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Biomedical subjects

C Pirich

Publications and source records attributed to C Pirich.

At least 37 records · Page 2Linked to original sources
PubMed1997

Effect of isradipine on in-vivo platelet function.

In animal studies calcium channel blockers (CCB's) and especially isradipine, a second generation dihydropyridine, interrupt the sequence of events culminating in the formation of atherosclerotic lesions. The effect of 4 weeks isradipine treatment (5mg daily) on blood pressure and in-vivo platelet function (measured with 111Indium-oxine labeled autologous platelets) were investigated in a randomized, double-blind and placebo controlled trial in 40 patients with mild to moderate hypertension and scintigraphically diagnosed active atherosclerotic lesions of the carotid arteries. The average supine systolic/diastolic blood pressure was significantly reduced at the end of the treatment period in the isradipine group (group 1; p < 0.0001) but remained unchanged in the placebo group (group P). The heart rate was not significantly altered in either group. There were no serious side effects. The platelet uptake ratio (PUR) measured over the atherosclerotic region of the carotid artery on 4 consecutive days before and after treatment decreased significantly in group I from 1.20 to 1.15 (within groups: p < 0.0001) but remained unchanged in group P. Platelet survival increased significantly in group I (mean 5.70 hours, lower quartile 4.50, upper quartile 4.50 hours, within groups: p < 0.0001) and remained unchanged in group P. Isradipine has a beneficial effect on in-vivo platelet function as evidenced by a decreased platelet deposition on vascular lesion sites and an associated prolonged platelet survival in patients with hypertension and active atherosclerotic lesions.

Adult↗
PubMed1997

Monitoring of the biodistribution and biokinetics of dysprosium-165 ferric hydroxide with a shadow-shield whole-body counter.

Radiation synovectomy is indicated when conventional pharmacological treatment of chronic synovitis has proved insufficient. In these cases dysprosium-165 ferric hydroxide (DFH) has been demonstrated to be clinically effective. After application of the agent, blood activity measurements and monitoring of activity distribution by gamma camera imaging over the local lymph nodes and the liver are commonly performed for control of possible leakage. In addition, we have used a shadow-shield whole-body counter with a profile facility to evaluate the biokinetics and biodistribution of 165Dy-DFH. Fifteen intra-articular injections were performed in 13 patients who received a median activity of 6.8 GBq (range 0.5-9.9 GBq) 165Dy-DFH. Activity profiles were obtained with the whole-body counter 2, 4 and 6 h after injection of 165Dy-DFH. The doses to non-target organs were calculated using the software MIRDOSE 3. In 10 of 15 treatments, absence of any leakage could be demonstrated. The effect of scattered rays could be observed in 14 measurements. In three patients small amounts of activity could be detected in the urinary bladder and in three patients activity was detected in the local inguinal lymph nodes, while no leakage could be detected by camera imaging. In these cases the individual doses to the bladder were 15 Gy, 65 mGy and 50 mGy, and those to the lymph nodes, 0.54 Gy, 0.89 Gy and 2.41 Gy. The whole-body counter also enabled the monitoring of activity profiles related to more complex pathological structures. In conclusion, using a whole-body counter activity leakage could be detected with much higher sensitivity than by using a gamma camera. The biodistribution of 165Dy-DFH could be determined, and leakage could be localised and related to organs. These results encourage the use of a whole-body counter to identify the site and extent of activity leakage.

Adult↗
PubMed1997

Pulmonary function and symptoms of welders.

OBJECTIVE: As the findings on changes in pulmonary function of welders have been inconsistent, this study aimed to analyze respiratory symptoms and pulmonary function among welders and controls with particular emphasis on small airways dysfunction. METHODS: Cross-sectional analysis, using spirometry and a standardized questionnaire, was used to evaluate 521 participants, 166 of whom (64 welders and 102 controls) were evaluated for pulmonary symptoms, occupational inhalative exposures, leisure time activities, and anamnestic data. RESULTS: The welders reported more pulmonary symptoms than the controls. They exhibited a decreased mean expiratory flow (MEF) at 25% and 50% of vital capacity (MEF25, MEF50) while the other parameters tested (forced vital capacity, forced expiratory volume in 1 s) were unchanged compared with the controls. Multivariate regression analysis revealed that smoking explained the observed variance; only in MEF25 the duration of welding exposure had a significant influence on this parameter. CONCLUSIONS: The significantly reduced flow values among the welders compared with the controls indicates the presence of small airways disease. Differences in smoking habits accounted for more than double the differences in MEF25 than did chronic welding fume exposure, confirming the role of the former as the main risk factor leading to the decline in lung function. Longitudinal studies are needed to evaluate the long-term effects of chronic welding fume exposure, in particular with a view to identifying especially susceptible workers.

Adult↗
PubMed1996

Decreased susceptibility of low-density lipoproteins to in-vitro oxidation after dextran-sulfate LDL-apheresis treatment.

Low-density lipoproteins (LDL)-apheresis is a well established treatment of severe hypercholesterolemia resulting in fast clinical improvement and angiographically proven regression after 6 months of therapy. The underlying mechanisms, beside lipoprotein removal, are still under debate. Recently, oxidized LDL were shown to be of key importance in foam cell formation and atherosclerotic lesion development. We examined the influence of dextran-sulfate LDL-apheresis on the susceptibility of LDL to oxidation in 6 patients (5 males, 1 female, age: 41-60 years) suffering from severe heterozygous hypercholesterolemia or combined hyperlipidemia. LDL-apheresis influenced the oxidizability of LDL by a significant (P < 0.01) prolongation of the median of lag time (min) for LDL samples (before treatment 75, range: 31-176 versus after treatment 129.5, range 45-286). A significant (P < 0.01) difference could be also observed in the amount of conjugated dienes as expressed by the maximum rate in absorbance (before treatment 15.39, range: 5.29-21.22 versus after treatment 20.20, range 12.88-72.33). Thiobarbituric acid reactive substances (TBARS) formation was significantly decreased in LDL obtained after apheresis treatment as compared to pretreatment LDL. Electrophoretic mobility (EM) of LDL obtained before and after LDL-apheresis revealed a significant increase (P < 0.05) from a mean of 8.8 +/- 0.5 to a mean of 10.5 +/- 0.5 mm. The titers of plasma autoantibodies against oxLDL (oLAb) which varied considerably interindividually, were not influenced by LDL-apheresis treatment. Levels of F2-isoprostanes, as measured by plasma levels of 8-iso-prostaglandin-F2 alpha (8-iso-PGF2 alpha), reflecting oxidative stress, did not change, either. In summary, our findings provide evidence that even one single dextran sulfate LDL-apheresis treatment decreases LDL-oxidizability, which is an additional beneficial effect to that of lipid lowering.

Adult↗
PubMed1996

Ex-vivo and in-vivo platelet function in patients with severe hypercholesterolemia undergoing LDL-apheresis.

Patients with severe familial hypercholesterolemia (HC) show abnormal platelet function and shortened platelet survival. Atherosclerosis is associated with platelet hyperactivity. Low-density lipoporotein (LDL)-apheresis eliminates the most atherogenic lipid fraction and inhibits the progression of atherosclerosis inducing even regression. In order to assess the influence of LDL-apheresis on platelet function ex-vivo and in-vivo, 6 patients with severe heterozygous HC, all of them being pharmacologically treated with HMG-CoA reductase inhibitors and anion exchange resins were investigated. Ex-vivo platelet function was assessed by the aggregation response to ADP before starting apheresis treatment, as well as after 2 and 24 weeks, respectively. In-vivo platelet function was determined by measuring platelet survival after radiolabeling with 111In-oxine before starting LDL-apheresis and after 24 weeks of twice monthly treatment. LDL-apheresis therapy induced a significant (p < 0.01) drop in cholesterol by 64%, LDL-cholesterol by 77% and in triglycerides by 46% over a period of 24 weeks. ADP-induced platelet aggregation revealed a decreased aggregability of platelets with a decline in the maximal amplitude and the slope of the response curve. Changes in platelet sensitivity to prostaglandins (PG) were significantly for PGI2, but did not reach statistical significance for PGE1. The results revealed a significant (p < 0.001) increase in platelet survival of 111In-oxine-radiolabeled autologous platelets from a mean of 106.50 hours before to 137.50 hours (p < 0.01) after treatment, being accompanied by an increase in labeling efficiency (p < 0.001) and recovery (p < 0.001). These data provide evidence for improved hemostatic regulation in vivo as a result of maintainance of lipid-lowering achieved with LDL-apheresis.

Adult↗
PubMed1996

Passive smoking and platelet thromboxane.

While active smoking is known to enhance platelet thromboxane production, no data on passive smoking is available yet. The influence of single and repeated exposure to passive smoke for 60 minutes in a 18 m3 room was assessed in non-smokers as compared to sex and age matched smokers. All the evaluated measures (malondialdehyde, plasma thromboxane B2, 11-dehydro-thromboxane B2, serum thromboxane B2, conversion of exogenous arachidonic acid to thromboxane B2 and to hydroxy-5, 8,10-heptadecatrienoic acid) were higher in smokers than non-smokers at baseline, immediately and 6 hours after passive exposure to cigarette smoke. Repeated exposure of non-smokers rendered their platelets more activated becoming close to the behaviour of smokers. These results indicate that passive smoking may activate thromboxane A2 release from the platelets, contributing to the development of hemostatic imbalance.

Adult↗
PubMed1996

Apolipoprotein A and biological half-life of prostaglandin I2 in HIV-1 infection.

Disturbances in lipid and lipoprotein metabolism being reported for HIV-1 infection are a common sign of severe infections. Apolipoprotein A being the main constituent protein of HDL has been described to function as the prostaglandinI2 (PGI2)-stabilising factor. PGI2 is not only one of the most potent biological antiaggregatory substances but seems to exert cell-protective properties in the central nervous system, too. PGI2 half-life as well as lipid [total-cholesterol (total-c), triglycerides] and (apo)lipoprotein [LDL-c, HDL-c and apolipoprotein (apo) AI] levels were investigated in 14 HIV-1 positive patients (13 males, 1 female, aged from 29 to 57 yrs). Patients exhibited decreased levels of total-c, LDL-c, HDL-c and apo AI, respectively, while elevated triglyceride levels were observed. PGI2 half-life was shortened (median 53, range: 15-161 seconds) in the patients' plasma as compared with normal controls ranging from 9-12 minutes. In patients with neurological manifestation (n = 8) the decrease of PGI2 half-life (median: 34 seconds, range: 15-67 seconds) was significantly more pronounced (p < 0.05) than in patients (n = 6) with the absence of any central nervous manifestation (median: 83.5, range: 29-161 seconds). The dramatic changes in both HDL-c and apolipoprotein AI as seen during HIV-1 infection are likely to impair PGI2-stabilisation thus being associated with the presence of peripheral neuropathy, dementia and haemostatic imbalance.

AIDS Dementia Complex↗
PubMed1995

Evidence for lipid regression in humans in vivo performed by 123iodine-low-density lipoprotein scintiscanning.

Radiolabeling of autologous LDL allows in vivo characterization of arterial wall lipid metabolism and LDL receptor imaging. Different kinetic types of arterial wall LDL entry reflect the de-, re-, and endothelialized segments in both animals and humans. In 36 male cholesterol-fed rabbits being treated with the calcium channel blocker isradipine (0.3 mg/kg daily), the retention of the radiolabeled (125I-LDL) was reduced, being related to the reduction in arterial wall cholesterol ester content and the decreased extent of Sudan III-positive areas. In parallel, a significant (p < 0.01) increase in vascular prostaglandin I2 (PGI2) generation was seen in endothelialized and reendothelialized segments of the abdominal aorta. These effects were completely abolished by concomitant treatment with acetylicsalicylic acid (ASA). These data could be confirmed in humans, too: a 4-week treatment with prostaglandin E1 (PGE1:5 ng/kg/min iv, 5 days/week, 6 h/day for 6 weeks) and isradipine (2 x 2.5 mg po daily for 4 weeks) did not change arterial 123I-LDL influx kinetics, which were examined over a total of 60 (PGE1) and 96 (isradipine) vascular regions. In contrast to this, the retention of the tracer was significantly diminished in different arterial segments. In isradipine-treated patients, 20 hours after reinjection of radiolabeled LDL, the quantitative LDL entry was reduced by at least 4.7% with a maximum of 23.5% (p < 0.01) in type I (n = 50 lesions) or type II lesions (n = 41). PGE1 treatment induced a 16.9% to 30.7% (p < 0.01) decrease of LDL retention in type I (n = 36 lesions) or type II lesions (n = 24), respectively. These findings support the hypothesis derived from earlier experimental studies that the antiatherosclerotic effects are likely to be due to the increase in PGE1 and/or PGI2 availability mediated by an increase in cAMP. The results demonstrate the potential of 123I-LDL scintigraphy for the characterization of vascular LDL kinetics and the monitoring of functional lipid lesion regression.

Alprostadil↗
PubMed1995

Umbilical arteries of babies born to cigarette smokers generate less prostacyclin and contain less arginine and citrulline compared with those of babies born to control subjects.

OBJECTIVE: The hypothesis of this study was that umbilical arteries of babies born to smoking mothers produce less nitric oxide and prostacyclin than do those of nonsmoking mothers. STUDY DESIGN: L-Arginine, L-citrulline, L-cysteine, and prostacyclin were measured in the umbilical arteries of 11 babies born to smoking mothers and 16 infants born to nonsmoking controls. The concentrations in the two groups were compared with the modified t test. RESULTS: The generation of prostacyclin was reduced in the umbilical arteries of infants of smoking mothers. Similarly, L-arginine and L-citrulline, but not L-cysteine levels, in these arteries were suppressed compared with those of the nonsmoking controls. CONCLUSION: Along with the known direct vasoconstrictive effect of nicotine, nitric oxide and prostacyclin deficiency may affect the uteroplacental blood flow and contribute to the impaired fetal nutrition and increased perinatal mortality of babies born to women who smoke.

Adolescent↗
PubMed1995

Atherogenic risk reduction in patients with dyslipidaemia. comparison between bezafibrate and lovastatin.

OBJECTIVE: To examine the atherogenic risk-reducing effect of bezafibrate and lovastatin. DESIGN, SETTING, PATIENTS, INTERVENTIONS: Double-blind, randomized clinical trial of male and female patients with moderate hypercholesterolaemia with or without hypertriglyceridaemia. Two months dietary treatment followed by 400 mg sustained release bezafibrate every day or 20 mg lovastatin every day for 6 months. Patients recruited (n = 561) and treated (n = 524) by primary care physicians throughout Austria. MAIN OUTCOME MEASURES: Multifactorial assessment of atherogenic risk profile. RESULTS: Bezafibrate increased high density lipoprotein cholesterol by 16%, lovastatin by 10% (P < 0.05). Bezafibrate decreased low density lipoprotein cholesterol by 20%, lovastatin by 27% (P < 0.001). Bezafibrate decreased total cholesterol by 15%, lovastatin by 18% (P < 0.001). Bezafibrate reduced triglycerides by 29%, lovastatin by 13% (P < 0.001); and fibrinogen by 9.4% and 3.0%, respectively. Fibrinogen reduction as a result of bezafibrate administration was dependent on starting levels. The risk ratio cholesterol:high density lipoprotein cholesterol (baseline both 6.1) reduction was 27% in both groups. The low:high density lipoprotein ratio (baseline: 4.1/4.2) reduction reached 31% and 34% respectively. Coronary events' probability (calculated from multifactorial risk functions) were greatly reduced by both agents (41%/33%). Hypertriglyceridaemic patients had a higher initial global coronary risk and profited more from treatment. Bezafibrate was significantly better tolerated (P < 0.001) than lovastatin; most events were gastrointestinal (6 vs 14, ns) or as a result of creatine phosphokinase elevations (3 vs 12, P < 0.05). CONCLUSIONS: Both treatments significantly reduced the risk parameters for developing coronary heart disease, and calculated multifactorial coronary risk was similarly decreased. When selecting a drug for moderate dyslipidaemia and if haemostatic regulation is disturbed, the additional effect of bezafibrate on elevated fibrinogen levels should be considered.

Adult↗
PubMed1995

[AV-block II and arthritis as manifestations of Lyme borreliosis].

A 23-year old patient suffered from transient oligoarthritis and second degree AV block. The diagnosis of stage II systemic Lyme borreliosis was supported by a history of tick bites and the detection of both IgG and IgM borrelia antibodies in the patient's serum. The ECG-findings (bradyarrhythmia and AV block II) were detected several weeks after the onset of arthritis, whilst the patient reported no cardiac symptoms. Treatment was started with ceftriaxone and then continued with doxycycline because of an allergic reaction to the first antibiotic.

Adult↗
PubMed1995

[Thrombocyte function of healthy probands taking 50 mg of acetylsalicylic acid per day].

The antithrombotic effect of acetylsalicylic acid (ASS) is attributed in part to its inhibitory action on platelet cyclooxygenase and, thereby, thromboxane A2 (TXA2) formation. The therapeutic goal of low-dose ASS regimens was the development of a preparation showing a high inhibitory capacity on platelet TXA2 generation whilst leaving vascular prostaglandin I2 (PGI2) synthesis unaffected, thereby minimizing side effects. The effect of a new acid-resistant preparation of 50 mg ASS (Thrombo-ASS 50 mg) on plasma levels of ASS, salicylate, TXB2, 11-dehydro-thromboxane B2, serum thromboxane B2 and malonyl dialdehyde, the conversion of exogenous 14C-arachidonic acid to TXB2 and hydroxy-5,8,10-heptadecatrienoic acid (HHT), as well as on the urinary metabolites 2,3-dinor-6-oxo-PGF1 alpha and 2,3-dinor TXB2, were compared in a crossover trial to those of a marketed preparation (Aspirin 100 mg) in healthy volunteers after a single dose and repeated administration of ASS. While platelet activity was inhibited by both the test and the reference substance to a comparable extent, vascular PGI2 production (as determined by urinary 2,3-dinor-6-oxo-PGF1 alpha excretion) was less affected by the test substance. These findings confirm the claim that a dosage of 50 mg ASS administered daily as an enteric coated or uncoated tablet is sufficient to almost completely block platelet cyclooxygenase, while the respective vascular enzyme is only minimally affected.

Adult↗
PubMed1994

The RED-LIP study--pravastatin in primary isolated hypercholesterolemia--an open, prospective, multicenter trial.

The therapeutic effects of the HMG-CoA reductase inhibitor pravastatin on plasma lipids were assessed in an open, prospective, multicenter trial over a treatment period of 3 months. Of a total of 1111 patients, the overall results were calculated from 715 evaluable patients (352 men and 363 women, mean age: 56.1 +/- 11.3 years) with primary isolated hypercholesterolemia (hyperlipoproteinemia type IIa according to Fredrickson) being at high risk for cardiovascular disease according to the classification of the national cholesterol consensus, whose guidelines are distinguishing between three risk levels (low, moderate, and high, respectively) of total-cholesterol (total-c) as well as LDL-c. The treatment period was preceded by a 3-month dietary counselling phase. Treatment with pravastatin significantly reduced total-c (23.8%, p < 0.001), LDL-c (31.9%, p < 0.001) and triglyceride (16.9%, p < 0.001) levels, concomitantly those of HDL-c were significantly raised (15%, p < 0.001). Pravastatin lowered the total-c/HDL-c ratio by nearly 36% from a mean of 8.1 +/- 2.5 to a mean of 5.2 +/- 1.6. At the end 476 patients (66.6%) received the standard dosage of 10 mg/day whereas 140 patients (19.6%) were recorded to take a dose of 20 mg/day. When comparing those patients (n = 456) having maintained consistently a dose of 10 mg pravastatin per day from week 0 to week 12 with patients (n = 113) who received 20 mg/day from week 4 to 12 similar efficacy was observed in both groups (reduction of total-c: 24.5% vs. 22.2%, n.s., reduction of LDL-c: 33.0% vs. 30.0%, n.s.).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Isradipine increases platelet--low-density lipoprotein binding: evidence from ex-vivo studies in humans.

The effects of isradipine (2.5 mg twice daily) on platelet--radioiodine-labeled [123I] low-density lipoprotein (LDL) binding were measured in 16 hypertensive patients (mean age 46.2 +/- 10.7 years) with (cholesterol > 250 mg/dl; n = 8) and without (cholesterol < 200 mg/dl; n = 8) hypercholesterolaemia during 4 weeks of isradipine treatment after 4 weeks of pretreatment placebo followed by 2 weeks of post-treatment placebo periods. Radioligand LDL-binding studies revealed that isradipine induced a significant (p < 0.001) rise in maximum binding capacity (Bmax) from a mean of 1148.6 +/- 244.3 ng protein/10(9) platelets to a mean of 1262.3 +/- 204.1 ng protein/10(9) platelets [dissociation constant (Kd): 9.7 +/- 4.9 micrograms protein/ml before treatment vs 7.8 +/- 3.7 g protein/ml after treatment]. After the post-treatment placebo phase, both Bmax and Kd returned to baseline levels. When the hypercholesterolaemic patients were compared with the normocholesterolaemics, the former revealed a more pronounced increase in platelet [125I]-LDL-binding capacity. Correspondingly, the dissociation constant showed a significantly (p < 0.05) greater decrease. In accordance with these results, both total and LDL cholesterol were reduced after 4 weeks of therapy with significant (p < 0.03) rises through to the end of the post-treatment placebo period. It is suggested that the observed increase in high-affinity platelet--LDL binding with isradipine treatment reflects a state of decreased in-vivo platelet activation, an effect which may be of particular clinical value in hyperlipidaemic patients.

Adult↗
PubMed1994

Isradipine decreases the entry of radioiodine-labelled low-density lipoproteins into the arterial wall.

Experimental studies have demonstrated that isradipine significantly decreases the entry of radioiodine-labelled (125I) low-density lipoproteins (LDL) into the aorta. This study aimed to investigate whether similar effects could be detected in humans as well. Twelve patients (nine men and three women, aged from 35 to 53 years), all of whom had both hyperlipoproteinaemia (either type IIa or type IIb; mean total cholesterol: 296 +/- 25 mg/dl; mean LDL cholesterol: 208 +/- 22 mg/dl) and mild-to-moderate hypertension [mean systolic blood pressure (SBP): 149 +/- 12 mmHg; mean diastolic blood pressure (DBP): 104 +/- 4 mmHg] received isradipine (2 x 2.5 mg). Autologous radiolabelled (123I) LDL was reinjected and a gamma camera used to study the LDL kinetics before (at 20 min, 2 h and 20 h) and after (at the same time intervals) treatment with isradipine. Of interest were those arterial regions that are typically sites of atherosclerotic lesions (carotid artery, femoral artery). Results revealed three different types of LDL kinetics which were not altered by isradipine treatment. The quantitative LDL entry, however, was reduced by at least 4.7% with a maximum of 23.5% (p < 0.01). Only five vascular sites with type III kinetics were detected. These data suggest that isradipine may induce functional regression of atherosclerotic lesions.

Adult↗
PubMed1994

Influence of calcium antagonists on platelet function and vascular prostacyclin production.

It is suggested that calcium antagonists can counteract the process of atherogenesis by influencing different cellular mechanisms, for example, inhibiting cellular migration and proliferation, as well as by having beneficial effects on lipid metabolism and platelet function. In an assessment of the activity of different calcium antagonists in various platelet function tests and prostacyclin (PGI2) synthesis, amlodipine, diltiazem, felodipine, isradipine, nicardipine, nifedipine, nitrendipine and verapamil were tested in vitro for their effects on adenosine diphosphate (ADP)- or collagen-induced platelet aggregation, malondialdehyde (MDA) formation and vascular PGI2 production. Nitrendipine, isradipine and nicardipine were shown to inhibit both ADP- and collagen-induced platelet aggregation at the lowest concentration (0.5 microgram/ml). The half-maximum inhibiting concentration (IC50) of isradipine (4.78 +/- 0.36 micrograms/ml for ADP-induced platelet aggregation) was significantly (p < 0.01) lower than the IC50 of all the other drugs. Nitrendipine, with an IC50 of 44.2 +/- 5.32 micrograms/ml, and nicardipine, with an IC50 of 46.74 +/- 3.83 micrograms/ml, were respectively the second and third most effective compounds. Formation of MDA was also inhibited the most by isradipine, which exerted its inhibitory properties at one-fifth the concentration needed with the other agents: the IC50 of isradipine was 0.98 +/- 0.16 microgram/ml, which was significantly different (p < 0.05) compared with the second most effective agent, verapamil, which had an IC50 of 14.92 +/- 3.78 micrograms/ml. In-vitro PGI2 production was stimulated the most by isradipine as well, producing a significant (p < 0.01) increase to 417.8 +/- 47.6 pg/mg tissue/h (control: 296.4 +/- 17.6 pg/mg tissue/h) at a concentration of 0.5 microgram/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1993

Lipoproteins and prostacyclin stability.

PGI2 is an important local mediator keeping circulating blood cells apart from the vessel wall, thus regulating hemostasis. Alterations of locally available amounts of this compound may be associated with either bleeding or thrombotic events. Factors influencing synthesis, transmission, and degradation coregulate the amount of biologically active PGI2 available at a certain vascular site. Plasmatic T1/2 of PGI2 is shortened either due to an inherited disorder or an acquired disease, its underlying cause being unknown. Generally, this is associated with thrombotic events and extremely low concentrations of both HDL cholesterol and apoA1. In contrast, the only patient we saw with a prolonged PGI2 T1/2 repeatedly experienced extremely severe bleeding complications. Recovery from severe diseases such as shock and malaria, for example, results in normalization of both PGI2 T1/2 and lipoprotein (HDL) and apoA values. Although these findings have not yet been verified at a molecular level, it is likely, that apoA1 contributes to the stabilization of PGI2 in human blood, thus representing one further link between lipid metabolism and hemostasis.

Adult↗