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Biomedical subjects

P Fitscha

Publications and source records attributed to P Fitscha.

At least 73 records · Page 4Linked to original sources
PubMed1988

[Defects in the prostaglandin system. VI. Acquired plasma factor defect].

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.

Adult↗
PubMed1988

[Defects in the prostaglandin system. VII. (Generalized, inherited [?]) cyclooxygenase defect].

Investigation of platelet function in a 55 year-old male suffering from peripheral vascular disease revealed platelet cyclooxygenase deficiency. Examination of femoral artery tissue at a later date likewise showed the presence of a cyclooxygenase defect. Investigated relatives were not affected. A 39 year-old male smoker admitted with an acute myocardial infarct without prodromal symptoms exhibited similar laboratory findings. In contrast to the cases reported in the literature so far, both our patients suffered from severe atherosclerosis, a relatively high platelet activity and an additional cyclooxygenase defect of cells other than the platelets. The patient with peripheral vascular disease died from sudden cardiac arrest.

Adult↗
PubMed1988

[Fibrinolytic activity, thrombocyte function and pharmacokinetics during intra-arterial or intravenous prostaglandin E1 infusion in patients with chronic arterial occlusive disease].

Monitoring various parameters of fibrinolytic activity in 6 patients with arterial occlusive disease during intra-arterial (i.a.) or intravenous (i.v.) prostaglandin (PG) E1 infusions indicated activation of the endogenous fibrinolytic system. However, due to the small number of patients not all test parameters revealed significant changes. None of the PGE1 infusion regimens used (1.25 or 2.5 ng/kg/min i.a. or 5 or 10 ng/kg/min i.v. for 120 min in each case) led to any significant change in various parameters checked for ex-vivo platelet function. In agreement with these data the radioimmunological determination of PGE1 in venous plasma did not reveal any significant rise. On the other hand, the circulating metabolite of PGE1, 15-keto-13, 14-dihydro-PGE1, reached plasma levels which correlated well with expected theoretical values taking the infusion rate into consideration. A potential mechanism by which even low plasma concentrations of PGE1 might affect platelet function in vivo is discussed.

Alprostadil↗
PubMed1988

[Liver function parameters and fibrinogen in intra-arterial and intravenous PGE1 infusion].

It has been claimed that PGE 1 pathologically alters liver function, the effect being less pronounced after intra-arterial administration. A retrospective data analysis of 4 different studies does not support this view. There was no effect on serum transaminases, fibrinogen or blood sedimentation rate. Furthermore, there was no difference between the i.a. and i.v. route of PGE 1 therapy under the investigated conditions. Thus, the claim that impaired liver function is less pronounced after i.a. PGE 1 administration is no longer valid.

Aged↗
PubMed1988

Comparable effect of prostaglandin E1 in decreasing in vivo platelet deposition on human lesion sites after intravenous and intraarterial application.

It had been claimed that prostaglandin E1 is degraded during first lung passage to a major extent. Clinical results, however, as well as various platelet function tests and coagulation parameters revealed no apparent difference after i.v. and i.a. infusion. Thus, we examined the question what the quantitative difference between i.v. and i.a. PGE1-application would be upon in-vivo platelet function assessed by platelet uptake over active lesion sites as well as platelet half-life monitoring after autologous 111-In-oxine platelet labelling. In patients suffering from peripheral vascular disease stage II according to Fontaine PGE1 was able to decrease platelet uptake after i.v. and i.a. therapy to a comparable extent; similarily, a significant prolongation in platelet half-life was noted, again revealing no difference. As the decrease in platelet uptake is assumed to be predominantly a vascular effect, it is hypothetized that more stable derivatives of PGE1 are active, counterbalancing a lower biological activity with a longer half-life.

Alprostadil↗
PubMed1988

Comparison of the acute haemodynamic effects of bopindolol and propranolol at rest and during supine exercise.

The acute cardiovascular effects of two beta-adrenoceptor blocking agents, bopindolol and propranolol, were compared in a randomized study in 16 male patients with coronary heart disease. All patients had had an uncomplicated acute myocardial infarction at least 8 weeks earlier. The two drugs reduced the arterial blood pressure to the same extent, both at rest and during exercise. As heart rate and stroke volume were also decreased, cardiac output was reduced, whereas systemic vascular resistance was increased at rest and during exercise. Left ventricular filling pressure was increased. No statistically significant differences in these variables were seen between the two groups.

Adrenergic beta-Antagonists↗
PubMed1988

Haemodynamic effects of short-term treatment with bopindolol in essential hypertension.

Ten patients (mean age 53 years) with essential hypertension have been studied at rest and during exercise following oral treatment for 6 weeks with a new beta-adrenoceptor blocking agent, bopindolol. The treatment caused a significant decrease in systolic and diastolic arterial blood pressure and heart rate, both at rest and during exercise. Stroke volume fell, too, and therefore so did cardiac output, whereas the systemic vascular resistance was increased. Left ventricular filling pressure was elevated both at rest and during exercise following bopindolol therapy. However, a different haemodynamic pattern was noted in patients with elevated total peripheral resistance prior to therapy (Group 1) compared to patients with normal or subnormal peripheral resistance (Group 2). A decrease in systemic vascular resistance seemed to be the cause of the fall in blood pressure in Group 1, as the expected increase in vascular resistance did not occur, whereas a reduction in cardiac output was of greater importance in Group 2. During exercise the lowering of arterial blood pressure in both groups was mediated by a reduction in cardiac output.

Adrenergic beta-Antagonists↗
PubMed1988

Diminished platelet residence time on active human atherosclerotic lesions in-vivo--evidence for an optimal dose of aspirin?

Although aspirin is an old drug, its optimal dose for the treatment of human atherosclerosis has not been finally proven. Various in-vitro and ex-vivo platelet function tests revealed a dose range from 1 to 3000 mg as being optimal. It was thus the goal to examine its in-vivo efficacy in human suffering from peripheral vascular disease in 7 different doses ranging from 1 mg to 1000 mg a day. All these patients have been treated for 3 months. Platelet half-life and platelet uptake ratio show an in part significant improvement being most pronounced at the daily doses of 20 and 1000 mg respectively. No change occurs in the placebo treated controls. These findings indicate, that 20 or 1000 mg aspirin taken daily per os, are superior to the other doses examined concerning the in-vivo platelet function (as measured by platelet half-life) and rendering the arterial surface less thrombogenic (as reflected by platelet uptake ratio-measurements).

Administration, Oral↗
PubMed1988

Epoprostenol in patients with Raynaud's disease.

Prostaglandin metabolism and the clinical effect of epoprostenol (prostacyclin, PGI2) infusions were studied in thirteen patients with Raynaud's disease. Epoprostenol was infused at 5 ng/kg/min for six hours daily for two consecutive five day periods, separated by a two day interval. No beneficial effects either during or after infusion could be detected in terms of frequency of severity of attacks or on skin temperature measurement. Raynaud's patients had significantly lower serum thromboxane B2 levels than normal controls though plasma levels of thromboxane B2, 6-oxo-PGF1 and the bicyclic metabolite of PGE2 did not differ between the two groups. Platelets from Raynaud's patients had a significantly lower conversion rate of arachidonic acid into thromboxane B2 and HHT and a significantly higher rate of HETE production than platelets from controls.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

The platelet rebound phenomenon during PGI2-infusion occurs at the receptor level.

In 6 patients treated with continuous prostaglandin I2 (PGI2)-infusion using a portable pump at a rate of 5 ng/kg/min for 7 days drug receptor interaction of [3H]Iloprost, a stable PGI2 analogue, with a particulate platelet membrane fraction was investigated. Saturation binding experiments of the high affinity platelet prostacyclin receptor performed before and at the end of PGI2 infusion revealed a significant increase of dissociation constant (Kd) and increase in maximal number of binding sites (Bmax). These findings suggest that continuous long-term PGI2 infusion results in a functional desensitization of the membrane-bound PGI2 platelet receptor with a decrease in receptor affinity and an increase in number of binding sites as suggested earlier based upon platelet sensitivity behaviour.

Aged↗
PubMed1988

In vivo modulation of platelet deposition on human atherosclerotic lesions by various antiaggregatory prostaglandins.

The influence of intravenous infusions of various prostaglandins on in vivo platelet function was studied after labelling of autologous platelets with 100 mu ci 111 indium-oxinesulfate in patients with peripheral vascular disease stage II according to FONTAINE. PGI2 (5 ng/kg/min) provoked a significant decrease of platelet deposition and a prolongation in platelet half-life time (74 +/- 6 vs 68 +/- 5 hours). PGE1 (25 ng/kg/min) failed to influence platelet deposition, but prolonged significantly platelet half-life time (82 +/- 6 vs 76 +/- 8 hours). CG 4203 (25 ng/kg/min) decreased significantly platelet deposition and prolonged significantly platelet half-life time (73 +/- 10 vs 67 +/- 11 hours). Iloprost (1 and 2 ng/kg/min) reduced significantly platelet deposition without dose relation. Half-life time was increased significantly after therapy compared to placebo (1 ng: 76 +/- 7 vs 69 +/- 7; 2 ng: 73 +/- 9 vs 67 +/- 9 hours).

Aged↗
PubMed1987

Prostaglandin I2 during radiolabelling improves recovery, but does not change platelet half-life and platelet uptake over active human lesion sites.

The fact that prostacyclin is able to preserve platelets in-vitro stimulated the question whether platelets being treated in presence of prostacyclin might behave different after reinjection in human. We therefore studied the effect of synthetic PG12 in-vitro, being added immediately after blood sampling. It is demonstrated that the presence of prostacyclin does not change the labelling efficiency and in-vitro viability beside the alterations induced by this compound itself, however, it results in a significantly improved recovery. Furthermore, the platelet half-life in the patients as well as the deposition of the radiolabelled platelets on active human atherosclerotic lesions does not seem to be affected. Thus, the addition of PGI2-improves cellular viability during the preparation without negatively interfering with the in-vitro and in-vivo results later on. Thus, the use of PGI2 can be strongly recommended.

Aged↗
PubMed1987

Prostaglandin I2 reduces activation of human arterial smooth muscle cells in-vivo.

Patients suffering from peripheral vascular disease have been "ultima ratio"-treated with PGI2 at a rate of 5 ng/kg/min for 6 hours a day and 5 consecutive days i.v. 20 of them underwent surgery thereafter as therapy was not sufficient. A histological examination and quantification of vascular tissue revealed that the number of activated smooth muscle cells was significantly lower in treated patients vascular segments than in untreated ones in all the different age groups. A comparable suppression was found in the intima and the media as well. It is thus concluded, that PGI2 inhibits smooth muscle cell proliferation most probably by inhibiting PDGF-release from the platelets and stimulation of smooth muscle cell cAMP. To achieve a more beneficial PGI2-effect at the vascular level, a prolonged PGI2-therapy looks rather promising.

Arteries↗