnail of Correlaci�n manom�trica, histol�gica e histoqu�mica en el estudio de megacolon en el ni�o

Research paper thumbnail of Effects of morphine on adrenaline responses of uteri from progesterone or estradiol treated mice

Comparative Biochemistry and Physiology Part C: Comparative Pharmacology, 1987

Abstrach-1. The effect of a chronic morphine treatment on the in oitro contractile responses of t... more Abstrach-1. The effect of a chronic morphine treatment on the in oitro contractile responses of the mouse uterus to adrenaline was studied. 2. Chronic morphine treatment induced a su~~ensiti~y state in the uteri from both progesterone and e&radio1 treated mice. 3. The acute administration of morphine to the uteri from morphine tolerant-dependent and progesterone treated mice induced a further increase of the contractile effect of adrenaline. 4. Reserpine administration did not further increase the supersensitivity of the mouse uterus to adrenaline induced by a chronic morphine treatment.

Research paper thumbnail of Possible involvement of adenine nucleotides in the neurotransmission of the mouse urinary bladder

Comparative Biochemistry and Physiology Part C: Comparative Pharmacology, 1985

The urinary bladder of the mouse contracts to several agonists, namely acetylcholine, noradrenali... more The urinary bladder of the mouse contracts to several agonists, namely acetylcholine, noradrenaline. adrenaline, histamine, angiotensin, serotonin, purine nucleotides and prostaglandin F?, 2. Atropine partially reduced the contraction induced by electrical stimulation, whereas propranolol and tolazoline were ineffective. 3. The atropine resistant component of the neurogenic response was reduced by indomethacin. Methysergide and diphenhydramine were ineffective. 4. Desensitization of the bladder by a$-methylene ATP abolished the response to ATP and greatly reduced the non-adrenergic non-cholinergic component of the neurogenic response. 5. The results suggest that ATP could be the transmitter responsible for the non-cholinergic non-adrenergic contraction of the mouse urinary bladder.

Research paper thumbnail of Effect of extracellular calcium and calcium channel antagonists on ATP and field stimulation induced contractions of the mouse urinary bladder

General Pharmacology: The Vascular System, 1989

The dependence on extracellular calcium of the responses to the electrical stimulation, ATP and h... more The dependence on extracellular calcium of the responses to the electrical stimulation, ATP and high K induced contractions has been studied in the mouse urinary bladder. 2. The responses to ATP, field stimulation and K induced depolarization were eliminated in calcium free EGTA medium. However, a small remanent of these responses was observed in the absence of calcium in the superfusing medium. 3. The calcium antagonists verapamil, nifedipine and diltiazem decreased in a close dependent manner the contractions induced by ATP and electrical stimulation of the mouse urinary bladder. 4. The responses of the mouse urinary bladder to high K concentration were antagonized by verapamil and diltiazem, but nifedipine was less effective in decreasing the tonic component of the contraction induced by K in the muscle. 5. The responses of the mouse urinary bladder to electrical stimulation, ATP and high concentration of K are mainly dependent on the extracellular calcium.

Research paper thumbnail of Correlación manométrica, histológica e histoquímica en el estudio de megacolon en el niño

Revista chilena de pediatría, 1982

Megacolon in children: Manometry, histology and histochemistry. Ninety-six anorectftl manometric ... more Megacolon in children: Manometry, histology and histochemistry. Ninety-six anorectftl manometric studies were performed in children with megacolon Sixteen patients had pressure records compatibles with Hirschsprung's disease: in twelve the rectal suction biopsy and study of acetylcholinesterase activity confirmed the diagnosis of aganglionosis. In two pacients with non conclusive manometry, acetylcholinesterase activity was highly positive: in one the diagnosis ofcolonicneuronal dysplasia through the study of succinic dehydrogenase was confirmed.

Research paper thumbnail of Effect of ethanol on human placental transport and metabolism of adenosine

Placenta, 1997

It has been suggested that adenosine is involved in the acute effects of ethanol in a number of t... more It has been suggested that adenosine is involved in the acute effects of ethanol in a number of tissues. The present study was undertaken to evaluate the role of adenosine on the vascular responses of perfused isolated human placental cotyledons after the acute administration of ethanol. The possibility that ethanol may effect the uptake and metabolism adenosine was also investigated. Uptake of adenosine was studied using the single-circulation paired-tracer dilution technique. Both adenosine and ethanol caused a dose-related increase in perfusion pressure of placental lobules. Pharmacologically relevant concentrations of ethanol (10-65 mM) significantly inhibited the uptake of [3H]adenosine between 25 and 50 per cent. Thin-layer chromatographic analysis of the perfusate after the administration of ethanol showed in a 17.9 +/- 0.6 per cent reduction of [3H]adenosine metabolism. These findings support the working hypothesis that placental adenosine, at least partially, mediates the placental disturbance elicited by the administration of acute ethanol, which may contribute to the pathogenesis of fetal alcohol syndrome.

Research paper thumbnail of Hypoxanthine uptake at the fetal side of human placenta proceeds through a nucleobase-preferring carrier and a non-saturable process

Placenta, 1997

ABSTRACT Uptake and metabolism of hypoxanthine by human placenta were studied using the single-ci... more ABSTRACT Uptake and metabolism of hypoxanthine by human placenta were studied using the single-circulation paired-tracer technique. In isolated cotyledons perfused through the fetal (basal) circulation, at mean pressures of 31.7 +/- 4.0 mmHg and mean flow rates maintained at 5.5 +/- 0.15 ml/min, the [3H]hypoxanthine uptake was 36 +/- 2.4 per cent (16.5 +/- 1.1 pmol/g wet weight). Hypoxanthine uptake was significantly inhibited by unlabelled (mM) hypoxanthine (0.5), adenine (0.5), guanine (0.5) and papaverine (15.0), but was unaffected by nitrobenzylthioinosine (0.01). Adenosine failed to inhibit hypoxanthine uptake. The kinetic analysis of hypoxanthine uptake showed it to be partially mediated by a saturable (apparent K(m) = 12.1 +/- 1.85 microns; Jmax = 7.1 +/- 0.52 nmol/min) and Na(+)-dependent mechanism. A greater fraction of hypoxanthine influx proceeded through a non-saturable process. Thin layer chromatographic analysis of venous perfusate after the intra-arterial injection of [3H]hypoxanthine showed a negligible degradation of nucleobase. These overall results show that hypoxanthine uptake at the fetal side of human placenta occurs by a saturable plus a non-saturable process. The carrier showed specificity for nucleobases and high affinity-low capacity for hypoxanthine. Since the fetal blood concentration of hypoxanthine is normally low, its uptake would be mediated by the high affinity transport system. Because the non-saturable mechanism can be operative at high concentrations of hypoxanthine, it may have primary importance to clear the nucleobase coming from the fetus during intrauterine hypoxia.

Research paper thumbnail of Bradykinin facilitates the purinergic motor component of the rat bladder neurotransmission

Neuroscience Letters, 1990

Research paper thumbnail of Insulin and nitric oxide stimulates glucose transport in human placenta

Life Sciences, 2005

The present work examines whether insulin and NO can act as regulators of glucose transport in pl... more The present work examines whether insulin and NO can act as regulators of glucose transport in placenta. Glucose uptake (2-deoxy D-[ 3 H]glucose) was measured in the absence (control or basal values) and in the presence of insulin (1200 AU/ml) or SNP (20 AM) in isolated perfused cotyledons and tissue slices preparations of human placenta. Both insulin and NO significantly increased glucose uptake by 20 and 27 per cent, respectively. Insulin decreased the Km of glucose transport from 42.5 F 2.69 to 35.1 F 2.58 mM. The stimulatory effect of SNP was mimicked by 8-CPT-cGMP and was completely blocked by the guanylate cyclase inhibitor, ODQ (10 AM). ODQ and the NOS inhibitor, L-NAME (100 AM), decreased basal glucose uptake but did not affect insulin-stimulated glucose transport. Taken together, these findings indicate that insulin and NO stimulate glucose uptake in human placenta and suggest that both potential regulators of glucose transport use different signaling pathways.

Research paper thumbnail of Ethanol inhibits L-arginine uptake and enhances NO formation in human placenta

Life Sciences, 2001

The acute effects of ethanol (20-60 mM) on L-arginine uptake and nitric oxide (NO) formation was ... more The acute effects of ethanol (20-60 mM) on L-arginine uptake and nitric oxide (NO) formation was investigated in human placental cotyledons perfused at constant flow. Ethanol (40 mM) decreased L-[3H]arginine uptake from 27.6 +/- 2.3 to 15.8 +/- 1.3 per cent (P < 0.05) of the injected dose and significantly enhanced NO levels in the perfusate from 0.88 +/- 0.11 to 2.80 +/- 0.39 microM. Ethanol also elicited the constriction of placental vessels. The effects of ethanol (20-60 mM) on L-arginine uptake and endothelial NO synthase (eNOS) activity were also investigated in cultured human umbilical vein endothelial cells (HUVEC). After 60 min of ethanol (40 mM) exposure, basal L-[3H]arginine uptake (4.7 +/- 0.3 pmol/microg protein/min) was inhibited by 60 per cent (P < 0.05). Basal eNOS activity in HUVEC determined under "no flow" (static) conditions was significantly increased (approximately 1.8 fold) by 60 mM ethanol. These data are consistent with a stimulatory effect of ethanol on eNOS activity in both basal and flow-stimulated conditions, which may serve a protective role against its vasoconstrictive acute effect. While acute ethanol administration inhibits L-arginine uptake, the present results do not allow us to speculate on the effects of chronic ethanol exposure on NO formation in the fetoplacental unity.

Research paper thumbnail of Endogenous Nitric Oxide Attenuates Ethanol-lnduced Vasoconstriction in the Human Placenta

Gynecologic and Obstetric Investigation, 1997

The purpose of this study was to clarify the role of endogenous nitric oxide and prostanoids in e... more The purpose of this study was to clarify the role of endogenous nitric oxide and prostanoids in ethanol-induced perturbation of microcirculation in perfused human placenta. Infusion of ethanol into chorionic plate vessels at 10–65 mM increases perfusion pressure in a concentration-dependent fashion, and is an indicator of fetal-placental vasoconstriction. Simultaneous infusion of Nω-nitro-L-arginine, methylene blue and endothelial cell removal significantly

Research paper thumbnail of L-Arginine Transport at the Fetal Side of Human Placenta: Effect of Aspirin in Pregnancy

Experimental Physiology, 1999

L-Arginine transport by the fetal side of human placenta was investigated through the characteriz... more L-Arginine transport by the fetal side of human placenta was investigated through the characterization of L-[3H]arginine uptake in isolated perfused cotyledon. Competitive inhibition experiments suggest the presence of at least two transport systems: a Na+-independent, pH-insensitive system inhibitable by cationic amino acids, similar to system y+, and a Na+-dependent system which recognizes both cationic and neutral amino acids only in the presence of Na+, i.e. a Bo,+-like system. The kinetic analysis of L-arginine uptake in the presence of Na+ revealed that the process is mediated by saturable components: a high-affinity system (Km = 167 +/- 18.0 microM; Vmax = 0.174 +/- 0.012 micromol min-1) and a low-affinity carrier (Km = 980 +/- 112 microM; Vmax = 1.60 +/- 0.12 micromol min-1). In the absence of Na+, L-arginine uptake was fitted by one model with a Michaelis-Menten constant of 200 +/- 24.8 microM. These results suggest that the high-affinity component corresponds to the Na+-independent system y+, whilst the low-affinity system may represent the activity of the Na+-dependent Bo,+ transporter. Kinetic studies in placentae taken from aspirin-treated pregnancies showed that L-arginine is transported with a significantly higher affinity (Km = 42.5 +/- 5.7 microM), but with a lower capacity (Vmax = 0.064 +/- 0.003 micromol min-1) than in the non-treated group. The latter finding suggests that aspirin would facilitate the uptake of the NO precursor only at very low arginine concentrations.

Research paper thumbnail of Correlaci�n manom�trica, histol�gica e histoqu�mica en el estudio de megacolon en el ni�o

Research paper thumbnail of Effects of morphine on adrenaline responses of uteri from progesterone or estradiol treated mice

Comparative Biochemistry and Physiology Part C: Comparative Pharmacology, 1987

Abstrach-1. The effect of a chronic morphine treatment on the in oitro contractile responses of t... more Abstrach-1. The effect of a chronic morphine treatment on the in oitro contractile responses of the mouse uterus to adrenaline was studied. 2. Chronic morphine treatment induced a su~~ensiti~y state in the uteri from both progesterone and e&radio1 treated mice. 3. The acute administration of morphine to the uteri from morphine tolerant-dependent and progesterone treated mice induced a further increase of the contractile effect of adrenaline. 4. Reserpine administration did not further increase the supersensitivity of the mouse uterus to adrenaline induced by a chronic morphine treatment.

Research paper thumbnail of Possible involvement of adenine nucleotides in the neurotransmission of the mouse urinary bladder

Comparative Biochemistry and Physiology Part C: Comparative Pharmacology, 1985

The urinary bladder of the mouse contracts to several agonists, namely acetylcholine, noradrenali... more The urinary bladder of the mouse contracts to several agonists, namely acetylcholine, noradrenaline. adrenaline, histamine, angiotensin, serotonin, purine nucleotides and prostaglandin F?, 2. Atropine partially reduced the contraction induced by electrical stimulation, whereas propranolol and tolazoline were ineffective. 3. The atropine resistant component of the neurogenic response was reduced by indomethacin. Methysergide and diphenhydramine were ineffective. 4. Desensitization of the bladder by a$-methylene ATP abolished the response to ATP and greatly reduced the non-adrenergic non-cholinergic component of the neurogenic response. 5. The results suggest that ATP could be the transmitter responsible for the non-cholinergic non-adrenergic contraction of the mouse urinary bladder.

Research paper thumbnail of Effect of extracellular calcium and calcium channel antagonists on ATP and field stimulation induced contractions of the mouse urinary bladder

General Pharmacology: The Vascular System, 1989

The dependence on extracellular calcium of the responses to the electrical stimulation, ATP and h... more The dependence on extracellular calcium of the responses to the electrical stimulation, ATP and high K induced contractions has been studied in the mouse urinary bladder. 2. The responses to ATP, field stimulation and K induced depolarization were eliminated in calcium free EGTA medium. However, a small remanent of these responses was observed in the absence of calcium in the superfusing medium. 3. The calcium antagonists verapamil, nifedipine and diltiazem decreased in a close dependent manner the contractions induced by ATP and electrical stimulation of the mouse urinary bladder. 4. The responses of the mouse urinary bladder to high K concentration were antagonized by verapamil and diltiazem, but nifedipine was less effective in decreasing the tonic component of the contraction induced by K in the muscle. 5. The responses of the mouse urinary bladder to electrical stimulation, ATP and high concentration of K are mainly dependent on the extracellular calcium.

Research paper thumbnail of Correlación manométrica, histológica e histoquímica en el estudio de megacolon en el niño

Revista chilena de pediatría, 1982

Megacolon in children: Manometry, histology and histochemistry. Ninety-six anorectftl manometric ... more Megacolon in children: Manometry, histology and histochemistry. Ninety-six anorectftl manometric studies were performed in children with megacolon Sixteen patients had pressure records compatibles with Hirschsprung's disease: in twelve the rectal suction biopsy and study of acetylcholinesterase activity confirmed the diagnosis of aganglionosis. In two pacients with non conclusive manometry, acetylcholinesterase activity was highly positive: in one the diagnosis ofcolonicneuronal dysplasia through the study of succinic dehydrogenase was confirmed.

Research paper thumbnail of Effect of ethanol on human placental transport and metabolism of adenosine

Placenta, 1997

It has been suggested that adenosine is involved in the acute effects of ethanol in a number of t... more It has been suggested that adenosine is involved in the acute effects of ethanol in a number of tissues. The present study was undertaken to evaluate the role of adenosine on the vascular responses of perfused isolated human placental cotyledons after the acute administration of ethanol. The possibility that ethanol may effect the uptake and metabolism adenosine was also investigated. Uptake of adenosine was studied using the single-circulation paired-tracer dilution technique. Both adenosine and ethanol caused a dose-related increase in perfusion pressure of placental lobules. Pharmacologically relevant concentrations of ethanol (10-65 mM) significantly inhibited the uptake of [3H]adenosine between 25 and 50 per cent. Thin-layer chromatographic analysis of the perfusate after the administration of ethanol showed in a 17.9 +/- 0.6 per cent reduction of [3H]adenosine metabolism. These findings support the working hypothesis that placental adenosine, at least partially, mediates the placental disturbance elicited by the administration of acute ethanol, which may contribute to the pathogenesis of fetal alcohol syndrome.

Research paper thumbnail of Hypoxanthine uptake at the fetal side of human placenta proceeds through a nucleobase-preferring carrier and a non-saturable process

Placenta, 1997

ABSTRACT Uptake and metabolism of hypoxanthine by human placenta were studied using the single-ci... more ABSTRACT Uptake and metabolism of hypoxanthine by human placenta were studied using the single-circulation paired-tracer technique. In isolated cotyledons perfused through the fetal (basal) circulation, at mean pressures of 31.7 +/- 4.0 mmHg and mean flow rates maintained at 5.5 +/- 0.15 ml/min, the [3H]hypoxanthine uptake was 36 +/- 2.4 per cent (16.5 +/- 1.1 pmol/g wet weight). Hypoxanthine uptake was significantly inhibited by unlabelled (mM) hypoxanthine (0.5), adenine (0.5), guanine (0.5) and papaverine (15.0), but was unaffected by nitrobenzylthioinosine (0.01). Adenosine failed to inhibit hypoxanthine uptake. The kinetic analysis of hypoxanthine uptake showed it to be partially mediated by a saturable (apparent K(m) = 12.1 +/- 1.85 microns; Jmax = 7.1 +/- 0.52 nmol/min) and Na(+)-dependent mechanism. A greater fraction of hypoxanthine influx proceeded through a non-saturable process. Thin layer chromatographic analysis of venous perfusate after the intra-arterial injection of [3H]hypoxanthine showed a negligible degradation of nucleobase. These overall results show that hypoxanthine uptake at the fetal side of human placenta occurs by a saturable plus a non-saturable process. The carrier showed specificity for nucleobases and high affinity-low capacity for hypoxanthine. Since the fetal blood concentration of hypoxanthine is normally low, its uptake would be mediated by the high affinity transport system. Because the non-saturable mechanism can be operative at high concentrations of hypoxanthine, it may have primary importance to clear the nucleobase coming from the fetus during intrauterine hypoxia.

Research paper thumbnail of Bradykinin facilitates the purinergic motor component of the rat bladder neurotransmission

Neuroscience Letters, 1990

Research paper thumbnail of Insulin and nitric oxide stimulates glucose transport in human placenta

Life Sciences, 2005

The present work examines whether insulin and NO can act as regulators of glucose transport in pl... more The present work examines whether insulin and NO can act as regulators of glucose transport in placenta. Glucose uptake (2-deoxy D-[ 3 H]glucose) was measured in the absence (control or basal values) and in the presence of insulin (1200 AU/ml) or SNP (20 AM) in isolated perfused cotyledons and tissue slices preparations of human placenta. Both insulin and NO significantly increased glucose uptake by 20 and 27 per cent, respectively. Insulin decreased the Km of glucose transport from 42.5 F 2.69 to 35.1 F 2.58 mM. The stimulatory effect of SNP was mimicked by 8-CPT-cGMP and was completely blocked by the guanylate cyclase inhibitor, ODQ (10 AM). ODQ and the NOS inhibitor, L-NAME (100 AM), decreased basal glucose uptake but did not affect insulin-stimulated glucose transport. Taken together, these findings indicate that insulin and NO stimulate glucose uptake in human placenta and suggest that both potential regulators of glucose transport use different signaling pathways.

Research paper thumbnail of Ethanol inhibits L-arginine uptake and enhances NO formation in human placenta

Life Sciences, 2001

The acute effects of ethanol (20-60 mM) on L-arginine uptake and nitric oxide (NO) formation was ... more The acute effects of ethanol (20-60 mM) on L-arginine uptake and nitric oxide (NO) formation was investigated in human placental cotyledons perfused at constant flow. Ethanol (40 mM) decreased L-[3H]arginine uptake from 27.6 +/- 2.3 to 15.8 +/- 1.3 per cent (P < 0.05) of the injected dose and significantly enhanced NO levels in the perfusate from 0.88 +/- 0.11 to 2.80 +/- 0.39 microM. Ethanol also elicited the constriction of placental vessels. The effects of ethanol (20-60 mM) on L-arginine uptake and endothelial NO synthase (eNOS) activity were also investigated in cultured human umbilical vein endothelial cells (HUVEC). After 60 min of ethanol (40 mM) exposure, basal L-[3H]arginine uptake (4.7 +/- 0.3 pmol/microg protein/min) was inhibited by 60 per cent (P < 0.05). Basal eNOS activity in HUVEC determined under "no flow" (static) conditions was significantly increased (approximately 1.8 fold) by 60 mM ethanol. These data are consistent with a stimulatory effect of ethanol on eNOS activity in both basal and flow-stimulated conditions, which may serve a protective role against its vasoconstrictive acute effect. While acute ethanol administration inhibits L-arginine uptake, the present results do not allow us to speculate on the effects of chronic ethanol exposure on NO formation in the fetoplacental unity.

Research paper thumbnail of Endogenous Nitric Oxide Attenuates Ethanol-lnduced Vasoconstriction in the Human Placenta

Gynecologic and Obstetric Investigation, 1997

The purpose of this study was to clarify the role of endogenous nitric oxide and prostanoids in e... more The purpose of this study was to clarify the role of endogenous nitric oxide and prostanoids in ethanol-induced perturbation of microcirculation in perfused human placenta. Infusion of ethanol into chorionic plate vessels at 10–65 mM increases perfusion pressure in a concentration-dependent fashion, and is an indicator of fetal-placental vasoconstriction. Simultaneous infusion of Nω-nitro-L-arginine, methylene blue and endothelial cell removal significantly

Research paper thumbnail of L-Arginine Transport at the Fetal Side of Human Placenta: Effect of Aspirin in Pregnancy

Experimental Physiology, 1999

L-Arginine transport by the fetal side of human placenta was investigated through the characteriz... more L-Arginine transport by the fetal side of human placenta was investigated through the characterization of L-[3H]arginine uptake in isolated perfused cotyledon. Competitive inhibition experiments suggest the presence of at least two transport systems: a Na+-independent, pH-insensitive system inhibitable by cationic amino acids, similar to system y+, and a Na+-dependent system which recognizes both cationic and neutral amino acids only in the presence of Na+, i.e. a Bo,+-like system. The kinetic analysis of L-arginine uptake in the presence of Na+ revealed that the process is mediated by saturable components: a high-affinity system (Km = 167 +/- 18.0 microM; Vmax = 0.174 +/- 0.012 micromol min-1) and a low-affinity carrier (Km = 980 +/- 112 microM; Vmax = 1.60 +/- 0.12 micromol min-1). In the absence of Na+, L-arginine uptake was fitted by one model with a Michaelis-Menten constant of 200 +/- 24.8 microM. These results suggest that the high-affinity component corresponds to the Na+-independent system y+, whilst the low-affinity system may represent the activity of the Na+-dependent Bo,+ transporter. Kinetic studies in placentae taken from aspirin-treated pregnancies showed that L-arginine is transported with a significantly higher affinity (Km = 42.5 +/- 5.7 microM), but with a lower capacity (Vmax = 0.064 +/- 0.003 micromol min-1) than in the non-treated group. The latter finding suggests that aspirin would facilitate the uptake of the NO precursor only at very low arginine concentrations.