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Biomedical subjects

E Jimenez

Publications and source records attributed to E Jimenez.

At least 91 records · Page 5Linked to original sources

Potassium-induced contraction in the lamb proximal urethra: involvement of norepinephrine and different calcium entry pathways.

The purpose of this work was to investigate the mechanisms involved in the peculiar biphasic response of the lamb urethral smooth muscle to high K+ solutions. The relative amplitude of the phasic and tonic components of the contraction and its reproducibility were dependent on the concentration of K+ used. Only concentrations higher than 80 mM (i.e., 120 mM) showed a tonic component greater in amplitude than the phasic one and manifested a tachyphylactic effect. Phentolamine (10(-6) M), prazosin (10(-6) M) and chemical denervation with 6-hydroxydopamine significantly inhibited the tonic component of the K+ (120 mM)-induced contraction, modifying its morphology. Reproducible contractions to K+ (120 mM) could be obtained in the presence of prazosin (10(-6) M) or cocaine (10(-6) M). The preparations were also shown to accumulate [3H]noradrenaline and release it upon depolarization with K+ (60 and 120 mM). Calcium removal inhibited the K+ (120 mM)-induced contraction. After addition of calcium (0.5-5 mM) the contractile activity was restored. Nifedipine (10(-6) M) and verapamil (10(-6) M) but not sodium nitroprusside (10(-6) M) significantly blocked the contractile response for calcium as well as the phasic component of the K+ contraction in calcium-containing medium. In preparations treated with prazosin (10(-6) M) the tonic component of the K+ (120 mM) contraction was more sensitive to nifedipine and removal of extracellular calcium than the phasic one.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗

Long-term contraception with the levonorgestrel 20 mcg/day (LNg 20) and the copper T 380Ag intrauterine devices: a five-year randomized study.

An intrauterine device, releasing approximately 20 micrograms/day of levonorgestrel (LNg 20), used by 1124 women, was studied in a randomized trial of five years duration in comparison with the Copper T, model TCu 380Agm in 1121 women. At five years, the gross cumulative pregnancy rate of 1.1 +/- 0.5 per 100 among users of the LNg 20 devices was not significantly different from the rate of 1.4 +/- 0.4 per 100 experienced by users of the Copper T 380Ag. The steroid-releasing IUD had significantly higher termination rates for expulsion and amenorrhea, a significantly lower termination rate for other menstrual problems and pain, and a lower continuation rate. The five-year continuation rate among women using the TCu 380Ag was 40.6 per 100 as compared with that of 33.0 per 100 among women randomized to the LNg 20 device (P less than .001). Terminations attributed to amenorrhea with the LNg device primarily account for differences in continuation. These two intrauterine devices are the most effective long-term, reversible IUDs yet reported in the literature. No other contraceptive methods have exhibited such low long-term pregnancy rates in randomized comparative trials.

Adolescent↗

Effects of low extracellular calcium on cytosolic calcium and ischemic contracture.

We have shown that myocardial cytosolic calcium [Cai] rises during ischemia. Simultaneously membrane bound stores are depleted. The [Cai] rise precedes the onset of irreversible ischemic contracture. We found that a low extracellular calcium [Cao] (100 microM) perfusate decreased peak contracture pressure and delayed the time to onset and to peak of ischemic contracture in the isolated retroperfused rabbit heart subjected to 37 degrees C ischemia. [Cai] was measured with the intracellular [Cai] fluorescent indicator Fura-2 AM (10 microM) in a separate group. In the group exposed to 2.45 mM Ca2+ there was a significant rise (P less than 0.05) in [Cai] to above 50% of preischemic value after 30 min of ischemia. The [Cai] in the low [Cao] perfused group at 30 min of ischemia was 30% below the preischemic value. The peak of the [Cai] rise in the low [Cao] perfusate group was markedly attenuated and delayed to 40 min. Taken together it appears that low calcium perfusate (100 microM) prior to ischemia attenuates the ischemia-induced [Cai] rise, delays the onset, and decreases the force of contracture with irreversible ischemic injury.

Adenosine Triphosphate↗

The effect of cardiac hypertrophy on changes in cytosolic free calcium concentration during ischemia.

Chronic ventricular hypertrophy caused by pressure overload is a common associated risk factor in congenital cardiac surgery. Because calcium controls contractile protein interaction, we postulated that inducing ventricular hypertrophy from birth alters the way myocytes are able to regulate free cytosolic calcium (Cai) during ischemia. In this study we measured Cai with a recently developed intracellular fluorescent probe trapped inside myocytes by deesterification. The probe shifts its fluorescence spectra (from 380 to 340 nm; fluorescence measured at 510 nm) when it binds to calcium in direct relation to Cai. We studied the effects of ischemia at 37 degrees C (up to 50 minutes) on Cai in newborn (3 to 5 days), adult control (2 to 4 months old), and hypertrophied (2 months old; aortic banding done at 10 days) isolated retroperfused rabbit hearts loaded with Fura-2. In a separate group of hearts (n = 6 per group) we measured isovolumic peak developed pressure with an intracavity balloon in hearts subjected to 30 minutes of ischemia at 37 degrees C and 30 minutes of reperfusion. The recovery of peak developed pressure (percent of preischemic control) was 101% +/- 6% in control, 85% +/- 4% (p less than 0.05 vs control) in newborn, and 67% +/- 7% (p less than 0.05 vs control) in hypertrophied hearts. Cai-dependent fluorescence rose to 160% +/- 30% of preischemic baseline levels by 30 minutes of ischemia in control versus a decline to 55% +/- 7% (p less than 0.05 vs control) in newborn and 51% +/- 2% (p less than 0.05 vs control) in hypertrophied hearts by 30 minutes of ischemia. We conclude that hypertrophied and newborn hearts have a lower Cai during ischemia compared with adult hearts, and this is associated with a worse recovery of cardiac function. The lower Cai may be the result of irreversible binding of calcium to contractile proteins.

Animals↗

Deferoxamine fails to improve postischemic cardiac function in hypertrophied hearts.

Myocardial hypertrophy is a well-recognized risk factor in congenital cardiac surgery. Hypertrophied hearts have been demonstrated to have an increased vulnerability to ischemia/reperfusion injury. We studied the effects of the iron chelator and hydroxyl radical scavenger deferoxamine given during early reperfusion in a model of isolated retroperfused rabbit hearts made hypertrophic by aortic banding early in life (1 week of age). The rabbits were studied at 6-8 weeks of age, and the hearts were subjected to 30 minutes of 37 degrees C ischemia followed by 30 minutes of reperfusion. Postischemic recovery of isovolumic developed pressure was measured by using an intracavitary balloon in both the untreated (n = 6) and the deferoxamine-treated (n = 6) groups and compared with normal age-matched controls. Deferoxamine (50 mumol/kg) was given to one group with the hypertrophied hearts during the first 10 minutes of reperfusion. The left ventricular weight/body weight ratio in the hypertrophied hearts was 2.9 +/- 0.4 x 10(-3) (n = 14) versus 2.0 +/- 0.1 x 10(-3) in the age-matched controls (p less than 0.05). Postischemic peak developed pressure recovered to 102 +/- 6% of the preischemic value in the normal hearts after 30 minutes of reperfusion compared with 75 +/- 5% for the untreated and 71 +/- 4% for the deferoxamine-treated hearts (p less than 0.05 vs. control). We conclude that chronic hypertrophy from early in life leads to increased susceptibility to ischemia and that the iron chelator deferoxamine is not effective in preventing the injury of reperfusion in hypertrophied hearts.

Animals↗

Subxiphoid pericardiotomy versus echocardiography: a prospective evaluation of the diagnosis of occult penetrating cardiac injury.

Diagnostic subxiphoid pericardiotomy (SP) is presently advocated for the diagnosis of occult cardiac injuries in patients with stable vital signs with juxta-cardiac-penetrating chest wounds. This approach, however, results in a reported 80% negative pericardial exploration rate. To investigate the reliability of bedside two-dimension echocardiography (2-D echo) in predicting cardiac injury as compared to SP, a prospective study was undertaken of patients with stable vital signs who were admitted with penetrating chest wounds that were located within the space bounded by the manubrium, nipples, and subcostal line. Initial evaluation of the patients with bedside 2-D echo was found to have a 96% accuracy, 97% specificity, and 90% sensitivity in predicting cardiac injury. The only false-negative findings were in a patient who consented to SP 18 hours after bedside 2-D echo was performed. The reliability of bedside 2-D echo compared to SP was not significantly different according to the kappa measure of reliability. These data suggest that bedside 2-D echo is an expeditious and reliable method to diagnose occult cardiac injuries during the initial assessment of a patient with stable vital signs who had penetrating chest trauma. This approach may allow for the selective use of SP on patients with positive bedside 2-D echo and could eliminate unnecessary surgical procedures.

Echocardiography↗

Human immunodeficiency virus-related lymphoreticular malignancies and peripheral neurologic disease. A report of four cases.

The most common human immunodeficiency virus-related (HIV) malignancies to date include Kaposi's sarcoma and the high-grade non-Hodgkin's lymphomas. There also appears to be an association between HIV and an aggressive form of Hodgkin's disease. In addition, there is a spectrum of HIV-related central and peripheral neurologic syndromes. This article documents four patients with HIV-associated lymphoma who presented with peripheral neurologic syndromes as part of their neoplastic process. Autopsy results obtained from two of these patients showed direct nerve infiltration by lymphoma. All patients had an elevated serum lactate dehydrogenase (LDH). It is recommended that HIV-related lymphoma be considered in a high-risk patient who presents with a peripheral neurologic syndrome especially if there is an elevated serum LDH.

Acquired Immunodeficiency Syndrome↗

Ranitidine prophylaxis in acute gastric mucosal damage in critically ill pediatric patients.

We determined the ranitidine dosage necessary to maintain gastric pH at or above 4 in 40 critically ill children. The patients were divided into four groups of ten patients each. They were treated with ranitidine in the following dosages: a) 2 mg/kg by NG tube every 12 h; b) 4 mg/kg by NG tube every 12 h; c) 0.75 mg/kg iv every 6 h; d) 1.5 mg/kg iv every 6 h. The fourth group had a higher median pH than the other groups, in spite of also having the highest risk of acute gastric mucosal damage (AGMD). Eight (80%) of ten patients in the fourth group had a pH greater than or equal to 4 or more than 80% of the study period. We recommend 1.5 mg/kg iv every 6 h for gastric acid inhibition in AGMD prophylaxis in children.

Adolescent↗

Obstetrical characteristics of a loss of end-diastolic velocities in the fetal aorta and/or umbilical artery using Doppler ultrasound.

In 30 of 137 high-risk pregnancies we observed absent end-diastolic velocities indicating a high downstream impedance, which could be proved by histomorphological findings of the placenta. On the average the loss of end-diastolic velocities occurred 2-3 days before suspicious and nearly 8 days before pathological cardiotocographic findings. The perinatal mortality was high when absent velocities had been observed before the 32nd week, a cesarean section was obligatory in all but 1 case. All fetuses were growth-retarded. In 9 cases we were able to determine the ratio of blood flow volume in the common carotid arteries to that of the fetal aorta. The values were significantly increased as compared to values of undisturbed pregnancies, demonstrating a redistribution of fetal blood in favor of cerebral circulation.

Aorta↗

Effect of thyroid hormones on angiotensinogen production in the rat in vivo and in vitro.

The influence of thyroid hormones on angiotensinogen production was studied in vitro and in vivo. In the in-vitro system, angiotensinogen production rate (APR) of monolayer cultures of rat hepatocytes in response to tri-iodothyronine (T3) and thyroxine (T4) was assayed. In the in-vivo system, plasma angiotensinogen concentration (PAC) and liver angiotensinogen content (LAC) were measured in hyper- and hypothyroid rats. In both thyroid dysfunctions, a significant decrease of PAC was found compared with that in control animals; however, LAC showed a significant increase in hyperthyroidism and a marked decrease in hypothyroidism. As PAC is dependent upon both angiotensinogen production by the liver and angiotensinogen degradation by renin, the decrease in PAC observed in hyperthyroidism could be due to an increase in plasma renin concentration, which would overcome the increased synthesis of liver angiotensinogen observed in these animals. In fact, addition of various concentrations of T4 or T3 to monolayer cultures of adult rat hepatocytes significantly enhanced APR. This increase was greater and started earlier with T3 (1196.1 +/- 143.7 (S.D.) pg/mg protein per 6-h incubation; significant differences at the third hour of incubation) than with T4 (858.3 +/- 88.2 pg/mg protein per 6-h incubation; significant differences at the sixth hour of incubation). In addition, a close dose-response relationship was found in the cultures supplemented with T3. The different time-course in the response elicited by T3 and T4 on APR could be a consequence of the necessary transformation of T4 into T3 to acquire biological activity.

Angiotensinogen↗

Iron deficiency anemia and iron therapy effects on infant developmental test performance.

The behavioral effects of iron deficiency and its treatment were evaluated in a double-blind randomized controlled community-based study of 191 Costa Rican infants, 12 to 23 months of age, with various degrees of iron deficiency. The Bayley Scales of Infant Development were administered before and both 1 week and 3 months after IM or oral administration of iron. Appropriate placebo-treated control infants were also tested. Infants with iron deficiency anemia showed significantly lower mental and motor test scores, even after considering factors relating to birth, nutrition, family background, parental IQ, and the home environment. After 1 week, neither IM nor oral iron treatments differed from placebo treatment in effects on scores. After 3 months, lower mental and motor test scores were no longer observed among iron-deficient anemic infants whose anemia and iron deficiency were both corrected (36%). However, significantly lower mental and motor test scores persisted among the majority of initially anemic infants (64%) who had more severe or chronic iron deficiency. Although no longer anemic, they still showed biochemical evidence of iron deficiency after 3 months of treatment. These persistent lower scores suggest either that iron therapy adequate for correcting anemia is insufficient to reverse behavioral and developmental disturbances in many infants or that certain ill effects are long-lasting, depending on the timing, severity, or chronicity of iron deficiency anemia in infancy.

Anemia, Hypochromic↗

Clearance and tissue distribution of intravenously injected Salmonella typhi polysaccharide in rabbits.

The interaction of Freeman polysaccharide of Salmonella typhi with blood and tissues of rabbits was studied by radioimmunoassay. After intravenous injection of 1.0 mg of S. typhi Freeman polysaccharide, a rapid clearance phase (t1/2, 6.0 min) was followed by a slower clearance period (t1/2, 55.2 min). These results suggest first, that the distribution of whole lipopolysaccharide is a function of how the polysaccharides are handled by the host; further, that the O side chain determines how and where lipopolysaccharide is cleared from the circulatory system; and finally, that Freeman polysaccharide regulates the toxicity of lipopolysaccharide by influencing its clearance from blood.

Animals↗