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Biomedical subjects

R Gonzales

Publications and source records attributed to R Gonzales.

At least 55 records · Page 3Linked to original sources
PubMed1994

Posthysteroscopic hyponatremia.

We report a case of severe hyponatremia following hysteroscopic myomectomy for uterine fibroids. This new technique, which requires large volumes of irrigation solution (1.5% glycine in this case), is being more widely applied as an alternative to open surgery. Thus, nephrologists may expect to encounter such cases as the female counterpart to transurethral resection of prostate-associated hyponatremia. Analysis of the dynamic features of this case, in the context of recent knowledge of glycine metabolism, suggests that the early severe hyponatremia is partly spurious, reflecting an osmotic effect of glycine (which is initially restricted to the extracellular space). As glycine progressively enters cells and is metabolized, the later phase of hyponatremia more accurately reflects true hypo-osmolality.

Adult↗
PubMed1993

Genomic structure of rat liver aryl sulfotransferase IV-encoding gene.

This report contains the first description of the genomic structure for a sulfotransferase (ST). The gene (ASTIV) encodes rat hepatic aryl ST IV, also known as tyrosine-ester ST (EC 2.8.2.9). A phage genomic clone containing 70% of the 3' AST gene coding sequence was isolated after screening a rat genomic library with an ASTIV cDNA. The remaining 5' sequence was determined from a PCR product obtained from rat genomic DNA and ASTIV cDNA-specific primers. ASTIV spans 3.5 kb and contains eight exons and seven introns. The fourth intron of this gene contains sequences homologous to rodent B1 repetitive elements and an Alu repeat found in rat. An alignment of the primary structures of ten different ST revealed several conserved regions, as well as a putative binding site for the cofactor for enzymatic sulfation reactions, 3'-phosphoadenosine-5'-phosphosulfate.

Amino Acid Sequence↗
PubMed1993

Effect of percutaneous balloon valvuloplasty on pulmonary hypertension in mitral stenosis.

Percutaneous mitral balloon valvuloplasty (PMBV) has been useful in decreasing mitral valve obstruction in mitral stenosis; however, the long-term effects of valvuloplasty on pulmonary artery pressure have not been extensively studied. Thirty-three patients underwent PMBV in our institution between January 1988 and December 1991. There were significant reductions in peak (19 +/- 1 to 12 +/- 1 mm Hg) and mean (10 +/- 0.7 to 6 +/- 0.4 mm Hg) mitral valve gradients estimated by Doppler techniques immediately after PMBV. The mitral valve area, as assessed by the pressure half-time method, increased from 1.06 +/- 0.05 to 1.98 +/- 0.08 cm2 (p < 0.001) after the procedure and remained significantly greater (1.68 +/- 0.11 cm2) at 17 +/- 2 months. Right ventricular systolic pressure (RVSP) was estimated in patients with tricuspid regurgitation (TR) using the modified Bernoulli equation. There was a good correlation between Doppler and catheterization for RVSP (r = 0.83 pre valvuloplasty; r = 0.87 post valvuloplasty). Right ventricular systolic pressure by Doppler was 56 +/- 4 mm Hg before valvuloplasty and 48 +/- 4 mm Hg immediately afterwards (p < 0.001). Nine patients had TR on follow-up Doppler studies with an estimated RVSP of 53 +/- 9 mm Hg (p = NS compared with pre- and post-valvuloplasty values). Six of these nine patients had moderate or severe mitral regurgitation (MR), compared with one patient without TR at follow-up (p < 0.05). There appears to be a good correlation between the RVSP determined by Doppler and measured at catheterization.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Norepinephrine-induced increase in sympathetic neuron-derived prostaglandins is independent of neuronal release mechanisms.

The contribution of exocytosis to norepinephrine-stimulated prostaglandin release from sympathetic postganglionic neurons was evaluated in homogenates of adult rat superior cervical ganglia. Incubation of ganglion homogenates with norepinephrine (1 mM) for 30 min caused an increased release of prostaglandin E2 and prostaglandin I2 (measured as the stable metabolite, 6-keto-PGF1a). Neither tetrodotoxin (10 mM), K+ (120 mM), nor EDTA in Ca(2+)-free buffer affected prostaglandin generation under basal and norepinephrine-stimulated conditions. These results suggest that the increase in prostaglandin production by sympathetic neurons after norepinephrine administration is not through the release of previously synthesized intracellular stores. Instead, the increase in prostaglandins in response to norepinephrine appears to be explained by de novo synthesis.

Animals↗
PubMed1991

Postnatal development of neurogenic inflammation in the rat.

We have studied the development in the rat of neurogenic inflammatory mechanisms that mediate cutaneous plasma extravasation. At birth and at postnatal day 10, intradermal injection of substance P, histamine, and bradykinin produced no significant plasma extravasation. At day 13 through adulthood (days 42-49), all test agents produced significant plasma extravasation which increased with increasing age. In the adult rat, pretreatment with 6-hydroxydopamine, to eliminate sympathetic postganglionic nerve terminals, attenuated the plasma extravasation elicited by substance P, histamine and bradykinin. The possible role of the sympathetic postganglionic neuron in the age-dependent changes in neurogenic inflammation is discussed.

Aging↗
PubMed1991

Noradrenaline-induced prostaglandin production by sympathetic postganglionic neurons is mediated by alpha 2-adrenergic receptors.

In this study we have demonstrated that noradrenaline increases the levels of prostaglandin E2 and prostaglandin I2 (detected as the stable metabolite 6-keto-prostaglandin F1 alpha) synthesized by homogenates of superior cervical ganglia from the adult rat. This noradrenaline-induced prostaglandin production was further characterized: (a) Selective destruction of adrenergic sympathetic postganglionic neurons in the ganglia using 6-hydroxydopamine abolished both basal and stimulated prostaglandin production. (b) Elimination of preganglionic cholinergic sympathetic nerve terminals in the ganglia had no effect. (c) Mepacrine (a phospholipase inhibitor) and indomethacin (a cyclooxygenase inhibitor) attenuated both basal and stimulated prostaglandin production. (d) Yohimbine, but not prazosin, suppressed the noradrenaline dose-response curve for prostaglandin production. The results of these experiments show that, in vitro, noradrenaline stimulates de novo synthesis of prostaglandin E2 and prostaglandin I2 by sympathetic postganglionic neurons. This stimulation by noradrenaline appears to result from action at an alpha 2-adrenergic receptor.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Hemodynamic effects of octreotide in patients with autonomic neuropathy.

BACKGROUND: The somatostatin analogue, ectrootide, is being used to treat postprandial hypotension in patients with autonomic neuropathy. Although the therapeutic effect of the drug is presumably secondary to a splanchnic vasoconstrictor action, its effect on splanchnic hemodynamics has never been characterized in patients with autonomic neuropathy. Moreover, it is unknown whether octreotide acts on other vascular beds in this group of patients or whether it affects cardiac output. We, therefore, measured splanchnic, forearm, and systemic vascular resistance and cardiac output before and after administering octreotide (0.4 microgram/kg s.c.) to patients with idiopathic autonomic neuropathy and diabetic autonomic neuropathy. METHODS AND RESULTS: Splanchnic blood flow was determined from the clearance of indocyanine green in seven patients. We observed that octreotide decreased splanchnic blood flow (from 850 +/- 77 to 664 +/- 48 ml/min, p less than 0.005), increased mean blood pressure (from 97 +/- 6 to 115 +/- 3 mm Hg, p less than 0.005), and increased splanchnic vascular resistance (from 0.118 +/- 0.012 to 0.18 +/- 0.018 mm Hg/ml/min, p less than 0.005). Forearm blood flow was measured by plethysmography in 13 patients. Octreotide increased forearm vascular resistance in patients with idiopathic autonomic neuropathy (n = 8) from 19.1 +/- 1.0 to 27.2 +/- 3.8 mm Hg/ml/min/100 ml forearm volume (p less than 0.01) and from 25.2 +/- 3.9 to 41.0 +/- 6.8 mm Hg/ml/min/100 ml (p less than 0.01) in patients with diabetic autonomic neuropathy (n = 5). Cardiac output was measured by two-dimensional echocardiography. Octreotide administration increased cardiac output in five of six patients with idiopathic autonomic neuropathy (from 4.4 +/- 0.4 to 5.0 +/- 0.5 l/min, p less than 0.02) and five of five patients with diabetic autonomic neuropathy (from 3.8 +/- 0.4 to 5.1 +/- 0.4 l/min, p less than 0.02). Systemic vascular resistance increased in patients with idiopathic autonomic neuropathy from 21.2 +/- 2 to 24.9 +/- 2.6 (p less than 0.05) but did not change in patients with diabetic autonomic neuropathy. CONCLUSION: The pressor effect of octreotide in patients with autonomic neuropathy is associated with increased splanchnic and forearm vascular resistance and with increased cardiac output.

Adolescent↗
PubMed1990

Noxious stimulus-induced increase in spinal prostaglandin E2 is noradrenergic terminal-dependent.

Prostaglandins (PGs) were measured in perfusate from the lumbar intrathecal (IT) space of pentobarbital anaesthetized rats. The level of PGE2, but not of PGF2 alpha or 6-keto PGF1 alpha, was increased by immersion of a hindpaw in water at a noxious temperature (50 degrees C). No increase in PGE2 was produced by non-noxious thermal stimulation (35 degrees C water). The noxious stimulus-evoked increase in PGE2, and increases in PGE2 during norepinephrine infusion (10 micrograms/ml), were significantly decreased in rats pretreated with intrathecal 6-hydroxydopamine. These data suggest that noxious stimuli induce an increase in the production of spinal PGE2 and that this production derives from, or requires the presence of noradrenergic terminals in the spinal cord.

Adrenergic Fibers↗
PubMed1990

Natural antibodies to IFN-gamma in man and their increase during viral infection.

Natural antibodies to IFN-gamma were found in healthy individuals ranging from newborn babies to adults and, at higher levels, in patients suffering from different viral infections. During a viral infection, the titer of anti-IFN-gamma antibodies was observed to be correlated with the stage of the disease. Antibodies specific to IFN-gamma were affinity purified both from sera taken from healthy individuals and sera from viral-infected patients, by using a rIFN-gamma-coupled CNBr-activated Sepharose 4B column. The antibodies were found to be of the IgG class, and maintained their ability to bind rIFN-gamma. They were then tested for neutralizing activity and none of the IgG preparations we analyzed impaired the antiviral activity of rIFN-gamma. This finding suggests that the antigenic determinants recognized by these antibodies on the IFN-gamma molecule are located outside the site, on the IFN-gamma molecule, responsible for its antiviral activity.

Age Factors↗
PubMed1990

Interferon-gamma marks activated T lymphocytes in AIDS patients.

Lymphocytes expressing interferon-gamma (IFN-gamma) on their surface were evaluated in 61 patients, all IV drug abusers, infected with human immunodeficiency virus type 1 (HIV-1), and in 85 healthy subjects (61 of whom were blood donors and 24 HIV-1 seronegative IV drug abusers). Data obtained demonstrated that IFN-gamma-expressing T lymphocytes, mostly CD8+ cells, were present in HIV-1-infected patients, and that their percentage, always higher in HIV-1-infected patients than in healthy subjects (p less than or equal to 0.001), increased with progressive stages of HIV-1 infection. At the same time other markers of T-cell activation, namely interleukin-2 receptor (rIL-2), transferrin receptor, and HLA-DR were also found to be positive in some of the HIV-1-infected subjects. The presence in the HIV-1-infected patients of activated CD8+ T cells, which are resistant to HIV-1 infection, may suggest that these cells are able to respond to continuous and progressive viral expression (HIV or/and other viruses) and may be a component of the specific response to HIV-1.

Acquired Immunodeficiency Syndrome↗
PubMed1990

A salivary vasodilator in the blood-sucking bug, Rhodnius prolixus.

1. Salivary gland homogenates of the blood-sucking bug, Rhodnius prolixus induced transient, dose-dependent relaxation of rabbit aortic preparations pre-constricted with 200 ng ml-1 noradrenaline, 1 microgram ml-1 histamine or 20 ng ml-1 angiotensin II. Such relaxations were less marked when the aorta was constricted by 60 mM KC1. These effects were observed with as little as 0.2 microgram ml-1 of crude salivary gland protein. 2. The vasodilator effect was endothelium-independent, abolished by 50 microM hydroquinone or 50 microM methylene blue, and potentiated by 30 mu ml-1 superoxide dismutase. 3. Salivary homogenates generated a coloured compound when reacted with sulfanilic acid in the presence of N-(1-naphthyl)-ethylediamine, indicating the presence of reactive nitrogen groups, equivalent to 35 +/- 3 ng of sodium nitrite per pair of glands. 4. Molecular sieving high performance liquid chromatography of salivary gland homogenates generated a single peak of vasorelaxant activity which coincided with the presence of platelet antiaggregating and spasmolytic (guinea-pig ileum contracted with histamine) activities, as well as with reactive nitrogen groups. 5. It is concluded that a protein of molecular weight 16.500 daltons in the salivary glands of R. prolixus contains reactive nitrogen groups which assist the bug during a blood meal. It is suggested that saliva of blood sucking anthropods is a natural resource of novel pharmacological activities.

Animals↗
PubMed1989

Antibacterial activity of the new carbapenem meropenem (SM-7338) against clinical isolates.

The in vitro antibacterial activity of the new carbapenem antibiotic meropenem (SM-7338) against 567 clinical isolates was evaluated. SM-7338 exhibited activity against a broad spectrum of organisms, including aerobes and anaerobes, and was superior to the other beta-lactam drugs tested (piperacillin, cefotaxime, ceftazidime, ceftriaxone, cefoxitin). SM-7338 was more active than imipenem, gentamicin and amikacin against Enterobacter cloacae and Pseudomonas aeruginosa. SM-7338 was less potent than imipenem against staphylococci and enterococci, but the activity of the two antibiotics against anaerobes was similar. SM-7338 and imipenem showed a high bactericidal activity at a concentration of 2-4 x MIC.

Anti-Bacterial Agents↗
PubMed1989

Production of hyperalgesic prostaglandins by sympathetic postganglionic neurons.

Prostaglandin E2 and prostacyclin (prostaglandin I2) produce hyperalgesia in animals and humans. Because there is evidence that prostaglandins contribute to pain maintained by sympathetic nervous system activity, we evaluated whether sympathetic postganglionic neurons synthesize these hyperalgesic prostaglandins, and whether production of prostaglandins by these neurons can contribute to sensitization of primary afferent nociceptors. Intradermal injection of arachidonic acid but not linoleic acid, in the rat hindpaw, produces a decrease in mechanical nociceptive threshold. This hyperalgesic effect is prevented by indomethacin, an inhibitor of prostaglandin synthesis or by prior surgical removal of the lumbar sympathetic chain. To test the hypothesis that sympathetic postganglionic neurons are the source of prostaglandins, we measured production of prostaglandin E2 and 6-keto-prostaglandin F1 alpha (the stable metabolite of prostacyclin) by homogenates of adult rat sympathetic postganglionic neurons from superior cervical ganglia. These homogenates produced significant amounts of prostaglandin E2 and 6-keto-prostaglandin F1 alpha, and most of this production is eliminated by neonatal administration of 6-hydroxydopamine which selectively destroys sympathetic postganglionic neurons. These results demonstrate that sympathetic postganglionic neurons produce prostaglandins, and supports further the hypothesis that the release of prostaglandins from sympathetic postganglionic neurons contributes to the hyperalgesia associated with sympathetically maintained pain.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Expression of gamma interferon on circulating lymphocytes in viral infections.

Peripheral blood lymphocytes from a total of 111 patients and 40 healthy individuals were studied for gamma interferon (IFN-gamma) expression on their surfaces by indirect immunofluorescence assay and flow cytometry, with a new anti-IFN-gamma monoclonal antibody (IGMB-14) as a specific reagent. Of 64 patients with proven acute viral infections, 59 had a significantly higher percentage of lymphocytes expressing IFN-gamma on their membranes than healthy individuals did. On the other hand, only 3 (8.9%) of 34 patients with proven bacterial infections had an increased percentage of IFN-gamma-expressing lymphocytes. None of the eight patients with other infections and none of the five with systemic lupus erythematosus showed an increased percentage of IFN-gamma-positive lymphocytes. The percentage of IFN-gamma-expressing lymphocytes during a viral infection was found to be related to different stages of the disease. Finally, some applications of this rapid IFN-gamma assay method in viral diseases are discussed.

Adolescent↗