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Biomedical subjects

M Orlandi

Publications and source records attributed to M Orlandi.

At least 73 records · Page 4Linked to original sources
PubMed1986

Are the vascular complications of diabetes mellitus preceded by an altered thromboxane/prostacyclin plasmatic ratio?

Although many data regarding the biosynthesis of thromboxane A2 and prostacyclin in diabetes mellitus have recently appeared in the literature, it is not clear whether an imbalance between the generation of the two prostaglandins might be connected to the vascular complications of diabetes. In the present review we have tried to emphasize the most significant aspects of these studies and we have focused on alterations of platelet prostacyclin receptors and on the effects of circulating immune complexes on platelets of diabetics. It is likely that studies on the release of platelet derived growth factor as well as more precise definitions of its action on vessel wall cells leading to a massive release of prostacyclin, will permit us to ascertain whether an alteration in prostaglandin ratio is linked to the genesis of the vascular complications in diabetics.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Prostaglandin and thromboxane biosynthesis in resting and activated platelet-free monocytes from aged subjects.

The main cyclo-oxygenase-dependent arachidonic acid (AA) derivatives, i.e. prostaglandin E2 (PGE2) and thromboxane A2 (TXA2), have been measured by radioimmunoassay in platelet-free cultures of human monocytes from young and old subjects, in presence and in absence of activating substances (10% fetal calf serum). No difference was found between cells from the two groups as far as the production of PGE2 and TXB2 (stable metabolite of TXA2) was concerned, at variance with reported data in young and old experimental animals. The addition to the cultures of exogenous AA caused a reorientation of cyclic endoperoxide metabolism resulting in a consistent decrease of the ratio TXB2/PGE2, but only in monocytes from young subjects. The data are discussed with respect to the claimed role of prostaglandins in the age-related immune derangement which is present in aged humans.

Adult↗
PubMed1986

Neoadjuvant chemotherapy for high grade osteosarcoma of the extremities: is a good response to preoperative treatment an indication to reduce postoperative chemotherapy?

Sixty-five patients with high grade central localized osteosarcoma of the extremities were treated according to a neoadjuvant chemotherapy schedule that was comprised of two methotrexate (MTX) cycles (high or moderate dosage) i.v. followed by cisplatinum (CDP) (continuous i.a. infusion for 24 hours). Thirty-four "good" responders (necrosis greater than 90%) were divide in two groups for post-operative treatment. The first group was treated for a short period (4 weeks) with i.v. MTX-CDP; the second group was treated for a longer period (24 weeks) with i.v. MTX-CDP and also adriamycin. Patients in the second group had far better results than the patients in the first group (19/19 vs. 5/15 continuously disease-free patients). Our results following this protocol indicate that even if patients are "good" responders to this neoadjuvant chemotherapy they should not undergo a shortened post-operative treatment, and the protocol should include adriamycin.

Adolescent↗
PubMed1985

Prostaglandin and thromboxane biosynthesis in isolated platelet-free human monocytes. I. A modified procedure for the characterization of the prostaglandin spectrum produced by resting and activated monocytes.

We have developed a technique to isolate monocytes from human peripheral blood. The technique takes special care of completely eliminating platelets which are usually present in other preparations. Monocytes obtained in good yields (2.5-5.0 X 10(5) cells/ml blood), were found to be 70-80% pure on the basis of morphological and histochemical criteria. Contamination was largely due to the presence of lymphocytes. Monocytes were incubated in the presence or absence of arachidonic acid and TXB2, PGE2 and 6-keto-PGF1 alpha were measured by specific and sensitive radio-immunoassays. It was found that when cells were incubated for up to 1 hr, the production of PGs was low or absent even in the presence of 10 microM arachidonic acid in the incubation medium. However, when incubations were carried out for 24 hrs in the presence of at least 1% fetal calf serum a dramatic increase in TXB2 production occurred, with levels as high as 150 ng X 10(6) cells. The ratio TXB2/PGE2 was around 3, while 6-keto-PGF1 alpha was produced at a much lower level. In the same conditions, when care was taken to evaluate PGs already present in fetal serum and/or cross reactivity due to media generally employed, purified human lymphocytes appeared unable to produce detectable levels of the three PGs tested.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Platelet aggregation and evaluation of the ratio thromboxane B2/6-keto-prostaglandin F1 alpha in the plasma of patients on long term cimetidine treatment.

It has been reported that a long term treatment with cimetidine may give rise to thrombotic complications and may cause reversible damage to blood cells. In 57 patients on long term cimetidine treatment, platelet aggregates, platelet aggregation in vitro, plasma 6-keto-PGF1 alpha/thromboxane B2 ratio and platelet cyclic AMP levels were assessed. In 52% of the patients, platelet aggregate ratios were abnormal and collagen and ADP-hypersensitive platelets were observed. Such alterations began occurring after the first month of therapy and were shown to worsen progressively during the administration. Four of these patients, who developed unexpected thrombotic compliances after about 7 months of therapy, showed higher than normal plasma thromboxane B2, lower plasma 6-keto-PGF1 alpha and two of them, lower platelet cyclic AMP concentrations. It is suggested that cimetidine, through an unknown mechanism which probably involves activation of endogenous cyclic AMP phosphodiesterase, may favour the action of platelet aggregating agents.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

[Is it useful to correct the immunological deficit in cancer patients? And with what modality?].

A certain degree of immunodepression appears to be present in some neoplastic patients. Many factors such as age and nutritional and hormonal state (particularly thymic factors and locally-acting hormones like prostaglandins of E series) are involved in this phenomenon. The literature shows that all these factors are very important in neoplastic processes and might strikingly contribute also to the extent of immunodepression observed in neoplastic patients. Moreover, the HLA genotype seems to effect the efficiency of the antineoplastic treatments. The authors think that immunodepression in neoplastic patients might be improved by immunomodulators such as zinc ions, thymic hormones and, possibly, inhibitors of prostaglandins of E series.

HLA Antigens↗
PubMed1984

[The cost of energy and cardiovascular expenditure in basketball players during a game].

Energy expenditure was evaluated for 6 Basket players while exercising on a cyclergometer. Oxygen consumption (VO2), pulmonary ventilation (VE), heart rate (HR), respiratory quotient (QR) and other parameters were estimated at various levels of load (25 Watt each step of 3 minutes duration), till to submaximal load of 175 Watt. The same subjects participate to a regular Basket game and their heart rate was continuously stored on a tape recorder (Holter). Arterial blood pressure was also taken whenever possible (timeout, etc). From the laboratory and field data, estimates were made for the oxygen consumption together with energy cost of the game. This can be assume a net value of 0.1339 Kcal X Kg-1 X min-1.

Blood Pressure↗
PubMed1983

Direct determination of distribution volume and disappearance rate of native creatine kinase in humans.

Distribution volume (DV) and disappearance rate (Kd) of native creatine kinase (CK), parameters needed for enzymatic estimation of infarct size, have not been characterized in humans. Values for these parameters have been determined in experimental models and extrapolated for use in humans. During hemodynamic monitoring, 100 to 150 ml of enzyme-rich plasma was collected from 10 patients with acute myocardial infarction, stored at -30 degrees C for a maximum of 6 days, and then rapidly reinfused back to the same patient after return of CK serum activity to baseline levels. After reinfusion, blood samples were obtained at 5- to 15-minute intervals for 2 hours and at 30- to 60-minute intervals for an additional 10 hours. In each specimen, total CK activity and MM-CK and MB-CK concentrations were determined by spectrophotometry and radioimmunoassay. Data were analyzed by either nonlinear least-squares approximation or the noncompartmental approach after baseline subtraction. Concentration of immunologically active molecules appeared to decline in parallel to enzymatic activity. In three patients a double exponential decay was demonstrated. All others exhibited single exponential decay, with a Kd of 0.0023 +/- 0.00057 (SD) min-1. DV averaged 3284 +/- 693 (SD) ml, 5% of body weight. There was no correlation between Kd estimated from terminal portions of CK time-activity curves following infarction and Kd calculated after reinfused plasma. It was concluded that a one-compartment model using values for Kd and a DV compatible with plasma volume is suitable for clinical application, and that true Kd cannot be determined from the terminal portion of CK time-activity curves after acute infarction.

Blood Transfusion, Autologous↗
PubMed1983

Plasmatic TXB2 and 6-keto-PGF1 alpha levels during charcoal hemoperfusion in chronic renal failure patients.

6 patients with end-stage renal disease underwent hemoperfusion with charcoal columns, for 60 min. Blood samples anticoagulated with 2% EDTA/aspirin solution were obtained from arteriovenous fistulas in the basal condition, 5 min after a bolus injection of heparin (7,500 U), at the end of hemoperfusion, and 30 min after. The study was repeated few days later, in the same patients, two hours after 100 mg aspirin by mouth. TXB2 and 6-keto-PGF1 alpha were assayed with RIA in unextracted (U) and extracted (E) and chromatographed platelet poor plasma (PPP). Platelet counts before and after hemoperfusion were also performed. Low levels of the two prostaglandins were found in plasma; this could be related to the procedures for collection and processing of plasma samples; no significant differences were observed between extracted and unextracted samples: there were slightly higher levels of 6-keto-PGF1 alpha in unextracted samples. After charcoal hemoperfusion there was only a slight and not significant increase of TXB2 and 6-keto-PGF1 alpha; low dose aspirin did not modify significantly plasma levels of the two prostaglandins before hemoperfusion but it reduced TXB2 and 6-keto-PGF1 alpha levels after charcoal hemoperfusion. The platelet count fell (-22%) after charcoal hemoperfusion with heparin alone and in similar manner after low-dose aspirin pretreatment (-24%, 7%).

6-Ketoprostaglandin F1 alpha↗
PubMed1979

Is a slow reacting substance-like compound involved in rat platelet agglutination.

Endoperoxide analogs at doses 100-fold higher than those required to aggregate human platelet-rich plasma (PRP), were ineffective on rat PRP. Indomethacin (20 microM) and imidazole did not affect arachidonate-induced aggregation of rat PRP. On the other hand, prostaglandin (PG) E1 inhibited aggregation at doses similar to those effective on human PRP, while high doses of PGI2 failed to inhibit arachidonate aggregation in the rat. Eicosatetraynoic acid (10 microgram) blocked the second phase of aggregation; the Ca2+-ionophore A 23187 potentiated the arachidonate effect. Thus, it appears that endoperoxides or thromboxane A2 may not be involved in rat platelet aggregation and that the formation of aggregants from arachidonate shares many properties with the biosynthesis of slow reacting substance, a metabolite of arachidonic acid containing a sulphate group. To test this, rat PRP was incubated with labeled sulphate and aggregated with arachidonate. After column and thin layer chromatography a labeled lipid was identified having a mobility higher than phospholipids but lower than PGF2 alpha. Treatment with arylsulphatase decreased radioactivity by at least 70%.

Adenosine Diphosphate↗
PubMed1978

[Long term electrophysiological study on patients with acute myocardial infarction and complete heart block. Is cardiac pacing always necessary? (author's transl)].

UNLABELLED: Of 335 consecutive patients (pts) admitted to the coronary care unit (CCU) for acute myocardial infarction (AMI), 34 (10%) evidenced complete heart block (HB). The overall inhospital mortality was 14% (47 pts) versus 39% of the HB group (13 pts). No previous conduction disturbances were documented in 58% of pts before appearance of complete HB. Complete HB was preceded in 52% of pts by first or second degree HB or bundle branch block. Of 21 pts with HB discharged from the hospital, 5 (23%) died between 5 and 24 months (mean 12): no patients had sudden death; 16 pts (76%) are still alive after 13 to 45 months (mean 30). His bundle electrophysiologic (HBE) study was performed in 10 pts of the HB group after 4 to 40 months: 4 pts with anterior versus 6 with inferior AMI. Conduction disturbances were no longer present in all but one pt who had H-V 60 msec. Ajmaline (50 + 50 mg iv) prolonged A-H over 130 msec in 4 pts; H-V was not significantly increased in 8 of the 10 pts, while in two pts was 100 msec. One pt in the acute phase and one pt 12 months later, required pacemaker (PM) implant (both had inferior MI). IN CONCLUSION: no sudden death was documented during the follow-up period. The late HBE study, before and after ajmaline, did not allow to recognize critical conduction abnormalities suggessting prophylactic PM implantation.

Adult↗