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Biomedical subjects

M A Cruz

Publications and source records attributed to M A Cruz.

63 records · Page 4Linked to original sources
PubMed1986

Adrenergic mechanisms in the control of myometrial activity in mice. Changes on estrous cycle.

Correlation between contractile activity and norepinephrine (NE) release induced by electrical stimulation or by high K+ depolarization has been analyzed in isolated preparations of mouse uterus throughout the different stages of the estrous cycle. Both the contractile activity induced by electrical stimulation and the capacity to maintain contracture, after changing the physiological bathing solution by high K+ solution, followed the same pattern: estrous greater than proestrous greater than diestrous greater than metestrous. High-K+ induced 3H-NE release was also different according to the stage of the estrous cycle. 3H-NE release was significantly less in estrous than in diestrous uterine horns. EC50 values for inhibiting contractile response, for isoprenaline, norepinephrine and phenylephrine were significantly greater in metestrous than in other stages of the estrous cycle. On the other hand, reserpinized mouse uteri showed an increase in EC50 values in the stages tested. The data support the hypothesis that in a mouse uterus, sex steroid hormones could affect beta-adrenergic receptor function indirectly, perhaps through an action on adrenergic neurons by a mechanism affecting NE release from sympathetic terminals.

Animals↗
PubMed1985

Effects of ethanol ingestion on amino acid uptake in the dog liver in vivo.

The effect of ethanol ingestion on the uptake of labeled amino acids was studied in the in situ autoperfused dog liver. Ethanol was administered orally, as a 15% water solution, in a dose of 4 g/kg body weight/day as the only source of water for 2 days. Amino acid uptake was measured in anesthetized dogs by means of the single-passage, multiple-tracer dilution technique. In control animals, hepatic uptake of 14C-glycine, 3H-alpha-aminoisobutyric acid (3H-AIB) and 3H-L-leucine were 50, 15 and 66%, respectively. In the ethanol-treated dogs, glycine and AIB uptake was reduced by 70 and 63%, respectively. L-leucine uptake was reduced by only 23%. The plasma concentration of the naturally occurring amino acids was significantly increased after ethanol treatment, probably due to a reduced influx into hepatocytes. Simultaneous measurements of hemodynamic parameters showed a significant increase in the portal vein pressure of ethanol-treated animals, whereas the portal vein blood flow and hepatic extracellular volume were unaffected.

Amino Acids↗
PubMedDate not supplied

Cardiac troponin T and cardiac dysfunction in extremely low-birth-weight infants.

Extremely low-birth-weight (ELBW) infants frequently manifest signs of cardiac dysfunction requiring inotropic support. It is not clear if this is due to cardiac injury, which can be monitored by measuring cardiac troponin T (cTnT). We performed a nested prospective cohort study at a university level III neonatal intensive care unit. The study included 27 infants weighing between 500 and 999 g. Exclusion criteria included evidence of sepsis, use of postnatal steroids, and cardiac anomalies. Measurements included serum cTnT and echocardiogram in the first 48 hours of life. The mean serum cTnT level of the study population was 0.52 +/- 0.38 ng/ml. It was higher in those with lower Apgar scores (0.89 +/- 0.37 if 5-minute Apgar < 4 vs 0.36 +/- 0.26 ng/ml, p < 0.001) and correlated to initial base deficit (r = -0.37, p < 0.05). Infants who required inotropic support had higher cTnT levels than those who did not (0.73 +/- 0.43 vs 0.39 +/- 0.29 ng/ml, p < 0.03). cTnT concentrations did not relate to simultaneous echocardiographic measures of cardiac function. In ELBW infants, serum cTnT levels are higher than normally seen in term infants and adults, and they are higher in infants with greater perinatal stress as well as those who show evidence of cardiac dysfunction requiring pressor support.

Apgar Score↗
PubMedDate not supplied

Serotonin-induced vasoconstriction is mediated by thromboxane release and action in the human fetal-placental circulation.

The possibility that prostanoids mediate the contractile response of serotonin on placental vessels was investigated. Rings of chorionic plate arteries and veins with and without endothelium were suspended in an organ bath for recording isometric mechanically activity. Serotonin caused dose-dependent contractions that were significantly attenuated by indomethacin (cyclo-oxygenase inhibitor, 10 microM) and SQ29,548 (thromboxane receptor antagonist, 1 microM). Pretreatment of placental venous and arterial rings with indomethacin decreased sensitivity (EC50) to serotonin of 2.3- and 1.9-fold, respectively. Pretreatment with SQ29,548 decreased sensitivity to serotonin of twofold in veins and 2.1-fold in arteries. In the endothelium-denuded placental arteries and veins, pretreatment with indomethacin and SQ29,548 reduced the serotonin-induced contraction in a similar way to that obtained in the endothelium-intact vessels. In isolated perfused cotyledon through the fetal circulation, serotonin caused a significant increase in perfusion pressure and stimulated thromboxane release 1.9-fold compared with basal values. Therefore, serotonin-induced vasoconstriction in the human fetoplacental circulation appears to be mediated in part by thromboxane release or action. This effect is not dependent on mediators released from the endothelium. The present study provides evidence for the participation of thromboxane A2 in the contractile response to serotonin in the human placental circulation. The ability of serotonin to release thromboxane A2 which is also a potent vasoconstrictor agent, may be important in increase fetoplacental resistance, one of the features of pre-eclampsia.

Endothelium, Vascular↗
PubMedDate not supplied

[Acne and immunity].

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Acne Vulgaris↗