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Biomedical subjects

M Porta

Publications and source records attributed to M Porta.

At least 181 records · Page 10Linked to original sources

Is the pro-adhesive activity of plasma von Willebrand factor counteracted by a physiological inhibitor of platelet adhesiveness?

1. Abnormal plasma levels of von Willebrand factor are accompanied by abnormal platelet function in some disease states. 2. Platelet retention in glass bead columns, platelet aggregation in vitro, beta-thromboglobulin and 6-oxo-prostaglandin F1 alpha were monitored in six normal male volunteers before and after an acute rise of von Willebrand factor, as induced by the intravenous administration of 1-deamino 8-D-arginine vasopressin (DDAVP). 3. After DDAVP a steady twofold rise of von Willebrand factor occurred. Platelet retention increased by 74% immediately after DDAVP but returned to baseline values within 60-120 min. No consistent changes of the other variables were observed. 4. These results suggest that as yet unidentified mechanism(s) inhibits the pro-adhesive activity of von Willebrand factor.

Adult↗

Increased platelet volume in diabetic retinopathy.

Platelet volume was measured in 30 healthy controls and 87 diabetic patients, the latter subdivided according to the absence, presence and severity of retinopathy, to investigate if platelet size is related to microangiopathy. The platelet volume of the whole diabetic population was increased (p less than 0.05) due to a higher percentage of large elements (p less than 0.05). The patients with various degrees of retinopathy had similar increases (p less than 0.05) in their platelet size, while those without complications occupied an intermediate position between normal controls and retinopathy patients. It is concluded that: (i) increased platelet size accompanies diabetic retinopathy, irrespective of its severity, and (ii) patients without this complication form a heterogeneous group, some of which already have alterations of platelet volume. The role of these abnormalities in the development and progression of diabetic microangiopathy remains to be established.

Adult↗

Evidence for functional endothelial cell damage in early diabetic retinopathy.

Two aspects of endothelial cell function were examined in two matched groups of male insulin-dependent diabetics, six with background retinopathy and seven without retinopathy. Leakage of fluorescein from the retinal capillaries was estimated by vitreous fluorophotometry. In addition, factors VIII/von Willebrand (vWF) and VIII-related antigen (VIII-RAG), which are synthesized by the endothelial cells, were measured, together with VIII-antihaemophilic factor (VIII-AHF). The patients without retinopathy had normal leakage of fluorescein in the macula (mean +/- SEM: 1.10 +/- 0.10 g X 10(-8)/ml) and the posterior vitreous (0.45 +/- 0.11 g X 10(-8)/ml), and normal circulating levels of vWF (123% of a normal reference plasma +/- 18%), VIII-RAG (137 +/- 14%) and VIII-AHF (112 +/- 18%). In contrast, the patients with background retinopathy showed higher leakage of fluorescein in the macula (6.34 +/- 1.74 g X 10(-8)/ml; p less than 0.01), and the posterior vitreous (3.09 +/- 0.94 g X 10(-8)/ml; p less than 0.02), as well as increased levels of vWF (177 +/- 16%; p less than 0.05). There was a trend towards increased VIII-RAG (195 +/- 24%; p less than 0.1), but not VIII-AHF (126 +/- 13%). Alterations of endothelial cell function thus accompany the development of retinopathy. It cannot be said from the present study whether these alterations also precede the appearance of retinopathy.

Adult↗

Twenty-four hour variations of von Willebrand factor and factor VIII-related antigen in diabetic retinopathy.

Factor VIII/von Willebrand factor (vWF) could play a role in the pathogenesis of diabetic microangiopathy. It has been suggested that its biologic activity is controlled by hormonal and metabolic mechanisms. To verify this hypothesis, vWF was monitored over a 24 hr period in 9 insulin treated patients with diabetic retinopathy, together with factor VIII-related antigen (VIII-RAG), plasma glucose, growth hormone (GH) and prolactin. vWF levels oscillated during the 24 hr, the mean values being higher during the day than at night-time, p less than 0.01. Compared to a group of normal controls in whom blood samples were taken randomly between 9.00 and 13.00, the levels of vWF were significantly increased at 11.00, p less than 0.02, and at 13.00, p less than 0.02, but at no other time. VIII-RAG values were also higher during the day than at night-time, p less than 0.01. The mean 24 hr levels of vWF correlated with those of VIII-RAG, p less than 0.01, with the age of the patients, p less than 0.01, and with the duration of disease, p less than 0.01. The levels of plasma glucose were higher during the day, while GH and prolactin rose at night-time. No correlations were found between vWF or VIII-RAG and plasma glucose, GH or prolactin, nor between the mean 24 hr levels of all these parameters and ponderal index, daily insulin dose, degree of metabolic control, severity of retinopathy. Insulin treated diabetics with microangiopathy show circadian variations in their plasma concentrations of vWF and VIII-RAG which should be taken into account when measuring these factors for clinical or research purposes.

Adult↗

Forearm ischaemia as a test of prostacyclin production: studies in normal subjects and in patients with diabetes mellitus.

Plasma levels of 6-oxo-PGF1 alpha, the hydrolysis product of prostacyclin, were significantly reduced in men with proliferative diabetic retinopathy, compared with normal controls. Male diabetics with background or no retinopathy formed an intermediate group with plasma levels of 6-oxo-PGF1 alpha lower than controls and higher than patients with proliferative retinopathy. Forearm ischaemia increased plasma levels of 6-oxo-PGF1 alpha by 30% in normal subjects. The increase occurred during arterial occlusion and was diminished by pretreatment with aspirin. The increase after ischaemia may reflect increased prostacyclin production. In diabetic patients forearm ischaemia produced an increase in plasma 6-oxo-PGF1 alpha similar to that seen in control subjects.

6-Ketoprostaglandin F1 alpha↗

24-Hour studies of prolactin and growth hormone levels in diabetic impotence.

Serum prolactin and growth hormone levels were measured hourly over 24 h in 8 insulin-treated diabetic males, 4 of whom were impotent. All patients showed normal sleep-related peaks of both hormones during the night. The mean 24-hour concentrations of prolactin and growth hormone were similar in patients with impotence (9.4 +/- 1.0 ng/ml and 3.8 +/- 0.4 microIU/ml, respectively) and without it (10.5 +/- 1.0 ng/ml and 4.7 +/- 1.1 microIU/ml, respectively). The mean prolactin and growth hormone concentration during the day time (7.00 a.m. to 7.00 p.m.) and the night time (7.00 p.m. to 7.00 a.m.) were also similar in patients with and without impotence. These results suggest that impotence in diabetic patients is not mediated by abnormalities of prolactin and growth hormone secretion.

Adult↗

Platelet abnormalities as related to diabetic retinopathy (with special reference to platelet shape change).

Abnormalities of platelet function may be related to the pathogenesis of diabetic retinopathy. A method for the in vitro assessment of platelet shape change (PSC), as induced by ADP in calcium-deprived platelet-rich plasma, is presented. The outcome of this test is dependent on the concentrations of ADP and of the chelating agent used. Studies in electron microscopy shoed that the parameter measured is not related to the disappearance of spiny-spherical forms. The values measured for PSC were significantly increased in a group of diabetic subjects, when compared to normal controls. In particular, patients with proliferative retinopathy showed more profound alterations of the PSC. No relations were found between the PSC values and ADP induced platelet aggregation, the plasma levels of von Willebrand factor and of factor VIII-related antigen.

Adenosine Diphosphate↗

Platelet shape change abnormalities in diabetic retinopathy.

In vitro platelet aggregation has been studied in 29 normal subjects and 35 diabetic patients with retinopathy by conventional aggregating agents and by a new technique which evaluates the platelet shape change. --Plate shape change, expressed as % light transmission variation induced by the addition of ADP (10 mumol/l) in calcium-deprived platelet rich plasma, was determined. Significant differences were found between the controls (12.6 +/- 0.7%) and the 35 diabetics (15.6 +/- 1.0%, p less than 0.02) and between controls and the subgroup of patients with proliferative retinopathy (17.3 +/- 1.1%, n = 15, p less than 0.001). Platelet aggregation induced by ADP, collagen and ristocetin did not show significant differences between normal and diabetic subjects. --The shape change is the physiological early phase of platelet aggregation and is related to energy requiring mechanisms. As yet unexplored metabolic abnormalities at this stage could account for previously described platelet abnormalities in diabetes.

Adenosine Diphosphate↗

[Variations of 3' 5' cyclic AMP level in CSF after SAH with or without vasospasm (author's transl)].

Levels of 3' 5' AMPc in CSF were analysed by radioimmunoassay in 56 patients. 12 were used as control and 33 had a Subarachnoid Haemorrage (SAH) between 1 and 22 days before sampling. Out of these 33 cases, 20 had an arterial aneurysm, 7 showed a more or less relevant degree of vasospasm on arteriography. 11 other patients presenting different neurological diseases were studied for comparison. (Ischemia, Hydrocephalus, Atrophy, Hematoma). 3' 5' AMPc level in CSF was found to be very low in case of SAH, especially in patients harboring a definite vasospasm. The significance of AMPc level in CSF is discussed in relation with impairment of consciousness, spasm, ischemia, cortical atrophy, hydrocephalus and hematoma.

Cyclic AMP↗

Vascular abnormalities in diabetes and their treatment.

The capillary abnormalities of diabetes include both dilatation and occlusion. Occlusion is the more important, as vision-threatening lesions are secondary to capillary occlusion. Capillary occlusion could result from abnormalities of blood coagulation and from endothelial cell disease. Evidence is presented of the predominant role of endothelial disease--abnormal coagulation is probably secondary. While there is no known treatment which can reliably prevent or reverse capillary changes, approaches by antiplatelet agents and normalization of blood sugar are possible methods.

Aneurysm↗

Surgical treatment of chronic subdural hematomas in infants.

Subdural hematomas in infants are associated with a high risk of recurrence. In an effort to combat this risk, a surgical procedure consisting of excision of the subdural membranes, a reduction of the craniocerebral disproportion and a restoration of the normal angle of junction of the cerebral bridging veins and the superior sagittal sinus is proposed.

Age Factors↗

Fibrinolytic activity in blood and cerebrospinal fluid in subarachnoid hemorrhage from ruptured intracranial saccular aneurysm before and during EACA treatment.

10 patients suffering from intracranial aneurysm causing subarachnoid hemorrhage (SAH) have been treated during the acute pre-and postoperatory phase with omega-aminocaproic acid. The blood and the cerebrospinal fluid of the treated patients have been analyzed in order to study fibrin(ogen) degradation products (FDP) and fibrinolytic activity (FA). The results so obtained show only an alteration of local fibrinolytic processes either inside or around the aneurysmatic clot: there were no alterations of the systemic FA. Furthermore, monitoring of FDP and FA was a very useful tool in those patients who took advantage of the treatment with omega-aminocaproic acid which protected them from rebleeding.

Aminocaproates↗

Carbamazepine and carbamazepine-10, 11-epoxide concentrations in human brain.

1 Carbamazepine (CBZ) brain and plasma concentrations were measured in twenty-one patients undergoing brain surgery for tumour removal. The drug was administered prophylactically at doses ranging from 6.9 to 14.8 mg/kg for 4-5 days before the intervention. 2 In seventeen cases where sample were collected 10-14 h after dosing, CBZ brain levels ranged from 2.2-14.5 microgram/g. A significant linear relationship (p less than 0.01) was observed between brain and plasma concentrations with a brain/plasma ratio of 1.1 +/- 0.1. 3 Carbamazepine 10,11-epoxide (CBZ-Epox), present in all samples, could be quantified in three brain specimens. Its brain concentrations ranged from 1.5-2.7 microgram/g with a brain/plasma ratio of 1.1-1.2. 4 Parieto-occipital areas tended to show higher CBZ concentrations while lower values were found in temporal regions. Very low CBZ levels were found in two gliomas while in meningiomas CBZ levels were similar to those observed in normal tissue. 5 The data, showing a linear relationship between brain and plasma concentrations of both CBZ and its epoxide, give additional significance to the plasma level monitoring of antiepileptic drugs.

Adult↗

Monoamine acid metabolites in ventricular CSF of patients with brain tumours.

Homovanillic acid (HVA) and 5-hydroxyindolacetic acid (5-HIAA) in ventricular CSF were determined in 19 patients (12 female 7 male) with brain tumours. No relationship was found between ventricular fluid pressure (VFP) and levels of HVA and 5-HIAA. A relationship was observed between ventricular CSF, HVA concentrations and tumour induced alterations in CSF dynamics. HVA concentrations were very high in patients whose tumours involved the third ventricle, the aqueduct, or the fourth ventricle, producing marked alterations in CSF flow. HVA concentrations significantly lower than in controls were observed in cases where tumours involved the lateral ventricles. Concentrations of acid metabolites in patients with little or no alteration in CSF dynamics corresponded with those in patients with other neurosurgical disorders.

Adolescent↗

[Monitoring of intracranial pressure].

An account of the significance of intracranial pressure is followed by a review of the various sites in which it can be recorded (spinal canal, lateral ventricles, subarachnoidal spaces, operation cavity, other sites). Monitoring of ventricular pressure is discussed in detail; this deals with the classic site and its technique has become part of clinical practice. The utilisation and interpretation of the data in the form of pressure levels and their changes in the course of time are also discussed. The clinical indications for monitoring are noted.

Brain Injuries↗