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Biomedical subjects

C Galli

Publications and source records attributed to C Galli.

At least 271 records · Page 15Linked to original sources
PubMed1986

Prostaglandin-induced storage and secretion of esteroproteases in the mouse submaxillary gland.

The submaxillary glands of adult C3H mice which received intraperitoneal injections of prostaglandins F2 alpha and E2 (PGF2 alpha and PGE2) were examined biochemically and ultrastructurally. Results indicated that the specific activity of esteroprotease in an homogenate of submaxillary glands was significantly increased when mice were treated with PGF2 alpha (96 or 480 micrograms/kg), and decreased when they were treated with PGE2 (96 or 480 micrograms/kg). Ultrastructural findings were correlated with these biochemical data. Thus, it appeared that PGF2 alpha stimulated the secretion and synthesis of bioactive proteins, and that PGE2 stimulated only the secretion.

Animals↗
PubMed1985

Heated fat, vitamin E and vascular eicosanoids.

A semisynthetic diet containing adequate amounts of vitamin E and 10% (w/w) of a mixture of polyunsaturated oils subjected to heating and characterized by elevated indexes of thermal alteration (polar component, dimer triglyceride, altered triglyceride contents and reduced alpha-tocopherol levels) was fed to growing male rats for a period of eight weeks. It resulted in a selective alteration of the production of vascular eicosanoids (elevation of platelet thromboxane formation and decrease of vascular prostacyclin release) compared to the values found in rats fed a diet containing a fresh mixture of polyunsaturated oils. Major nutritional parameters, plasma lipids and the fatty acid profiles of plasma, liver and heart lipids were not different in the two groups of animals. Supplementation of an excess vitamin E (300 mg/kg) to the diet containing heated fat neutralized the adverse effects of heated fat on vascular eicosanoid production.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Oral polyunsaturated phosphatidylcholine reduces platelet lipid and cholesterol contents in healthy volunteers.

The effects of orally administered polyunsaturated phosphatidylcholine (PPC) on plasma lipids, lipoproteins and platelet function and composition were studied in seven healthy male volunteers. PPC (Nattermann & Cie, GmbH, Cologne, Federal Republic of Germany), 10 g/day, was given for a 6-week period after a 4-week wash out; laboratory tests were repeated after a further 4-week period after the end of treatment. PPC did not appear, during treatment, to modify the levels of plasma total cholesterol and triglycerides. High density lipoprotein (HDL) cholesterol levels were, however, increased after six weeks of PPC. The most dramatic changes occurred in platelet membrane composition: the total lipid/total protein and the cholesterol/protein ratios were reduced significantly, whereas increases of the phospholipid/total lipid ratio and of the linoleic acid membrane content were observed. Platelet function tests, both in whole blood and in platelet rich plasma, were not modified. Similarly, the thromboxane B2 formation after standard stimuli and the sensitivity to exogenous prostaglandin I2 also were unchanged. During the final wash out period following treatment, a reduction of plasma total and low density lipoprotein (LDL) cholesterol levels also was recorded. PPC appears to be capable of modulating lipid exchanges between cell membranes and the plasma compartment.

Administration, Oral↗
PubMed1985

Differential effects of various vasoactive drugs on basal and stimulated levels of TXB2 and 6-keto-PGF1 alpha in rat brain.

Thromboxane B2 and 6-keto-PGF1 alpha (6KPGF1 alpha), the major stable metabolites of thromboxane and prostacyclin, are present in the CNS, where they appear to be mainly produced within and/or acting upon the vascular district. Their concentrations are of few pg/mg protein in rat brain cortex of animals sacrificed by microwave (MW) radiation, procedure which inactivates tissue enzymes and allows the determination of endogenous "basal" levels of eicosanoids. Levels of 6KPGF1 alpha and especially those of TxB2 increase several fold over the basal values in brain cortex of animals sacrificed by decapitation followed by a few minute interval before analysis (post-decapitation ischemia, PDI). Pretreatment of animals with the vasoactive drug papaverine, resulted in elevation of brain basal levels of 6KPGF1 alpha and with the carbochromene derivative AD6 in reduction of basal levels of TxB2, whereas the calcium antagonist nifedipine and dipyridamole did not modify basal levels of the two eicosanoids. Treatments with papaverine and AD6 reduced the accumulation of TxB2 and enhanced that of 6KPGF1 alpha occurring after PDI, to different extents, both resulting, however, in reduction of the TxB2/6KPGF1 alpha ratio. Nifedipine instead, decreased the release of both eicosanoids and resulted in elevation of the TxB2/6KPGF1 alpha ratio, whereas dipyridamole had no effect. In conclusion, the evaluation of the overall effects of drug treatments on the TxB2/6KPGF1 alpha ratio in cerebral tissue, provided useful informations on the pharmacological modulation of vascular eicosanoids in this district.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Effects of acute and chronic ethanol administration on thromboxane and prostacyclin levels and release in rat brain cortex.

The effects of acute (3 g/kg i.p. two hours before sacrifice) and chronic (6% in drinking water and libitum for 15 days) ethanol administration to male rats (200 g body weight) on basal levels and release of TxB2 and 6-keto-PGF1 alpha in brain cortex were studied. Also the effects of chronic ethanol (30 days) on the fatty acid composition of brain cortical tissue and liver phospholipids were investigated. Acute treatment reduced basal levels of 6-keto- PGF1 alpha in brain cortical tissue (rats sacrificed by microwave radiation) and decreased the accumulation of 6-keto-PGF1 alpha in brain cortex after post-decapitation ischemia (PDI). Basal TxB2 levels were also reduced in brain cortex, but TxB2 release during PDI was enhanced. Chronic treatment (15 days) induced changes of TxB2 and 6-keto-PGF1 alpha levels and release during PDI in brain cortex less pronounced than those observed after acute treatment. The reduced effectiveness of chronic ethanol on brain vasoactive eicosanoids suggest adaptation processes. After chronic treatment (30 days), the fatty acid composition of brain cortex total phospholipids were not significantly modified. Changes of eicosanoid production after ethanol were thus independent from modifications of the fatty acid precursor pool(s). Ethanol-induced changes in the production of vascular eicosanoids in the CNS may be of relevance to the action of the compound on the CNS and may also have implications for the clinic.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Platelets from aged rats aggregate more, but are more sensitive to prostacyclin.

The balance between vascular eicosanoids has been explored in young (1 month of age) and aged (11 month of age) rats. PRP from mature rats was more reactive to collagen (lower threshold, greater amplitude of aggregation curve and higher TxB2 formation) than PRP from young animals. Release of 6-keto-PGF1 alpha from PRP-perfused isolated aortas (pg@ul) was higher and the inhibition of PRP aggregation after perfusion correspondingly greater, in mature rats. Platelets from aged rats were more sensitive to exogenous prostacyclin (higher inhibition of aggregation and greater accumulation of cAMP). The fatty acid compositions of plasma and platelet lipids were not different in the two age groups. Compensatory mechanisms were operating in the aged rats, counteracting the greater platelet aggregability with higher vascular prostacyclin production and greater sensitivity of platelets to this eicosanoid.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Costs and benefits of the passive prophylaxis of hepatitis B in an Italian hospital.

The authors report the clinical results and the cost/benefit analysis of a protocol of passive prophylaxis of hepatitis B based on the administration of two doses of three ml each of HBIG and on the control of anti-HBs levels by RIA for six months after accidental exposure in health-care personnel. Only two out of 351 susceptible subjects developed viral hepatitis instead of the expected 70 if passive prophylaxis had not been performed. The cost/benefit analysis showed a saving of 356 509 US$ in the past 36 months. Furthermore, the cost of each case of hepatitis prevented was 2194 US$, whereas the cost of one case of acute, benign hepatitis was 6180 US$. Since a saving of 3.39 US$ for each dollar spent is achieved, this protocol of passive prophylaxis appears more than adequate both clinically and economically. It is believed that the adoption of some general prophylactic measures will further stress the advantages of this procedure.

Adult↗
PubMed1985

Modification of brain vascular eicosanoids after pharmacological treatment and ischemia in the rat: drugs and brain vascular eicosanoids.

Vascular eicosanoids (E) thromboxane (measured as T X B2) and prostacyclin (measured as 6-keto-PGF1 alpha) may modulate hemodynamic parameters in brain circulation. We have studied (a) the effects of the administration of vasoactive drugs, in the rat, on T X B2 and 6-keto-PGF1 alpha levels and release in brain cortex, and (b) changes of brain vascular E levels during hypoxia and recovery, in the same animal species. Administration of vasoactive drugs (papaverine, dipyridamole, the carbochromene derivative AD6 and nifedipine) to rats resulted in differential effects on endogenous levels and post-decapitation release of both compounds. Reduction of the T X B2/6-keto-PGF1 alpha balance in brain cortex was obtained with papaverine and AD6, whereas nifedipine reduced 6-keto-PGF1 alpha more than T X B2. During hypoxia there was no significant modification of brain vascular E, but during recovery both compounds were decreased. Thus pharmacological treatments during recovery from hypoxia may normalize brain vascular E levels.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

[Nifedipine as a vasodilator antihypertensive with a rapid action].

On occasion, blood pressure rises so precipitously and severily, or the clinical setting in which hypertension occurs is so critical, that prompt pressure lowering becomes crucial to prevent disabling, or even lethal complications. Such hypertensive emergencies more commonly complicate the accelerated phase of untreated or poorly treated hypertension of various etiologies. There is also a group of conditions that qualify as hypertensive emergencies not so much because of the actual height of the pressure, but rather because of complicating disorders that make even moderate pressure elevation harmful. These include aortic dissection, intracranial bleeding and acute left ventricular failure. Two fundamental concepts in the management of hypertensive emergencies are: immediate and effective therapy is required and takes precedence over time-consuming diagnostic procedures; the choice of the drugs will depend on how their time course of action and hemodynamic and metabolic effects meet the needs of the clinical situation. It is well proven that nifedipine reduces Ca-dependent vascular smooth muscle tone by direct interference with transmembrane Ca supply and thereby counteracts every kind of contractile tension development of the vascular wall: the higher the wall tension, the easier relaxation in induced by a given concentration of the compound. Because of this, it has become quite clear from recent studies that: nifedipine is a potent antihypertensive agent.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Gland Neoplasms↗
PubMed1985

Retroperitoneal nodal aplasia, asplenia, chylous effusion and lymphatic dysplasia: an acquired immunodeficiency syndrome?

Two adult patients (one in Italy and the other in the USA) are described with similar findings of paraaortic nodal aplasia, asplenism, multiple serous and chylous effusions, and retroperitoneal lymphatic dysplasia. Although the clinical courses are incomplete, this unusual constellation of signs in the setting of normal peripheral lymph trunks suggest an acquired rather than inborn anomaly and possibly a variant acquired immunodeficiency syndrome.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Fractionation and characterization of hydatid fluid antigens with identification of an antigen similar to human serum albumin.

Human and sheep hydatid fluids were separated by ultrafiltration, gel chromatography and immunoabsorption into several immunogenic fractions in which both parasite antigens and host substances were present. The immunological characterization of proteic antigens was carried out by immunodiffusion and immunoelectrophoresis with rabbit and ram antisera. A line of identity was observed between a human fraction (labelled as III) and a sheep fraction (labelled as 2B). Further evidence of the presence of a parasitic antigen in fraction III was given by its reaction against an antiserum from ram directed against sheep fraction 2B. The immunological characterization of fraction III indicated a close similarity between human serum albumin and parasitic antigens.

Animals↗
PubMed1984

Sex differences in platelet thromboxane and arterial prostacyclin production in control and n-6 fatty acid supplemented rats.

Sex differences in eicosanoid production in platelets and vessel walls have been studied in control and n-6 fatty acid supplemented rats. In platelet rich plasma (PRP) of control female rats, arachidonic acid (AA) levels in phospholipids (PL), thromboxane B2 (TxB2) formation following collagen stimulation and aggregatory responses to collagen were higher than in PRP of male rats. 6 keto PGF1 alpha release from PRP-perfused isolated aortas were the same for both sexes, but the antiaggregatory activity of the wall was higher in males than in females, in association with a greater sensitivity of male platelets to prostacyclin. The administration of n-6 fatty acid supplements increased AA level in PL, TxB2 production and aggregation only in male platelets. Production of 6 keto PGF1 alpha and the antiaggregatory activity of aortic walls were reduced after dietary treatment in males, but biochemical and functional parameters were not correlated in females. The results indicate complex sex-related differences in fatty acid metabolism and eicosanoid production, and in responses to n-6 dietary fatty acids in platelets and the vascular system in the rat.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Calcium-channel blockade with nifedipine and angiotensin converting-enzyme inhibition with captopril in the therapy of patients with severe primary hypertension.

Nifedipine (10 mg qid) and captopril (25 mg qid) were tested alone and in combination in 14 patients suffering from severe primary hypertension. Each study period was of 1 week's duration. Circulatory response was evaluated through hourly pressure and pulse rate readings. The fall in pressure after oral nifedipine was maximal within 1 hr or less and was generally accompanied by palpitation and increase in pulse rate; with a six hourly dosing regimen the tendency of blood pressure to recover after each dose was interrupted by the next dose, so that values remained significantly reduced throughout the 24 hr, although pressure fluctuations were evident. Promptness of the antihypertensive action of captopril was similar, but the magnitude and the duration of the fall in pressure were less pronounced. When the converting-enzyme inhibitor was combined with the calcium-channel blocker, pressure fluctuations were not abolished, but the antihypertensive response was definitely enhanced, so that normal blood pressure was maintained for several hours during the day. Additional positive effects of captopril were mitigation of the heart rate reaction and prevention of the ankle pitting or edema elicited by nifedipine. A balance in arteriolar and venular dilatation promoted by captopril is the suggested mechanism for these effects. With the two-drug combination the function of the left ventricle was not reduced and possibly improved; blood urea nitrogen and serum electrolyte and creatinine concentration were not affected. Plasma renin activity increased with captopril and reverted toward baseline with the addition of nifedipine, suggesting an interference of the calcium-channel blocker with the release of renin.

Adult↗
PubMed1984

Acute effects of ethanol, caffeine, or both on platelet aggregation, thromboxane formation, and plasma-free fatty acids in normal subjects.

The acute effects of ethanol (0.5 ml/kg b.w.) and caffeine (200 mg), alone or in combination, on platelet function and plasma lipid-lipoprotein levels, were tested in four healthy volunteers according to a Latin Square design. The effects of ethanol alone on platelet function (adrenaline- and collagen-induced aggregation, thromboxane B2 formation induced by arachidonic acid) were negligible. Conversely, caffeine significantly reduced maximal aggregation of platelets following adrenaline and collagen, 3 hours after administration; it also significantly increased thromboxane B2 formation 1 hour from administration. The intakes of caffeine and, to some extent, of ethanol at doses in the common daily range, although not profoundly affecting platelet function or lipid parameters, should be given consideration when treatments with platelet-active drugs are prescribed.

Adult↗