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Biomedical subjects

L Vargas

Publications and source records attributed to L Vargas.

At least 19 recordsLinked to original sources

Comparative analgesic efficacy of patient-controlled analgesia with ketorolac versus morphine after elective intraabdominal operations.

We conducted a randomized, double-blind trial to compare analgesia and side effects produced by ketorolac and morphine during postoperative patient-controlled analgesia (PCA). Fifty-one patients (ASA classes I and II) undergoing elective intraabdominal procedures were assigned to one of two groups. When postoperative pain first increased to 4/10 (by visual analog scale [VAS]), patients were randomly assigned to one of two groups. Group 1 (n = 25) received up to two intravenous (IV) boluses of 5 mg of morphine followed by IV morphine PCA, whereas those in Group 2 (n = 26) received up to two IV boluses of 30 mg ketorolac, then IV ketorolac PCA. Up to two rescue doses of morphine (5 mg per dose, subcutaneously) were given in either group when pain during deep inhalation exceeded 5/10 on VAS. Ten patients from Group 1 required rescue doses of morphine compared to 22 patients from Group 2 (P < 0.0011). Two and 16 patients from Groups 1 and 2, respectively, were withdrawn because of inadequate analgesia (P < 0.01). Mean pain scores were less in Group 1 than in Group 2 at each time, but only significantly so at 15 min (P < 0.0021), 30 min (P < 0.0336), and 24 h (P < 0.0358) after starting PCA. Time to acceptance of oral liquids was equivalent in Groups 1 and 2 (22 h and 21 h, respectively). IV ketorolac PCA, although well tolerated, has limited effectiveness as the sole postoperative analgesic after intraabdominal operations.

Abdomen

[Cytogenetic studies of Chilean children with acute lymphoblastic leukemia].

Acute lymphoblastic leukemia (ALL) is the most frequent childhood cancer. The leukemic cells of ALL patients show several well defined numeric and structural chromosomal abnormalities which are universally known for its prognostic implications. We studied a group of 44 children with ALL, to investigate the incidence of chromosome aberrations in ALL, its lymphocyte lineage and some clinical feature associations, and the finding of non previously described aberrations. A high proportion of patients (79.5%) showed chromosomal abnormalities. Most of them had a pseudodiploid karyotype (46 chromosomes), characterized mainly by a translocation. In relation to chromosome number, 27% of them were hyperdiploid with more than 50; 9% hyperdiploid between 47-50 and 7% hypodiploid (less than 46). Among structural aberrations found, were the following recurrent translocations: t (1; 19), t (4; 11), t (9; 22) in 6.8%, 9.1% and 2.3% of cases respectively, all related to an early B immunophenotype. Other translocations found, compromised regions 7q22, 9p21 - 24. Two new translocations in ALL were found: t (1; 5)(q23; q33), apparently balanced, and t (13; 21)(q14; q22), unbalanced. Other recurrent structural changes found were: deletion (6q), (7q), (9p), (11q), (12p), inversion (3q), isochromosome (7q), maker chromosomes and double minutes. The distribution of chromosome abnormalities in this group of patients was in agreement with previous reports from other investigators.

Adolescent

Stress-induced hyperglycemia and hypoinsulinemia are suppressed by sulfonylurea. Predominant role of insulin.

Based on the in vitro blockade of adrenal catecholamines release by sulfonylurea, we searched for an anti-stress activity of this drug. Stress-induced hyperglycemia and insulin inhibition were employed as adrenergic stress indicators. A standard dose of the oral sulfonylurea glipizide (200 micrograms/100 g), administered 15 min before a 1-h restraint stress to intact or 80% pancreatectomized rats, produced total suppression of the stress-induced hyperglycemia-hypoinsulinemia, an effect followed by a significant post-stress hypoglycemia of 1 h duration. The latter effect was elicited by all the sulfonylureas assayed. In the 80% pancreatectomized rats, glipizide nearly halved the increases in plasma catecholamines at 30 min of stress, but did not modify those attained at 60 min, when glycemia was decreasing and insulinemia was still increasing. Moreover, behavioral experiments in intact stressed rats showed that the adrenergic overt behavior inhibition caused by propranolol was not produced either by glipizide or insulin, reinforcing that glipizide affect was not mediated by catecholamine inhibition. These findings suggest a blockade of catecholamines hepatic receptors by the anticipated insulin release induced by sulfonylurea. Thus, insulin fully dominated when insulin and catecholamines were administered in a stress-like sequence. A confirmation of these findings in diabetic patients subjected to surgical stress would allow a new therapeutic application of sulfonylurea. It is concluded that an anticipated insulin release plus an insulin dominant role over catecholamines activity might explain the anti-stress effect of sulfonylurea.

Analysis of Variance

Induction of peroxisomal fatty acyl-coenzyme A oxidase and total carnitine acetyl-coenzyme A transferase in primary cultures of rat hepatocytes by garlic extracts.

Garlic has been proposed as a natural hypolipidemic substance. Most hypolipidemic compounds induce peroxisomal proliferation and increase enzyme activities associated with peroxisomal beta-oxidation in rat liver. Here we report that garlic methanol-extracts behave as hypolipidemic drugs, increasing the activity of peroxisomal fatty acyl-coenzyme A oxidase and of total carnitine acetyl-coenzyme A transferase in primary cultures of rat hepatocytes. Both enzymes are considered markers associated with increased peroxisomal beta-oxidation. As in the case of hypolipidemic peroxisome proliferators, garlic extracts partially prevented the decrease in fatty acyl-coenzyme A oxidase as the culture aged. No changes were observed in the activity of microsomal NADPH cytochrome c reductase or of mitochondrial glutamate dehydrogenase.

Acyl-CoA Oxidase

Absorption of oral ethinylestradiol is delayed by its eutectic mixture with cholesterol.

A solid dispersion of ethinylestradiol-cholesterol (EE & CHOL; eutectic 1:4 W/W) was prepared by melting and rapid cooling. The fused material was then mixed with lactose as vehicle. Soft gelatin capsules were filled with 50 mg of the final mixture to give 0.050 mg of ethinylestradiol. Six female volunteers received, one capsule of the eutectic combination of EE:CHOL or one 50 micrograms tablet of ethinylestradiol (Dianor, Syntex), in a cross-over study and in fasting state. Venous blood samples were drawn at 0, 10, 20, 30, 40, 50, 60, 90, 120, 240, 360, 480, 720, 1440 minutes after dosing. Immunoreactive EE was measured by radioimmunoassay to assess the serum concentration-time course. All subjects exhibited a significant increase in EE levels after oral administration. Mean peak EE levels, 1350 pg/ml vs 91 pg/ml (p less than 0.001), were achieved 360 minutes and 90 minutes (p less than 0.01), after administration of the eutectic and reference formulation, respectively. Eutectic mixture showed a greater area under the serum concentration-time curve, longer mean residence time of the drug in the body, and four times the value of the elimination half-life of the reference formulation. It is concluded that the combination of ethinylestradiol with cholesterol forming an eutectic mixture, when administered orally to normal women, modulates the absorption and the bioavailability of the EE. This approach may be suitable for long-acting oral treatment with sex steroids.

Administration, Oral

Short-lived suppressor cell activity during normal human pregnancy.

Short-lived suppressor cell (SLSC) activity was determined in normal pregnant women. This activity was significantly increased in all three trimesters of pregnancy and during the first week postpartum. When pregnant women were divided into primiparous and multiparous groups, no significant differences were found between the two groups in any of the periods studied. These results suggest that increased SLSC activity may play a role in the materno-fetal tolerance and that parity has no influence on this activity.

Adult

Bradykinin-induced vasoconstriction of rat mesenteric arteries precontracted with noradrenaline.

1. Administration of bradykinin caused dose-dependent vasoconstriction in rat isolated perfused mesenteric arteries precontracted with noradrenaline. 2. The vasoconstrictor response was not mediated by BK1-bradykinin receptors. 3. Inhibition of cyclo-oxygenase with indomethacin, aspirin or meclofenamate abolished the vasoconstrictor effect of bradykinin, showing that a member of the arachidonic acid cascade may be involved. 4. Inhibitors of thromboxane synthesis (imidazole and UK 38485) did not affect or only reduced the bradykinin-induced vasoconstriction. 5. The endoperoxide H2/thromboxane A2 receptor antagonist SQ 29548 significantly reduced the vasoconstrictor effect of bradykinin, but did not affect the vasoconstrictor response to noradrenaline, adrenaline, vasopressin, 5-hydroxytryptamine or prostaglandins. 6. The eicosanoid(s) that mediate bradykinin-induced vasoconstriction appear to be synthesized outside the arterial endothelium. 7. The data suggest that the vasoconstrictor effect of bradykinin in the rat isolated mesenteric artery is mediated by vasoconstrictor arachidonic acid metabolites including the cyclic endoperoxides and/or the thromboxanes.

Animals

[The determination of immunological parameters in splenectomized patients].

We studied 15 patients submitted to splenectomy. Humoral immunity was studied with protein electrophoresis and quantification of immunoglobulins; cellular immunity was studied by total and subpopulation lymphocyte counts and evaluation of phagocytosis. Increased levels of IgG, IgM and IgA, a decrease in circulating T-lymphocytes and an increased phagocytosis was seen after operation. These findings correlated to the presence of viral and parasitic infections postoperatively. Preoperative antipneumococcal vaccination prevented infections by this agent. Thus, appropriate preventive measures must be taken to deal with altered immunological responses after splenectomy.

Adolescent

[Glucose overload test. Screening of gestational diabetes in population of pregnant women with risk factors for diabetes. Clinical experience].

UNLABELLED: Clinical utility of the Overload Test with 50 g. of Oral Glucose (PSG) is evaluated, in 513 pregnancies with risk factors for diabetes. Of the 933 PSG which were made, 13.7% were positive (limit value: plasma glucose of much less than 150 mg/dl at 1 hour); the test were made after 20 weeks of gestation in 82.8% of the cases. Of the 128 positive PSG, 73 positive Oral Glucose Tolerance Test were obtained (O'Sullivan criteria). The prevalence of gestational diabetes found in this group was 15.2%. There was no difference on the most frequent risk factors (family history, obesity and macrosomia) between the general population in the study and the group of Gestational diabetes. CONCLUSION: PSG, because of its easy application, low cost and excellent tolerance is a test which should be included among the prenatal routine test as screening for gestational diabetes in our media.

Adult

Organic and inorganic calcium blockers on voltage and receptor operated channels of resistance arteries of the rat.

The vasoconstrictor responses induced by noradrenaline (NA), adrenaline (AD), serotonin (ST) and vasopressin (VP) on the anterior mesenteric artery of the rat and its branches, were maintained, although somewhat reduced when perfused with a Ca free solution that depletes extracellular Ca. The vasoconstrictor responses were abolished when Lanthanum, EDTA, Verapamil or Nifedipine were added to the Ca free solution. These drugs are known to displace plasmalemmal bound Ca that triggers vasoconstriction when the agonists attach to the receptors thus blocking the vasoconstrictor responses. When the mesenteric arteries were perfused with a Ca containing solution, to block the vasoconstriction induced by the agonists the concentration of La3+, EDTA, Verapamil and Nifedipine must be raised. Thus these drugs appear to compete with extracellular ionic Ca for the membranal sites involved in the activity of the agonists. K induced vasoconstriction was abolished when extracellular Ca was depleted by a Ca free solution and with lower concentrations of the anticalcic drug than those used to cancel the effect of the agonists. Ca appears to be attached to voltage operated channels less firmly than to receptor operated channels. NA, AD, ST and VP showed different sensitivity to the blocking effect of the various anticalcic drugs. This is probably explained by small differences in the structure of the Ca channels operated by the agonists.

Animals

Inhibition of stress-induced hyperglycemia by tail pinching or intraventricular enkephalin administration in the rat.

The tail pinch (t-p) method added to a basal restraint stress produced inhibition of the stress-induced hyperglycemia, an effect that was neutralized with intrathecal anesthesia but not with intracerebroventricular (i.c.v.) naloxone (50, 100, 1000 ng/100 g) or with intraperitoneal naloxone injections (0.1-0.3 mg/100 g). A similar negative result was obtained with i.c.v. administration of 500 and 1000 ng/100 g of beta-endorphin. In contrast, a single i.c.v. injection of 1000 ng/100 g of Met-enkephalin reproduced the t-p inhibitory effect. The latter was not elicited by i.c.v. FK 33824, an enkephalin analogue, a result that supports the specific participation of the delta-opioid receptors. The results obtained with central alpha-adrenoceptor antagonists and central noradrenergic chemical destruction, or central alpha-adrenoceptor agonists, support the production of a reinforcement of the alpha-adrenoceptor stress stimulation by the t-p procedure, probably through noradrenaline and enkephalin mediation.

Animals

Sympathetic nervous system mediates urinary kallikrein excretion in conscious rats.

1. The influence of the sympathetic nervous system on urinary kallikrein excretion (UKal) was investigated in conscious rats during stress produced by inserting a silastic catheter through the urethra into the bladder. The effect of this stress on blood glucose (BG), mean arterial pressure (MAP), urinary volume (Uv), urinary sodium (UVNa), and glomerular filtration rate (GFR) was also studied. 2. In intact animals stress of 120 min duration produced a non-significant increase of MAP, a significant increase of BG and a decrease of UNa (P less than 0.001 t-test, 9 d.f.), but it did not affect Uv and GFR. In stressed rats UKal was considerably lower (52 milli Amidasic Units [mAU] per 100 g bodyweight, s.e.m. = 5, n = 6) than in control rats (170 mAU per 100 g, s.e.m. = 21, n = 5). The inhibitory effect on UKal was also observed when kallikrein was measured by the kininogenase method. 3. Adrenal medullectomy, performed 1 week before the experiment, suppressed the stress hyperglycaemia but did not affect the reduction of urinary kallikrein or the anti-natriuresis. 4. Intracerebroventricular (i.c.v.) injection of saline also had no effect in the control or in the stressed rats, while i.c.v. d-l-propranolol decreased MAP, suppressed the stress hyperglycaemia and the anti-natriuresis and stimulated UKal, without changes in Uv and GFR. Non-stressed control rats i.c.v. injected with saline excreted considerably less kallikrein than rats i.c.v. injected with d-l-propranolol (control saline: 162, s.e.m. = 14, n = 6; vs control d-l-propranolol: 559, s.e.m. = 20, n = 6). Even in stressed rats this difference was registered (stressed saline: 56, s.e.m. = 8, n = 6; vs stressed d-l-propranolol: 554 mAU per 100 g, s.e.m. = 33, n = 6). 5. Peripheral sympathectomy with 6-hydroxydopamine (6-OHDA) did not suppress the hyperglycaemic response to stress, but it stimulated UKal. Kallikrein excretion was similar in 6-OHDA stressed (534 mAU per 100 g, s.e.m. = 30, n = 6) than in 6-OHDA control rats (491 mAU per 100 g, s.e.m. = 34, n = 6). No differences were observed on UNa and GFR between control 6-OHDA treated rats and stressed 6-OHDA treated rats. 6. The present results suggest strongly that urinary kallikrein excretion is modulated by sympathetic activity. Results after central beta-adrenergic blockade and peripheral sympathectomy led to the hypothesis that normal sympathetic tone in the kidney inhibits the release of kallikrein into the urine.

Adrenal Medulla