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Biomedical subjects

I Rovira

Publications and source records attributed to I Rovira.

At least 19 recordsLinked to original sources

Antifungal activity of three spermidine conjugates.

Three tri-substituted spermidines, di-p-coumaroyl-caffeoylspermidine, tri-caffeoylspermidine and tri-p-coumaroylspermidine, isolated from pollen of Quercus alba, were examined for antifungal activity. Both di-p-coumaroyl-caffeoylspermidine and tri-p-coumaroylspermidine reduced mycelial growth of the oat leaf stripe pathogen, Pyrenophora avenae and reduced powdery mildew (Blumeria graminis f. sp. hordei) infection of barley seedlings when applied as a post-inoculation treatment. When used as a pre-inoculation treatment, only di-p-coumaroyl-caffeoylspermidine reduced powdery mildew infection significantly. Growth of P. avenae in the presence of 100 microM di-p-coumaroyl-caffeoylspermidine reduced activity of S-adenosylmethionine decarboxylase (AdoMetDC), and led to a reduction in the incorporation of labelled ornithine into spermidine. The other two spermidine conjugates increased AdoMetDC activity and the flux label from ornithine into spermine in P. avenae significantly.

Antifungal Agents↗

Plasma magnesium in patients submitted to cardiac surgery and its influence on perioperative morbidity.

BACKGROUND: To determine the changes in magnesaemia in cardiac surgical patients submitted to cardiopulmonary bypass (CPB) and their influence on perioperative morbidity. METHODS SETTING: the cardiovascular surgery department of a university hospital. PATIENTS: 60 patients of both sexes, mean age 60+/-12 yrs, operated on consecutively for myocardial revascularization or valve replacement. INTERVENTIONS: plasma Mg2+ levels were measured preoperatively, during CPB, postCPB and throughout the first 24 hrs after operation. Preoperative plasma Mg2+ levels of these patients were compared with those of 15 non-cardiac surgical patients and 11 healthy volunteers. RESULTS: Mean values of Mg2+ similar in the three populations although in the group of cardiac patients the number of hypomagnesaemic patients was significantly higher (16 patients=26.6%). In these 16 patients, preoperative hypomagnesaemia had a statistically significant relationship with the preoperative treatment with beta-blockers and previous history of arrhythmias (p<0.05). A progressive statistically significant decrease of Mg2+ was observed throughout the surgery that remained low at 24 hours postoperatively (p<0.05). Normomagnesemic patients needed significantly more shocks and electrical energy to obtain heart defibrillation after CPB. The incidence of both postoperative arrhythmias and postoperative low cardiac index (<2.5 L.m2) was statistically significantly more frequent in hypomagnesaemic patients (p<0.05). CONCLUSIONS: Preoperative hypomagnesaemia was more frequent in this small sample of cardiac surgical patients than in non-cardiac surgical patients and was related to preoperative treatment with b-blockers. Hypomagne-saemia caused by CPB persisted 24 hrs after operation and was associated with higher incidence of both postoperative arrhythmias and low cardiac index.

Adrenergic beta-Antagonists↗

[Esmolol in anesthesiology: pharmacology and indications].

Esmolol is a beta-adrenergic receptor antagonist with a relatively specific affinity for beta 1 adrenergic receptors. Its mechanism of action is therefore largely cardioselective and only high doses block beta 2 adrenergic receptors. The pharmacologic features of the drug give it rapid onset of beta-blocking action (distribution half-life = 2 minutes) and a short duration of action due to rapid clearance (clearance half-life = 9 minutes). The rapid metabolism of esmolol allows its beta-blocking activity to be lowered rapidly by changing the rate of infusion and obtaining rapid reversibility of effect in the minutes following interruption of the infusion. The esmolol dose is therefore manageable and individual adjustments can be made in function of a patient's clinical status. Such properties mean that esmolol is indicated for short-term treatment of hypertension and tachycardia during the perioperative period and in clinical situations that require easy unblocking of beta receptors. Hypertension and bradycardia are the most frequent complications associated with the administration of esmolol, such that blood pressure, heart rate and electrocardiographic data must be monitored.

Adrenergic beta-Antagonists↗

[Changes in oxygen saturation in the jugular bulb during cardiac surgery].

OBJECTIVE: Heart surgery with cardiopulmonary bypass (CPB) leads to changes in supply and consumption of cerebral oxygen (DO2 and VO2C). Monitoring jugular bulb oxygen saturation (SjO2) detects changes in the DO2C/VO2C ratio that occur in patients undergoing heart surgery. The objective of this study was to determine the evolution of SjO2, of the arteriovenous difference of cerebral oxygen and of cerebral oxygen extraction, as well as the possible relation between those variables and changes in mean arterial pressure, hemoglobin counts and temperature in patients undergoing heart surgery with CPB. PATIENTS AND METHOD: A prospective study carried out in 31 patients who underwent coronary valve surgery. To monitor SjO2, each patient's internal jugular vein was cannulated with an oximetric catheter in a retrograde direction to monitor SjO2. RESULTS: Baseline SjO2 (68 +/- 7.4%), obtained after anesthetic induction, was similar to SjO2 before (65 +/- 6%) and after (67 +/- 8.2%) CPB. However, SjO2 upon starting CPB (60 +/- 8.6%) and during rewarming (63 +/- 3%) were significantly lower than at baseline. SjO2 was significantly higher during hypothermic bypass (78 +/- 5%) than at baseline. SjO2 ranged from a low of 60 +/- 8% as CPB was initiated to a high of 78 +/- 5% during hypothermic CPB. Mean arterial pressure was significantly lower at the start of bypass (44 +/- 6 mmHg) than anesthetic induction (83.5 +/- 13.1 mmHg) and the decrease correlated with a significant decrease in SjO2. Changes in mean arterial pressure were unrelated to significant changes in SjO2 at other moments, however. Nor was there a significant relation between changes in temperature or hemoglobin and the evolution of SjO2. At least one episode of SjO2 desaturation (= 50%) occurred in 29% of the patients, with the lowest values being recorded at the start of CPB and during rewarming. CONCLUSIONS: The greatest risk of cerebral oxygen imbalance between supply and demand occurs at the start of CPB and during rewarming, as shown by decreases in SjO2 levels below baseline at those times.

Blood Pressure↗

Isolated lichen planus of the lip successfully treated with chloroquine phosphate.

Solitary lesions of lichen planus (LP) are often confused with other inflammatory or malignant epithelial lesions. We describe a 51-year-old woman who had had an LP of the lower lip for 11 years. She had undergone several oral and topical therapies with little improvement. The patient had an excellent response to chloroquine phosphate within 3 months. This report represents the third case of LP exclusively localized on the lower lip.

Anti-Inflammatory Agents, Non-Steroidal↗

Nitric oxide inhalation during exercise in chronic obstructive pulmonary disease.

Patients with chronic obstructive pulmonary disease (COPD) may develop hypoxemia and pulmonary hypertension when exercising. To investigate whether inhaled nitric oxide (NO), a selective pulmonary vasodilator, modifies the changes induced by exercise in pulmonary hemodynamics and gas exchange in COPD, we studied nine patients (FEV1, = 39 +/- 2% predicted), at rest and at submaximal exercise, during breathing of room air and NO (40 ppm). NO inhalation decreased pulmonary artery pressure (Ppa) both at rest and during exercise (analysis of variance [ANOVA] p < 0.05). However, the effect of NO on PaO2 was different at rest than during exercise. At rest, NO decreased PaO2 from 72 +/- 3 mm Hg to 65 +/- 2 mm Hg, due to an increase in ventilation-perfusion (VA/Q) inequality (dispersion of blood flow distribution from 0.9 +/- 0.1 to 1.1 +/- 0.1). During exercise, PaO2 decreased during breathing of room air (-5 +/- 3 mm Hg), whereas it remained essentially unchanged during inhalation of NO (+2 +/- 3 mm Hg), with both changes being significantly different (p < 0.05). VA/Q relationships improved during exercise during breathing of both room air and NO, as a result of a reduction in the dispersion of ventilation distribution. Moreover, NO administered on exertion contributed to redistribute blood flow from alveolar units with low VA/Q ratios to units with normal ratios (p < 0.05). We conclude that in patients with COPD, the inhalation of NO during exercise moderately reduces pulmonary hypertension, and that in contrast with the effects of such inhalation at rest, it may prevent the exercise-associated decrease of PaO2. This effect is probably explained by a preferential distribution of inhaled NO during exercise to well-ventilated alveolar units with faster time constants and normal VA/Q ratios.

Administration, Inhalation↗

Insulin receptor structural requirements for the formation of a ternary complex with IRS-1 and PI 3-kinase.

Insulin receptor substrate-1 (IRS-1) is a major substrate of the insulin receptor tyrosine kinase and is an intermediate in insulin signaling. Phosphotyrosyl-IRS-1 binds to other signaling proteins including phosphatidylinositol 3-kinase (PI 3-kinase). We examined the role of three insulin receptor tyrosine autophosphorylation domains in association of the receptor with IRS-1. Our data support the idea that tyrosine phosphorylation of the insulin receptor juxtamembrane domain is necessary for receptor association with IRS-1. We provide evidence that the kinase regulatory domain, which is part of a loop structure at the mouth of the catalytic cleft, when mutated to replace Tyr1146, Tyr1150, and Tyr1151 with phenylalanine can bind receptor substrates without tyrosine phosphorylation of residues in the receptor juxtamembrane region. In addition, our data show that the amount of PI 3-kinase directly associated with the insulin receptor C-terminus is low when compared to the PI 3-kinase associating with IRS-1. We also demonstrate that a substantial amount (approximately 25%) of the IRS-1 associated PI 3-kinase is associated with the insulin receptor in a ternary complex of insulin receptor/IRS-1/PI 3-kinase.

Adenosine Triphosphate↗

Worsening of pulmonary gas exchange with nitric oxide inhalation in chronic obstructive pulmonary disease.

BACKGROUND: Inhalation of nitric oxide (NO) causes selective pulmonary vasodilation and improves arterial oxygenation in acute respiratory distress syndrome. But some patients do not respond or gas exchange worsens when inhaling NO. We hypothesised that this detrimental effect might be related to the reversion of hypoxic vasoconstriction in those patients where this mechanism contributes to ventilation-perfusion (V(A)/Q) matching. METHODS: We studied 13 patients with advanced chronic obstructive pulmonary disease (COPD). We compared their responses to breathing room air, NO at 40 parts per million in air, and 100% O2. Changes in pulmonary haemodynamics, blood gases, and V(A)/Q distributions were assessed. FINDINGS: NO inhalation decreased the mean (SE) pulmonary artery pressure from 25.9 (2.0) to 21.5 (1.7) mm Hg (p = 0.001) and PaO2 from 56 (2) 53 (2) mm Hg (p = 0.014). The decrease in PaO2 resulted from worsening of V(A)/Q distributions, as shown by a greater dispersion of the blood-flow distribution (logSD Q) from 1.11 (0.1) to 1.22 (0.1) (p = 0.018). O2 breathing reduced the mean pulmonary arterial pressure to 23.4 (2.1) mm Hg and caused greater V(A)/Q mismatch (logSD Q, 1.49 [0.1]). The intrapulmonary shunt on room air was small (2.7 [0.9]%) and did not change when breathing NO or O2. INTERPRETATION: We conclude that in patients with COPD, in whom hypoxaemia is caused essentially by V(A)/Q imbalance rather than by shunt, inhaled NO can worsen gas exchange because of impaired hypoxic regulation of the matching between ventilation and perfusion.

Administration, Inhalation↗

A regulatory role in mammalian salivary glands for 5-hydroxytryptamine receptors coupled to increased cyclic AMP production.

Although a functional role for serotonin (5-hydroxytryptamine, 5-HT) has been defined in the salivary glands of some lower species, relatively few data supporting a role for 5-HT in the regulation of mammalian salivary glands have been presented. Our initial results from polymerase chain reaction studies in cells of mammalian submandibular gland origin using consensus sequence primers from G protein-coupled receptors suggested the presence of mRNA for a 5-HT receptor in these cells. Based on this observation, the question of a role for 5-HT in mammalian submandibular gland function was re-addressed, using isolated, perfused rat submandibular glands and dispersed-cell aggregates from this gland. In perfused glands, 5-HT decreased the rate of saliva flow initiated by acetylcholine by about 50% and increased the amount of protein in the saliva two-fold. In dispersed-cell aggregates, 5-HT elicited a concentration-dependent increase in the accumulation of adenosine 3',5' monophosphate (cyclic AMP; EC50 = 660 +/- 110 nM). In addition, functional studies, as well as radioligand binding experiments, indicated that the effects of 5-HT are independent of beta-adrenoceptors. Accumulation of cAMP in gland cells was consistent with a direct action of 5-HT on adenylyl cyclase. Similar cyclic AMP responses to 5-HT were observed in cells isolated from mouse and opossum submandibular glands and rat sublingual and parotid glands. Our findings suggest the presence of a 5-HT receptor in mammalian salivary glands coupled to the stimulation of adenylyl cyclase and, at least in rat submandibular gland, involved in modifying the volume and protein content of saliva.

Animals↗

Annular elastolytic giant cell granuloma--actinic granuloma?

A 56-year-old woman with annular elastolytic giant cell granuloma is reported. She had annular, slowly growing lesions on sun-exposed areas and the dorsum of one foot. Biopsies from both areas revealed a mid-dermal inflammatory infiltrate with many giant cells engulfing elastic fibres. The current nosological situation of this process is discussed. Actinic granuloma (AG) is a term coined by O'Brien in 1975 to describe a cutaneous process characterized by multiple annular lesions located on sun-exposed skin areas. The histopathology is defined by the presence of multinucleated giant cells containing elastic fibres at the lesion edge, and the absence of these fibres at the lesion centre. The nosology of this disease and the role of actinic exposure as a triggering factor for it has been much discussed in recent years. We report a new case of AG not limited to photo-exposed areas.

Female↗

[Nitric oxide].

Nitric oxide was identified as the relaxing factor derived from the endothelium in 1987. Nitric oxide synthesis allows the vascular system to maintain a state of vasodilation, thereby regulating arterial pressure. Nitric oxide is also found in platelets, where it inhibits adhesion and aggregation; in the immune system, where it is responsible for the cytotoxic action of macrophages; and in the nervous system, where it acts as neurotransmitter. A deficit in endogenous synthesis of nitric oxide contributes to such conditions as essential arterial hypertension, pulmonary hypertension and heart disease. An excess of nitrous oxide induced by endotoxins and cytokinins, meanwhile, is believed to be responsible for hypotension in septic shock and for hyperdynamic circulatory state in cirrhosis of the liver. Nitric oxide has also been implicated in the rejection of transplanted organs and in cell damage after reperfusion. Inhaled nitrous oxide gas reduces pulmonary hypertension without triggering systemic hypotension in both experimental and clinical conditions. It also produces selective vasodilation when used to ventilate specific pulmonary areas, thereby improving the ventilation/perfusion ratio and, hence, oxygenation. Nitric oxide inhalation is effective in pulmonary hypertension-coincident with chronic obstructive lung disease, in persistent neonatal pulmonary hypertension and in pulmonary hypertension with congenital or acquired heart disease. Likewise, it reduces intrapulmonary shunt in acute respiratory failure and improves gas exchange. Under experimental conditions nitric oxide acts as a bronchodilator, although it seems to be less effective for this purpose in clinical use.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗

Effects of inhaled nitric oxide on pulmonary hemodynamics and gas exchange in an ovine model of ARDS.

Inhaling low concentrations of nitric oxide (NO) gas causes selective pulmonary vasodilation of ventilated lung regions. NO activates soluble guanylate cyclase, increasing guanosine 3',5'-cyclic monophosphate (cGMP). Inhibition of NO synthesis enhances hypoxic pulmonary vasoconstriction. Therefore we examined independent and combined effects of NO inhalation and infusion of NG-nitro-L-arginine methyl ester (L-NAME), an NO synthesis inhibitor, on pulmonary vascular pressure-flow relationships, gas exchange, and plasma cGMP levels in anesthetized and mechanically ventilated sheep with acute lung injury induced by bilateral lavage. After lavage, inhaling 60 ppm by volume of NO decreased pulmonary arterial pressure (PAP) and resistance without any systemic hemodynamic effects, increased arterial PO2, and decreased venous admixture (Qva/QT; all P < 0.05) without altering cardiac output (QT), mixed venous PO2, or O2 uptake, major determinants of intrapulmonary shunt. During NO inhalation, PAP-left atrial pressure gradient (PAP-LAP) and Qva/QT were reduced (both P < 0.05) independently of QT, which was varied mechanically. L-NAME infusion produced systemic and pulmonary vasoconstriction and increased PAP-LAP gradient across the entire range of QT, whereas Qva/QT, was not changed. NO inhalation after L-NAME infusion produced pulmonary vasodilation and decreased Qva/QT to the same degree as NO inhalation alone. Five to 10 min after inhalation of 60 ppm NO, before and after L-NAME infusion, arterial plasma cGMP levels were increased by 80% (both P < 0.05). With NO breathing after L-NAME, we measured a consistent transpulmonary cGMP arteriovenous gradient [31 +/- 8 and 33 +/- 7 (SE) pmol/ml at 5 and 10 min, respectively; both P < 0.05]. NO inhalation before or after L-NAME administration in this acute lung injury model reduced Qva/QT, most likely by increasing cGMP concentration in ventilated lung regions and causing selective pulmonary vasodilation.

Administration, Inhalation↗

[Stevens-Johnson syndrome associated with esophageal stenosis].

Stevens-Johnson syndrome consists of inflammatory bullous lesions of the skin and mucous membranes and seems to be associated to several pharmacologic and/or infectious triggering factors which might share a common immunologic way. Esophageal stenosis secondary to Stevens-Johnson syndrome is very rare. During the last 40 years, only two cases in children have been reported. In the present work, we report clinical features and anesthetic management of a 6-year-old girl requiring seven general anesthesia procedures with ketamine and isoflurane for correction of esophageal stenosis.

Anesthesia↗