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Biomedical subjects

M Livio

Publications and source records attributed to M Livio.

At least 55 records · Page 3Linked to original sources
PubMed1980

Arachidonic acid-induced malondialdehyde formation in rat platelets. Kinetic aspects and inhibition by acetylsalicylic acid and indomethacin.

Malondialdehyde (MDA) is a stable product of arachidonic acid metabolism, catalyzed by the enzyme cyclo-oxygenase. The experimental conditions for measuring the kinetic of MDA formation in rat platelet-rich plasma were defined. In platelets stimulated with arachidonic acid MDA formation was almost linear for a limited period of time (between 0 and 2 min) and was concentration-dependent with saturation kinetics. The hyperbolic curves obtained were recast in a linear plot (according to transformation S/V versus S) and straight lines fitting all experimental points were obtained. The apparent Km value of arachidonic acid was 0.49 +/- 0.09 mM and Vmax 1.44 +/- 0.06 nmoles MDA/1.4 x 10(9) platelets/min. The apparent type of inhibition and the relative potency of acetylsalicylic acid and indomethacin on MDA formation were also investigated. Inhibition by both drugs was concentration-dependent, and was much stronger when either drug was preincubated with platelets for 10 min than for 1 min. Analysis of the data by Dixon plots (1/V versus inhibitor concentrations) revealed an apparently competitive type of inhibition. It is suggested that both acetylsalicylic acid and indomethacin inhibit cyclo-oxygenase in platelet-rich plasma by a similar mechanism, not involving covalent binding of either drug to the enzyme.

Animals↗
PubMed1980

Impaired thromboxane production by newly formed platelets after aspirin administration to thrombocytopenic rats.

The in vivo inhibitory effect of aspirin on platelet cyclo-oxygenase is irreversible and lasts for the entire platelet life-span. Reappearance of cyclo-oxygenase activity in blood after aspirin has been proposed as a measure of the formation of new platelets and as an indirect indicator of platelet survival. A delay of 24--72 h in recovery, however, has been observed and it has been suggested that aspirin might also inhibit megakaryocyte cyclo-oxygenase. To test this possibility, aspirin (100 mg/kg) or saline were administered i.p. to rats made thrombocytopenic 2 h later (platelet count less than 5% of basal value) by a specific antiplatelet antiserum. Malondialdehyde (MDA) and thromboxane B2 (TxB2) production by platelets was measured by spectrophotometry and radioimmunoassay respectively, during the period of platelet count restoration. By 24 h after thrombocytopenia was induced, platelet count was about 15% of basal values in control and aspirin-treated rats. However, while in controls MDA and TxB2 production was restored to about 20% of basal values, in aspirin-treated rats less than 5% return of activity was detected. A marked difference between the two groups was still found 96 h after induction of thrombocytopenia, when platelet count restoration was similar. Since aspirin disappeared very rapidly from the circulation, the delay in recovery of cyclo-oxygenase activity supports the hypothesis of a megakaryocyte effect of this drug.

Animals↗
PubMed1980

Haemolytic uraemic syndrome: report of a case and new pathogenetic concepts.

Haemolytic uraemic syndrome (HUS) is a severe clinical condition characterised by thrombocytopenia, microangiopathic haemolytic anaemia and renal impairment [1]. At histological examination hyaline microthrombi occluding terminal arterioles and capillaries are generally found. Other syndromes share major clinical and histological diagnostic criteria with HUS. In particular, there is no method at present which clearly differentiates HUS from thrombotic thrombocytopenic purpura (TTP) [2]. We propose therefore the term thrombotic microangiopathy (TMA) to discuss both syndromes. The pathogenesis of TMA is unclear and many forms of therapy have been attempted without definitive proof of efficacy. The recently reported [3] successful results with exchange transfusion and plasma infusion represented a consistent advance in the management of these diseases. The beneficial effect of these procedures was attributed to replacement of an unknown 'missing' factor in plasma. This finding generated recent observations possibly relevant in understanding the pathogenesis of these diseases.

Adult↗
PubMed1979

Prostacyclin and human foetal circulation.

Tissues from human umbilical cord arteries and placental veins generated much greater prostacyclin activity than vessels from normal adults. High prostacyclin generation could contribute to maintaining the low peripheral vascular resistance typical of foetal circulation in which blood pressure is low despite very high cardiac output.

Adolescent↗
PubMed1979

Bleeding in renal failure: a possible role of vascular prostacyclin (PGI2).

Specimens of venous tissues from a group of 25 patients with chronic uremia and 7 patients with acute renal failure generated significantly higher PGI2-like (platelet aggregation inhibiting) activity than venous tissues from 30 normal subjects. After repeated washings, when this activity could barely be detected in the controls, pronounced inhibitory activity was still evident in samples containing venous tissues from uremic patients. Both prolonged bleeding times and increased PGI2-like activity returned to normal in 4 acute uremic patients on restoration of their renal function. These findings may be relevant to the pathogenesis of bleeding in renal failure.

Acute Kidney Injury↗
PubMed1979

Treatment of the hemolytic uremic syndrome with plasma.

Two patients with the hemolytic uremic syndrome were treated with plasma exchange an infusion: in both cases, the reduced platelet count reverted to normal values and the microangiopathic anemia ceased within a few days. Systemic blood pressure and requirement for antihypertensive drug therapy were also markedly reduced following treatment with plasma. Venousprostacyclin (antiplatelet aggregating) activity was undetectable in both patients before but was restored after treatment with plasma. The plasma samples collected before, but not those collected at various intervals after replacement therapy, had decreased capacity to stimulate prostacyclin activity in rat aortic rings. It is suggested that in patients with the hemolytic uremic syndrome or with other clinical conditions which can be included under this rubric (such as thrombotic thrombocytopenic purpura) a plasma factor is lacking which stimulates prostacyclin activity. Plasma would supply such a missing factor, thus representing a rational treatment for some of the life-threatening manifestations (thrombocytopenia, hemolytic anemia, hypertension) of this severe syndrome.

Antihypertensive Agents↗
PubMed1978

Haemolytic-uraemic syndrome: deficiency of plasma factor(s) regulating prostacyclin activity?

It is suggested that patients with the haemolytic-uraemic syndrome and related disorders (such as thrombotic thrombocytopenic purpura) lack a plasma factor which stimulates prostacyclin (P.G.I2) activity. Normal plasma would supply the missing factor and is a rational treatment for some life-threatening symptoms (thrombocytopenia, haemolytic anaemia, hypertension) of this syndrome.

Anemia, Hemolytic↗
PubMed1978

Platelet aggregation: methodology and physiopathology.

The physiopathological role of platelet aggregation in some thromboembolic and atherosclerotic complications is strongly suggested on the basis of many indirect findings. The qualitative methodological approach to this problem generally used until recently is rapidly giving way to a quantitative, biochemical approach. Platelet aggregation, however, even if expressed in terms of nanomoles of a product obtained in a sophisticated reaction system, will continue to deceive investigators and clinicians who fail to view it in the adequate (although still uncertain) context of rheological and vascular interactions.

Animals↗
PubMed1978

Bleeding in renal failure: altered platelet function in chronic uraemia only partially corrected by haemodialysis.

Bleeding time, blood loss and platelet retention by glass beads, measured by standardized techniques, were significantly altered in a group of 30 non-thrombocytopenic patients with chronic renal failure undergoing maintenance haemodialysis. Bleeding time or blood loss did not correlate with platelet retention either before or after haemodialysis. No correlation could be found between the above tests and a number of biochemical parameters characterizing the uraemic condition. Haemodialysis only partially corrected the abnormal bleeding time, blood loss and platelet retention. These tests were still significantly different after haemodialysis from those of 30 normal subjects. It is suggested that some non-dialyzable material could play an important role in the aetiology of uraemic bleeding.

Adult↗
PubMed1978

Vascular factors in the pathogenesis of uraemic bleeding.

To determine the possible role of vascular factors in the bleeding tendency of uraemic patients, three major factors of the haemostatic system normally present in vascular tissues were studied. Factor VIII-related protein (F VIII) was detected on the vascular intima of 13 patients and 10 normal subjects. Comparable values of plasminogen activator (PA) were found in tissue slices from 7 patients and 7 controls. In contrast, prostacyclin like (PGI2) activity, measured as platelet aggregation inhibitory potency, was significantly higher in specimens from 15 patients with either acute or chronic uraemia than in 10 controls. The latter abnormality, leading to impaired platelet-vessel wall interaction, might contribute to the disturbed haemostasis of uraemic patients.

Adult↗