Effect of amlodipine and cilazapril treatment on platelet Ca2+ handling in spontaneously hypertensive rats.

Abnormal Ca2+ handling and enhanced aggregation response have been reported in platelets from spontaneously hypertensive rats (SHR) and patients with essential hypertension, and thought to be involved in the progression of target organ damage of hypertension. It is important to examine whether antihypertensive therapy can improve the abnormal platelet response in hypertension. We investigated the effect of antihypertensive treatment such as amlodipine and cilazapril on Ca2+ handling and aggregation response in SHR platelets. Four-week-old male SHR were divided into three groups. Each group was treated with amiodipine (A: 10 mg/kg/day), cilazapril (C: 10 mg/kg/day) or vehicle (V) for 8 weeks by gavage. At 12-week-old, platelet [Ca2+]i was measured with fura-2 in each group of SHR and age-matched Wistar-Kyoto rats (WKY) as normal control. Systolic blood pressure in amlodipine and cilazapril treated groups were similar with WKY and significantly lower than vehicle treated group (A: 124 +/- 9, C: 126 +/- 9, WKY: 122 +/- 10 and V: 180 +/- 9 mmHg, respectively). The basal [Ca2+]i in the three groups of SHR were similar and higher than WKY (A: 47 +/- 1.7, C: 47 +/- 1.2, V: 48 +/- 3.9 and WKY: 40 +/- 4.0 nmol/l, respectively). There were no significant differences in thrombin (0.1 U/ml)-stimulated [Ca2+]i rise in the presence or absence of extracellular Ca2+ among the three groups of SHR and these were higher than WKY. Intracellular Ca2+ discharge capacity, assessed by the ionomycinstimulation was similar in the all groups. Thrombin-induced maximum platelet aggregation responses in the three groups of SHR were similar and higher than WKY. The antihypertensive treatment of Ca2+ antagonist or ACE inhibitor gave no change in intraplatelet Ca2+ metabolism in SHR. These results support the hypothesis that an abnormal Ca2+ handling in SHR platelet is genetically determined and not improved by hypotensive therapy.     

Crossed aphasia with left spatial neglect and visual imperception: a case report

A 64-year-old right-handed woman with no left-handers in the family developed aphasia associated with moderate left hemiparesis and dense left homonymous hemianopia following rupture of a right middle cerebral artery aneurysm and subsequent selective surgery confined to the right hemisphere. Severe left spatial neglect and constructional apraxia were also present. The patient was an achondroplasic dwarf whose previous medical and neurological history was otherwise unremarkable. Computed tomography of the brain showed a large right temporo-insulofrontoparietal lesion. Language and nonverbal cognitive functions were assessed after 2 and 6 months, and then four years later. A reportedly overall language disruption in the acute period evolved into Wernicke's aphasia and then into a mild form of conduction aphasia. The associated left spatial neglect eventually shrank to a minimum. The patient never had clinically detectable visual agnosia, but on specific tests of visual recognition and perception some impairment was found four years after onset. The left hemiparesis disappeared in time while the left hemianopia persisted. This case is a convincing example of an entirely righthanded person in whom both linguistic and visuospatial functions are represented in the right hemisphere. Received: 12 May 2002 / Accepted in revised form: 18 November 2002 Correspondence to L.A. Vignolo     

Alpha-Fetoprotein und cystische Fibrose

Zusammenfassung Kürzlich wurde über signifikant höhere Serumspiegel von Alpha-Fetoprotein (AFP) sowohl bei Patienten mit cystischer Fibrose (CF) als auch deren Eltern und einem Teil der Geschwister berichtet; es wurde daraufhin die Bestimmung von AFP zur Erfassung von heterozygoten Trägern des CF-Gens empfohlen. In eigenen Untersuchungen gleichfalls mit einem Radioimmunassay konnten diese Befunde nicht bestätigt werden.     

Prognosis of symptoms in patients with diagnosed chronic organic solvent Intoxication

Summary The profile and prognosis of symptoms of 87 patients (mean age 38.6 years) in whom a chronic organic solvent intoxication due to tri- or perchloroethylene or mixtures of solvents had been diagnosed 3–9 years earlier were examined by means of an interview.Both at the time of diagnosis and upon reexamination, the most common symptoms were abnormal fatigue, memory disturbances and headache. Also dizziness, sleep disturbances, sensory symptoms in the extremities, mental depression, concentration difficulties, psychic irritability, emotional lability, tremor and nausea were present in over 60% of patients at the time of diagnosis. Upon reexamination, 52% of the intoxication patients with no other contributing neurological disease felt that their overall subjective condition was better than at the time of diagnosis, 21% felt that it was worse, and 27% reported no change. Most of the individual symptoms had more often changed for the better than for the worse; the differences were statistically significant with regard to abnormal fatigue, headache, dizziness, sleep disturbances, nausea, and emotional lability, whereas memory disturbances had changed in the opposite direction. Younger persons, who had had a longer follow-up period and without regular check-ups at the Institute of Occupational Health seemed to have better prognosis at the group level. Due to the great variation between the individuals, the prognosis was, however, impossible to predict in individual cases.     

Effect of proteases on plasminogen activator release from isolated perfused dog leg

The present study was undertaken to determine which proteases could induce the release of plasminogen activator from isolated perfused dog hind leg. The proteases tested were thrombin, trypsin, chymotrypsin and factor Xa which show restricted specificities of various kinds, and papain which shows a broader specificity. Thrombin at concentrations of between 2 × 10⁻⁸ M and 6 × 10⁻⁷ M released plasminogen activator dose-dependently. Trypsin released plasminogen activator as strongly as thrombin. On the other hand, chymotrypsin exerted little effect on plasminogen activator release even at 5 × 10⁻⁶ M, and factor Xa at concentrations of between 10⁻⁷ M and 5 × 10⁻⁷ M showed no activity to release plasminogen activator. The effect of papain on plasminogen activator release was very weak and not dose-dependent. These results indicate that plasminogen activator release from the vessel wall was induced specifically by only particular proteases such as thrombin and trypsin. This suggests that certain arginine residues of the reactive sites on the vessel wall may participate in the release of plasminogen activator by proteases.