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Biomedical subjects

J Pascual

Publications and source records attributed to J Pascual.

At least 361 records · Page 20Linked to original sources
PubMed1988

Localized CNS brucellosis: report of 7 cases.

Seven patients with brucellar infection localized in the central nervous system (CNS) are reported. This series represent 3.5% of all brucellosis cases in our hospital. There was a conspicuous absence of systemic signs and symptoms. The clinical course was characteristically protracted. Meningitis (acute, chronic, transient and recurrent) and progressive myeloradiculopathy were the 2 clinical patterns. Cranial nerve neuropathy was frequent, eight nerve involvement being present in 4 cases; transitory ischemic attacks and subarachnoid haemorrhage occurred in 2. Routine laboratory determinations were negative or non-specific. Cerebrospinal fluid (CSF) findings included hypoglycorrhachia, lymphocytic pleocytosis and hyperproteinorrhachia. There was also a remarkable increase in the gamma-globulin and IgG values with morphology of oligoclonal bands in CSF electrophoresis. Brucella agglutination titers were low or absent in serum and/or CSF. By contrast, Coombs tests were always positive and higher titers were found in serum and CSF. After treatment a persistent CSF positive Coombs test at low titers together with an isolated increase in CSF gamma-globulin and IgG values were detected in cured patients. Brucella blood cultures were negative, but CSF cultures were positive in four cases. Rifampin and doxycycline seems to be the treatment of choice. These agents must be maintained at least for 4 months in order to avoid relapses. Corticosteroids may be helpful at the beginning of treatment. Outcome is generally favourable in this disorder. We conclude that clinical and biological characteristics of localized CNS brucellosis are in accordance with those already described in other types of localized brucellosis.

Anti-Bacterial Agents↗
PubMed1988

Hypersensitivity to calcium associated with an increased sarcolemmal Ca2+-ATPase activity in diabetic rat heart.

Sarcolemmal Ca2+-dependent ATPase activity and the mechanical response to calcium and verapamil were studied in myocardium from normal rats and those with diabetes induced by streptozotocin. Sarcolemmal Ca2+-ATPase activity was increased in diabetic animals, depending on the duration of the diabetes. Both the maximal velocity and the affinity were greater in hearts of diabetic rats compared with normal controls. In insulin treated diabetic hearts the affinity of the enzyme for calcium decreased but the maximal velocity was not modified. The enzyme activity was stimulated maximally by millimolar concentrations of calcium and inhibited by lanthanum chloride. Calcium induced a concentration dependent increase in dF/dt in normal and diabetic hearts, but in diabetes the dose-response curve to calcium chloride was shifted to the left. Verapamil depressed the dF/dt in a concentration dependent manner in normal and diabetic hearts; but the drug was more effective in diabetic than in normal rats. These results suggest that an increase in sarcolemmal Ca2+-ATPase activity may be of critical importance in the hypersensitivity of diabetic heart in the presence of low extracellular calcium and calcium blockade.

Animals↗
PubMed1987

Effects of GABA on gastric acid secretion and ulcer formation in rats.

The effects of gamma-aminobutyric acid (GABA), bicuculline and baclofen, orally and intraperitoneally (i.p.) administered, on the development of stress and pyloric ligation-induced gastric ulcers, were studied in rats. GABA, but not baclofen, significantly reduced the frequency and severity of both models as assessed by ulcer index, incidence and number of ulcers/animal. Gastric protection was dose-related in both experimental models and was completely antagonized by pretreatment with bicuculline methiodide, that blocks peripheral, but not central GABA receptors. All GABA effects were observed after oral and i.p. administration, but inhibition of gastric lesions was greater by the last route. Furthermore, GABA did not affect the acidity or the volume of gastric secretion in pylorus-ligated rats. Consequently its antiulcer activity appears to be mediated by factors unrelated to gastric acid secretion. Since the entry of GABA across blood-brain barrier is greatly restricted it may be concluded that stimulation of peripheral GABA receptors is primarily involved in its antiulcer action.

Animals↗
PubMed1987

Chagasic IgG modifies the activity of sarcolemmal ATPases through a beta adrenergic mechanism.

The effect of anti beta adrenoceptor IgG from chagasic sera upon Ca2+-ATPase and Na++K+-ATPase of myocardial membrane was studied. Chagasic IgG stimulated Ca2+-ATPase and inhibited Na++K+-ATPase activities. Both enzymatic effects of the IgG could be prevented after beta adrenoceptor blockade or after the absorption of chagasic IgG with turkey red blood cells. Isoproterenol acted similarly. These results provide information concerning to the biochemical mechanism, by which an antibody, known to activate adenylate cyclase system coupled to cardiac beta adrenoceptor, produces stimulation of myocardial contractility.

Adrenergic beta-Agonists↗
PubMed1987

Intraventricular haemorrhage complicating a brain abscess.

Intraventricular haemorrhage occurred in a patient with a parietal rim-enhancing mass on computed tomographic scan. At operation a brain abscess was identified and removed. Peptostreptococcus and fusobacterium were isolated, possibly of dental origin. The possible sources of this intracranial bleeding are discussed. A neoplasm should not always be considered in the case of a cerebral ring-enhancing mass complicated with intracranial bleeding; in selected cases, brain abscess should be excluded too.

Brain↗
PubMed1987

The release of phosphate from contracting atria as a parameter of (Na+ + K+)-ATPase activity. Effect of ouabain.

An experimental situation that permits simultaneous evaluation of the mechanical activity and inorganic phosphate (Pi) release by beating atria was developed. It concerned cell membrane integrity and compartmentalization of the cells. The Pi released by isolated rat and guinea pig atria was measured in a physiological salt solution. The preparations were incubated under preload for the simultaneous recording of dF/dt and Pi. The substrate of this reaction was the endogenous ATP. Pi release by atria increased with time. It was stimulated at high K+ concentrations (30 mmol/l) and inhibited at very low ones (1.2 mmol/l). The lack of Mg2+ in the incubation media did not affect it. Ouabain induced different effects upon Pi release; at low concentrations it was increased while at higher ones it was inhibited. The relationship between ouabain concentrations, mechanical responses and liberation of Pi by isolated atria from rat and guinea pig showed that at low concentrations ouabain simultaneously increased dF/dt and Pi release. On the contrary, at high concentrations of ouabain dF/dt decreased, contracture occurred and the Pi release decreased. Isoproterenol, norepinephrine and calcium, at concentrations that increased dF/dt, did not modify Pi release. Different concentrations of potassium and ouabain also modulated the 32P Pi efflux in a fashion similar to that with the Pi released by beating atria. We propose that Pi release by living cells appears to be correlated with manipulations which either stimulate or inhibit (Na+ + K+)-ATPase activity.

Animals↗
PubMed1986

Modification of sarcolemmal enzymes by chagasic IgG and its effect on cardiac contractility.

It has been shown that sera from chagasic patients contain an antibody which binds to beta-adrenoceptors of myocardium and modulates their activity. Chagasic IgG triggered a marked stimulation of myocardial contractility with an increase in intramyocardial cyclic AMP and inhibition of (Na+ + K+)-ATPase activity. Both the mechanical and enzymatic effects of the IgG could be prevented by beta-adrenoceptor blockade or after the absorption of chagasic IgG with turkey red blood cells. In contrast, guinea pig red blood cells were unable to remove the beta-reactivity of chagasic IgG. These findings suggest that the IgG from chagasic patients increases myocardial contractility by behaving as a beta-agonist. This effect is likely related to stimulation of the adenylate cyclase coupled to the cardiac beta-adrenoceptor.

Adenylyl Cyclase Inhibitors↗
PubMed1986

Chagasic IgG binds and interacts with cardiac beta adrenoceptor-coupled adenylate cyclase system.

It has been previously shown that sera from chagasic patients have an antibody specific for beta adrenoceptors, independently of other tissue-reactive antibodies as the EVI (endocardium, blood vessels, interstitium) system, and it is highly specific to other heart diseases. In this paper we demonstrate that the IgG present in chagasic sera was able to bind to beta adrenoceptors of the heart and also to interact with the membrane bound adenylate cyclase complex, inducing stimulation of enzymatic activity. Moreover, this antibody stimulated contractile activity of guinea pig myocardium, that could be blocked by a specific beta adrenoceptor antagonist. Chagasic IgG inhibited the binding of (-)-(3H)-dyhidroalprenolol to a beta-adrenergic receptor of purified guinea pig myocardial membranes behaving as non-competitive inhibitor. This IgG also exerted a non-competitive inhibition upon the mechanical effect of exogenous norepinephrine.

Adenylyl Cyclases↗
PubMed1985

Synthesis of PAF-acether and blood volume changes in gram-negative sepsis.

Gram-negative sepsis was induced in rats by intraperitoneal injection of Escherichia coli. The development of bacterial peritonitis and septicemia was monitored by counting the number of peritoneal cells and by performing cultures of blood samples. Mortality reached a 50% rate when rats were injected with 2 X 10(8) colony-forming units. Rats injected with the doses of bacteria which induced mortality showed a time- and dose-dependent increase of vascular permeability as judged by the presence of abundant peritoneal exudate and by the depletion of the circulating volume. In order to know whether the generation of PAF-acether could be involved in the development of the permeability changes, the formation of this mediator was measured in the peritoneal cells and spleen of animals at different times and in response to different doses of E. coli. Significant amounts of PAF-acether could be obtained preceding the development of blood volume depletion in response to the injection of doses of E. coli which induced both mortality and the development of permeability. These data suggest that PAF-acether might be one of the inflammatory mediators involved in the pathogenesis of the hemodynamic changes observed in endotoxemia.

Animals↗