Diferencias de protección frente al riesgo biológico laboral en relación al sistema preventivo elegido por la empresa / Differences of occupational biohazard protection in relation to preventive system chosen by the company

El objetivo de este trabajo ha sido obtener información sobre el nivel de exposición y protección de los trabajadores a los agentes biológicos laborales en diferentes sectores de actividad valorando sus diferencias en relación al sistema preventivo elegido por las empresas. Se realizó un estudio en el que participaron 590 trabajadores de 59 empresas españolas en las que se pasaron 2 cuestionarios, uno para la empresa y otro para los trabajadores, obteniéndose una muestra definitiva de 518 trabajadores pertenecientes a 51 empresas en las que existía exposición a agentes biológicos. Se encontraron diferencias significativas en la gestión del riesgo biológico laboral en función del sistema preventivo elegido por la empresa concluyendo que la protección a la exposición laboral a agentes biológicos no está desarrollada por completo porque no se dispone de herramientas que permitan su fácil realización y por lo tanto la gestión de los riesgos biológicos general no es adecuada (AU)

The aim of this study was to obtain information on the level of exposure and protection of workers to biological agents at work in relation to the preventive system choosen for the companies. An study in which 590 workers from 59 Spanish companies in which 2 questionnaires were given, one for the company and other for the workers, yielding a final sample of 518 workers from 51 companies in which there is exposure to biological agents. Our results provide significant differences in the management of occupational exposure to biological agents depending on the preventive system chosen by the company concluding that the protection is not fully developed because there are not enough tools available that allow easy implementation and the overall management of biological risks is inadequate (AU)

Hypertension and the absence of EDHF-mediated responses favour endothelium-dependent contractions in renal arteries of the rat.

BACKGROUND AND PURPOSE: Experiments were designed to determine the modulation by nitric oxide (NO) and endothelium-dependent hyperpolarizations (EDHF-mediated responses) of endothelium-dependent contractions in renal arteries of normotensive and hypertensive rats. EXPERIMENTAL APPROACH: Rings, with or without endothelium, of renal arteries of 8-month-old Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were suspended in myographs for isometric force recording. KEY RESULTS: ACh evoked relaxations in preparations contracted with phenylephrine. L-NAME (inhibitor of NOS) attenuated (WKY) or abolished (SHR) these relaxations. TRAM-34 plus UCL 1684 (inhibitors of EDHF-mediated responses) did not decrease the relaxation, except in rings of WKY when L-NAME was also present. High concentrations of ACh caused a secondary increase in tension, augmented in rings of WKY by L-NAME or TRAM-34 plus UCL 1684. The increase in tension was prevented by indomethacin. Under baseline tension, ACh induced endothelium-dependent contractions, prevented by indomethacin (COX inhibitor) or terutroban (TP receptor antagonist). The calculated endothelium-dependent contractions were larger in rings of SHR compared with those of WKY. In preparations of SHR, the contractions were augmented by L-NAME in the presence of SC19220 (EP-1 receptor antagonist). In arteries of WKY, the endothelium-dependent contractions were augmented by TRAM-34 plus UCL 1684. The responses were reduced by SC19220. CONCLUSIONS AND IMPLICATIONS: In the renal artery of the rat, EDCF-mediated contractions are augmented by hypertension. The endothelium-dependent contractions are facilitated by NOS inhibition (in the presence of an EP-1 receptor antagonist) and by the withdrawal of EDHF-mediated responses.

The endothelium-derived hyperpolarizing factor: insights from genetic animal models.

In the late eighties, several studies revealed the existence of a third vasodilating factor next to nitric oxide (NO) and prostacyclin (PGI2). As the action of this third factor is closely related to smooth muscle hyperpolarization, this factor was termed endothelium-derived hyperpolarizing factor (EDHF). The story of its investigation is a confusing one and several different candidate molecules and pathways have been proposed to account for the EDHF phenomenon. Major candidate molecules/mediators of EDHF signalling are K+, electrical coupling through gap junctions, cytochrome P450 metabolites, and endothelial small- and intermediate Ca2+-activated K+ channels (SK(Ca) and IK(Ca)). In this mini review, we wish to convey that EDHF is as powerful as NO and PGI2 in terms of blood pressure regulation and that deficiency in EDHF signalling contribute to several cardiovascular pathologies such as hypertension, chronic renal failure, and diabetes. In addition, we focus on recent insight into the EDHF phenomenon provided by novel genetic animal models, such as mice deficient of either endothelial SK(Ca) or IK(Ca) and the impact of channel deficiency on endothelial function, EDHF signalling, and arterial blood pressure.

Is a (n inborn) deficiency of prostacyclin synthesis stimulating plasma factor associated with increased lipoprotein(a)?

Patients with the antiphospholipid syndrome as well as those with a lack in the prostacyclin synthesis stimulating plasma factor (PF) are prone to develop thrombophilia and are at a higher clinical risk for vascular disease. As patients with the antiphospholipid syndrome have been reported to show elevated lipoprotein (Lp)(a) levels, we re-examined all our patients known to have an inborn or an acquired persistent deficiency of PF. Their non-affected relatives served as controls. In addition, 36 patients suffering from clinically manifested atherosclerosis as well as 16 healthy adults, all of them having elevated Lp(a) levels (> 30 mg/dl), were screened for a PF deficiency. In fact, all the patients with a deficient PF activity showed elevated Lp(a) values. While the prevalence of PF deficiency ranges about 1-2%, in 7 (19%) patients with clinically manifested atherosclerosis and 3 (19%) healthy adults with elevated Lp(a) this defect was found. The findings demonstrate an association between PF deficiency and Lp(a), indicating a biochemical interaction which needs to be further elucidated.

A case of myocardial infarction complicating pregnancy--a role for prostacyclin synthesis stimulating plasma factor and lipoprotein (a)?

Coronary heart disease and myocardial infarction (MI) is rarely seen in women below the age of 40 years and even more rarely during pregnancy. The first case of MI during pregnancy was described by Katz in 1992 (1). Current literature reviewed by Samara et al. 1989 (2) listed only 62 cases of proven MI during pregnancy or in the puerperium, the maternal mortality rate being as high as 24%. In this paper we are going to report on a 26-year old pregnant woman suffering from MI, probably as a result of a haemostatic imbalance caused by a lack of prostacyclin synthesis stimulating plasma factor (PF) and elevated lipoprotein (a) (Lp (a)). The potentially deleterious thromboembolic complications in patients with PF-deficiency, especially in combination with elevated Lp (a), should be carefully considered.

Radiation-induced vascular damage.

A 55-year-old male underwent detailed angiological and biochemical investigation because his daughter suffered from myocardial infarction in the 29th gestational week. An inborn familial plasma factor defect and increased Lp(a) were detected. Localized vascular changes were found in the right femoral artery while the resting vascular system was normal. Anamnestic data revealed a testicular cancer and therapeutic irradiation in that area (5000 rad) 12 years ago.

[Deficiency of prostacyclin stimulating factor in type I diabetes mellitus. Correlation with the duration of the disease]. / Deficiencia del factor estimulante de la prostaciclina en la diabetes tipo I. Correlación con la duración de la enfermedad.

The prostacyclin stimulating plasma factor (PSPF) was studied in 40 children affected by insulin dependent diabetes (type I), using smooth muscle cells of rat aorta as substrate. The patients were divided into three groups according to the duration of the disease; recently diagnosed patients (n = 10), patients with less than 5 years of evolution (23 cases), and patients with more than 5 years duration (n = 7). The most significant data were that all the patients with more than 5 years duration had decreased PSPF with values below I SD (p less than 0.001). No statistically significant differences were found among the group with less than 5 years duration, recently diagnosed patients and the normal control group. Neither could a correlation be found between the value of PSPF and the dose of insulin required by each patient, or the rate of hyperglycemia, triglycerides, cholesterol and Hb A1C.

Deficient activity of prostacyclin stimulating plasma factor (PSPF) in newborns.

The activity of PSPF was studied in 38 normal newborns. The production of 6-keto-PGF1 (PGI2 stable metabolite) after stimulation with cord blood plasma, 0.72 +/- 0.50 pmol/10(5) cells, was lesser than after stimulation with plasma from 2-3 years old children, 3.00 +/- 0.89 pmol/10(5) cells (p less than 0.01), or from adults, 7.74 +/- 5.00 pmol/10(5) cells (p less than 0.001). No differences were shown during neonatal period. The presence of a circulating inhibitor factor in newborns was dismissed by mixed cultures. The behaviour of neonatal plasma after consecutive stimulations with AA was similar to adult plasma response. We proved that newborns show a deficient capacity to stimulate PGI2, which is not due to circulating inhibitor factor, and we think that this deficiency is due to a weaker action of stimuli, rather than to an immaturity.

[Defects in the prostaglandin system. VI. Acquired plasma factor defect]. / Defekte im Prostaglandinsystem. VI. Erworbener Plasmafaktordefekt.

A 44 year-old male was admitted to hospital in October 1984 presenting with enzymatic and electrocardiographic signs of posterior wall myocardial infarction. At this time 2 separate examinations revealed normal plasma factor activity. At the 1 year follow-up (November 1985) plasma factor activity was still present. However, in February 1987 for the first time, the patient's plasma failed to enhance PGI2 synthesis from vascular tissue in vitro. 3 further follow-up examinations within the next 6 weeks again revealed an acquired absence of plasma factor activity of unknown cause. No deterioration in clinical condition occurred. All relatives tested showed normal plasma factor activity.

[Prevalence of plasma factor deficiency in the Vienna population. Results of a screening study of 1,300 adults]. / Prävalenz des Plasmafaktormangels in der Wiener Bevölkerung. Ergebnisse einer Screening-Untersuchung an 1300 Erwachsenen.

A screening investigation for the presence of risk factors for the development of atherosclerosis demonstrates a plasma factor deficiency in 0.8% in the Viennese population. These findings are in agreement with the data of a newborn screening performed earlier. All the persons were clinically healthy. In 4 of them at least 1 family member suffered from the same defect. The pathogenetic relevance of the plasma factor defect for thrombophilia at young age is discussed.