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Biomedical subjects

A Zmuda

Publications and source records attributed to A Zmuda.

At least 19 recordsLinked to original sources
PubMed1994

[Hydroxyproline in serum and urine in children with pulmonary hypertension in the course of congenital heart defects].

In accordance to contemporary views on the pathology of biochemical changes in the fibrotic process at pulmonary hypertension, the authors took a trial to investigate the convection of excessive blood flow through lungs and changes of collagen metabolism in lungs. The possibility of following the metabolism of collagen through naming its metabolites (hydroxyproline-Hp) made us to connect the intended surveys with practical trail of its use, and diagnostic methods at children with congenital shunt cardiac defects. The survey was taken up in three groups of children with different levels of pulmonary advancement hypertension process: 39 children with dynamic elevation of pulmonary artery pressure (I st and II nd group age range: 12 months to 2 years), and 17 children with marks of pulmonary vascular obstructive disease. III rd group age range: 12 months to 6 years. It was stated, that between children from the first and second group before operational treatment, clear growth of Hp contents in serum and in urine returned to its correct value within the 1 to 6 months observation period since the cardiac defect has been corrected. In the third group, in spite of surgical treatment, the increased Hp content remained in the post operative period, therefore testifying the non-retreated fibrotic changes. It was stated, that Hp content control in serum and excretion in urine can possess clinical usage as an auxiliary exam estimating the advancement of pulmonary hypertension before surgical treatment and at the post-operative monitoring of the lungs.

Child↗
PubMed1993

A treatment algorithm for neuropathic (Charcot) midfoot deformity.

Forty-nine feet in 47 patients with midfoot neuropathic foot deformity were referred for care to a comprehensive foot salvage clinic and followed for an average of 3.6 years. Twenty-three initially presented without open ulcers. Two underwent elective Syme's ankle disarticulation amputation, and the others were kept ambulatory with a combination of periods of nonweightbearing cast immobilization, accommodative extra-depth shoes with custom orthotics, and ankle-foot orthoses. Twenty-six of the feet initially presented for care with open ulcers and/or chronic osteomyelitis. Twenty-two of these patients underwent 32 surgical procedures. Sixteen underwent debridement of the infected bone and surrounding soft tissues. Excision of large, nonaccommodative boney prominence, termed exostectomy, was performed in eight. Partial excision of the deformed midfoot combined with boney stabilization and attempted arthrodesis, termed partial tarsectomy, were performed in seven. All surgical patients were managed postoperatively with long-term custom accommodative bracing. Follow-up at an average of 3.6 years revealed that all but one of the patients remained ambulatory. Six walk with accommodative shoe gear and persistent stable chronic open ulcers. None required below-knee amputation. Five amputations were performed, three at the Syme's ankle disarticulation level, one at the Chopart's hind-foot level, and one at the mid-foot level.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Selectin-P-mediated adherence of platelets to neutrophils is regulated by prostanoids and nitric oxide.

The expression of Selectin-P was measured in terms of formation of "rosettes" by human gel-filtrated thrombin (30-50 mU)-stimulated platelets on the surface of isolated homologous neutrophilic leucocytes (PMNs) according to Jungi (1986). The monoclonal anti-Selectin-P antibody completely prevented the formation of "rosettes", proving the specificity of Selectin-P-mediated adhesion. The Selectin-P-mediated adhesion of platelets to PMNs was inhibited by both iloprost (ILO) (IC50 = 5.0 nM) and sodium nitroprusside (NaNP) (IC50 = 0.93 microM); thus ILO is ca. 180 times more potent an inhibitor of "rosette" formation than NaNP. The NOS-inhibitors L-NO2Arg (10-30 microM) and L-MetArg (3-30 microM) each suppressed the adhesion, while at lower and higher concentrations these NOS-inhibitors did not influence rosette formation. L-Arginine (up to 1 mM) was not able to influence significantly the Selectin-P-mediated adhesion of platelets to PMNs. The COX inhibitor aspirin (10-30 microM) promoted the adhesion. We conclude that the Selectin-P-mediated adhesion of platelets to PMNs is inhibited by both ILO and NaNP, whereas endogenous prostanoids and nitric oxide seem to exert an antagonist effect on the adhesion of platelets to PMNs.

Antigens, CD↗
PubMed1991

Influence of no-donor (SIN-1) on functions of inflammatory cells.

NO-donor SIN-1 (0.01-1.0 mM) dose-dependently inhibited the basal and FMLP (30.0 mM)-stimulated release of beta-glucuronidase from rat peritoneal leukocytes and antigen-specific stimulation of Interleukin-2 production by T-hybridomas. I-123 LDL binding to human lymphocytes was inhibited by Iloprost (1 mM) but activated by SIN-1 (0.3 mM). We conclude that beside the smooth muscle cells and platelets the blood inflammatory/immune cells are under the PGI2/NO control, however, the precise regulation as well as physiological importance need further investigation.

Animals↗
PubMed1989

[Effectiveness of etofibrate in arteriosclerosis obliterans. Pilot study in hyperlipidemic patients with arteriosclerosis obliterans].

In a pilot study the therapeutic effect of 2 x 500 mg etofibrate (Lipo Merz retard) on lipids and lipoproteins, fibrinolytic activity and clinical parameters was studied for four weeks in hyperlipidemic patients suffering from arteriosclerosis obliterans (Fontaine stage II/III). The study parameters were evaluated prior to and after the four weeks of treatment. Administration of etofibrate resulted in a significant decrease in serum cholesterol and triglyceride levels, the decrease in LDL-/HDL-cholesterol-ratio due mainly to an elevation of the HDL-cholesterol fraction, an increase in plasma fibrinolytic activity, an increased peripheral blood flow in the ischemic leg, and an increase in the pain-free walking distance. Thus, etofibrate applied twice daily might be recommended for the treatment of hyperlipidemic patients with signs of arteriosclerosis obliterans, Fontaine stage II/III.

Adult↗
PubMed1987

On the mechanism of thrombolytic action of thromboxane synthetase inhibitors.

Using our in vivo model for studying drugs which prevent deposition of thrombi or dissipate thrombi formed in extra-corporeal circulation over a collagen strip superfused with arterial blood of anaesthetized and heparinized cats, we have found that dazoxiben--a thromboxane synthetase inhibitor--possesses not only antithrombotic but also thrombolytic potency in vivo (ED50 = 3.8 mg/kg i.v.). The thrombolytic potency of dazoxiben was antagonized by aspirin at a dose of 50 mg/kg i.v. Moreover, dazoxiben stimulated the generation of prostacyclin in isolated rat aortic slices incubated in platelet rich plasma, but not in platelet poor plasma. It is suggested that the thrombolytic potency of thromboxane synthetase inhibitors after their systemic administration is associated with the release of prostacyclin and/or prostacyclin-stable metabolites by the vascular endothelium owing to feeding of prostacyclin synthetase with prostaglandin endoperoxides accumulated in platelets following the inhibition of thromboxane synthetase.

Animals↗
PubMed1986

Eicosanoid balance at early stages of experimental atherosclerosis. Its relationship with plasma fibrinolytic activity and platelet aggregation.

We have studied generation of eicosanoids in blood vessels and platelets of rabbits in relation to platelet aggregation and plasma fibrinolytic activity at early stages of experimental atherosclerosis. A level of lipid peroxides in plasma augmented progressively from the 2-nd to 12-th week of atherogenic diet. In parallel, platelets generated more TXA2 and 12-HETE while in blood vessels a gradual reduction of prostacyclin formation was observed. Reduction in generation of PGI2 was accompanied by steady formation of PGE2. In the second week of the diet a slight decrease appeared of aggregatory response while later aggregability of platelets was increased. At first, plasma fibrinolytic activity was decreased, but it significantly augmented after 12 weeks of the diet. The above data indicate that changes of arachidonic acid metabolism in platelets and blood vessels appear at a very early stage of atherosclerosis and they influence platelet function and plasma fibrinolytic activity.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1984

Dihomo-gamma-linolenic acid in patients with atherosclerosis: effects on platelet aggregation, plasma lipids and low-density lipoprotein-induced inhibition of prostacyclin generation.

Dihomo-gamma-linolenic acid ( DHLA ), a precursor of monoenoic anti-aggregatory prostaglandins (PGE1, PGD2), was administered for 4 weeks in a daily dose of 1.0 g into 33 patients with atherosclerosis on a basis of a double-blind trial. Comparison of treatment and placebo groups revealed elevation of DHLA in red cell lipids in DHLA -treated subjects. No differences, however, between the two groups could be observed in platelet aggregability, thromboxane A2 generation by platelets, serum cholesterol, PGE1 and PGE2 levels, and in inhibitory activity of low-density lipoproteins against prostacyclin synthetizing system in arteries. The dietary supplementation used did not lead to distinct antithrombotic effects.

8,11,14-Eicosatrienoic Acid↗
PubMed1984

Formation of lipoxygenase and cyclooxygenase metabolites of arachidonic acid by brain tissue.

Rat brain slices released spontaneously and after challenge with A23187 LTC4-like radioimmunoactivity. Total cat brain ischemia followed by short postischemic reperfusion period resulted in the increased release of lipid peroxides and PGE2 but not in LTC4-like substance by brain slices. In lumbar cerebrospinal fluid of patients with completed stroke presence of LTC4-like material was observed.

Animals↗
PubMed1983

The use of carprofen, a non-steroidal antiinflammatory agent, in peptic ulcer diseases.

The effects of carprofen (Roche), a nonsteroid antiinflammatory agent, on gastric secretion, serum gastrin level, electropotential difference (PD), gastric microbleeding, DNA loss, and the generation of mucosal prostaglandins (PGs) were examined in 20 duodenal ulcer patients with active ulcer (15 patients) or in remission (5 patients). Carprofen administered for one-week period at a therapeutic dose (300 mg/day) was well tolerated by all ulcer patients and no adverse effects were observed during or after treatment. Endoscopy performed after carprofen treatment showed complete ulcer healing in 9 out of 15 patients and no exacerbations were observed in the rest of patients. No significant changes were observed in basal or pentagastrin-induced secretion, PD, gastric microbleeding and DNA loss. The generation of PGE2, 6-keto-PGF1 alpha and thromboxane B2 was not affected by the treatment with carprofen. This study indicates that carprofen shows excellent gastrointestinal tolerance in ulcer patients, and it might be useful in the treatment of arthritic patients with peptic ulcer disease.

Action Potentials↗
PubMed1981

Aspirin-induced gastric ulcers in cats. Prevention by prostacyclin.

Gastric ulcers were produced in conscious cats in 3 hr by simultaneous intravenous or intragastric administration of acetylsalicylic acid (ASA), plus intravenous infusion of histamine (80 micrograms/kg/hr), pentagastrin (8 micrograms/kg/hr), or intragastric instillation of HCl. The formation of these ulcers was accompanied by almost complete inhibition of prostaglandin (PG) biosynthesis, suggesting that the withdrawal of normal protection of gastric mucosa by PGs may be major factor in pathogenesis of ASA-induced gastric lesions. Prostacyclin (PGI2), infused at a dose producing about 50% inhibition of histamine or pentagastrin-induced acid secretion, significantly reduced the formation of gastric ulcers produced by ASA + histamine or pentagastrin. Inhibition of gastric acid secretion by about 50% using ranitidine, a new H2-receptor antagonist, also decreased the formation of gastric ulcers induced by ASA + gastric secretagogue, but the degree of this reduction was significantly smaller than after PGI2. In addition, PGI2 decreased significantly the severity of gastric ulcers produced by a combination of ASA plus gastric perfusion of HCl, the antiulcer effect being more pronounced when PGI2 infusion was started prior to, rather than during, ASA administration. This study confirms that the administration of ASA plus gastric secretagogue or gastric instillation of HCl is a reliable model of gastric ulcerations probably resulting from withdrawal of biosynthesis of mucosal PGs and shows that PGI2 is capable of preventing the formation of these ulcers by means other than its effect on gastric acid secretion.

Animals↗
PubMed1981

Prostacyclin and blood glucose levels in humans and rabbits.

In patients with peripheral vascular disease and in healthy rabbits, infusion of PGI2 but not of 6-keto PGF1 alpha induced a rise in blood glucose level and a pathological deviation in glucose tolerance test. In experiments in vitro, the increased concentrations of glucose produced dose-dependent inhibition of PGI2 release from isolated rat aortic rings. The link between PGI2 and carbohydrate metabolism is discussed.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Serum lipoproteins, lipid peroxides and prostacyclin biosynthesis in patients with coronary heart disease.

Serum low-density lipoproteins (LDL) and high-density lipoproteins (HDL) were prepared by gradient ultracentrifugation and dialysis from 12 healthy subjects and 15 patients with coronary heart disease and hyperlipoproteinemia. In both lipoprotein fractions cholesterol and lipid peroxides were determined. The effect of these lipoproteins on spontaneous prostacyclin biosynthesis in rat aortic slices was studied. Serum lipoproteins were susceptible to peroxidation during the preparation procedure. LDL were more prone to peroxidation than HDL. Little lipid peroxides were formed in lipoproteins when calcium ions had been removed by EDTA, and when butylated hydroxytoluene (BHT) was present at all stages of their preparation. LDL when prepared without these precautions either from healthy subjects or from patients with coronary heart disease markedly suppressed prostacyclin generation by rat aortic slices. This inhibition was unrelated to LDL-cholesterol, but was due to LDL-lipid peroxides. Peroxide-low LDL prepared from most of the healthy subjects and patients with coronary heart disease and concomitant hyperlipoproteinemia, did not inhibit prostacyclin biosynthesis. However, in one quarter of the patients, LDL was inhibitory. Consequently, in some patients with coronary heart disease, there operate unknown mechanisms which are responsible for the inhibitory activity of LDL on prostacyclin generation.

Adult↗
PubMed1981

Increased platelet activity after termination of prostacyclin infusion into man.

Infusion of PGI2 at a dose of 5 or 10 ng/kg/min during 72 hours into patients with peripheral vascular disease was followed by increased susceptibility of platelets to proaggregatory action of ADP and collagen but not that of arachidonate. The above effects were observed 24 hours after termination of infusion of PGI2. A tendency to an increased formation of TXA2 in PRP aggregated by arachidonate was also noticed. Infusion of PGI2 at a dose of 2 mg/kg/min during 72 hours into the patients caused the decreased platelet aggregability to ADP and arachidonate but not to collagen, and a decreased tendency to production of TXA2 in PRP aggregated by arachidonate. The existence of a "rebound effect" in platelets after a long term PGI2 therapy is suggested.

Adenosine Diphosphate↗
PubMed1981

Role of mucosal prostaglandins and DNA synthesis in gastric cytoprotection by luminal epidermal growth factor.

This study compares the effect of epidermal growth factor and prostaglandins (PGE2 or PGI2), applied topically to gastric mucosa, on gastric secretion and formation of ASA-induced gastric ulcerations in rats. Epidermal growth factor given topically in non-antisecretory doses prevented dose-dependently the formation of ASA-induced ulcers without affecting prostaglandin generation but with a significant rise in DNA synthesis in the oxyntic mucosa. The anti-ulcer effect of topical prostaglandins was also accompanied by an increase in DNA synthesis. This study indicates that topical epidermal growth factor, like PGE2 or PGI2, is cytoprotective and that this cytoprotection is not mediated by the inhibition of gastric secretion or prostaglandin formation but related to the increase in DNA synthesis in oxyntic mucosa.

Animals↗
PubMed1981

Prostaglandin E2 in gastric mucosa and its role in the prevention of ulcers induced by acetyl salicylic acid in cats.

Gastric mucosa of the cat generates PGE2 activity at a significantly higher concentration in the antral 59.25 +/- 7.42 ng/g) than in the oxyntic (28.06 +/- 4.50 ng/ml) gland area. Intravenous (i.v.) infusion of histamine 80 micrograms/kg/h) or intragastric (i.g.) instillation of 0.1 N HCl (4 mEq/h) for 3 h significantly decreased the generation of PGE2 in antral and fundic mucosa, but did not result in the formation of gastric lesions. Aspirin (ASA) given i.v. or i.g. for 3 h caused a further fall in the generation of PGE2 in the mucosa and when combined with i.v. histamine or i.g. HCl, it caused almost complete disappearance of PGE2 activity and the formation of antral ulcers in all tested cats. Exogenous PGE2, given i.v. in a dose (30 micrograms/kg/h) reducing histamine-stimulated (80 micrograms/kg/h) acid secretion by about 50%, prevented almost completely the formation of gastric ulcers induced by a combination of ASA plus i.v. histamine or i.g. HCl. This study indicates that the gastric mucosa generates PGE2 which is capable of preventing gastric ulcers induced by ASA combined with histamine or mucosal acidification.

Animals↗
PubMed1981

Gastric cytoprotection by prostaglandins, ranitidine, and probanthine in rats. Role of endogenous prostaglandins.

Intragastric administration of aspirin (ASA) plus 0.15 M HCl to fasted rats produced typical gastric ulcers accompanied by almost complete disappearance of mucosal prostaglandins (PGs). Pretreatment with various exogenous PGs that were biologically inactive (e.g. 6-keto-PGF1 alpha or PGF2 beta) or active (PGE2 and PGI2) but used in non-antisecretory doses prevented the formation of these gastric lesions ('cytoprotection'). Besides PGs, antisecretory compounds such as ranitidine, a new H2-receptor antagonist, and probanthine were also found to be cytoprotective, even when given in non-antisecretory doses. Mucosal generation of PGs in animals treated with ASA and HCl plus ranitidine or probanthine was very low and not significantly different from those receiving only ASA and HCl. Thus, the cytoprotection appears to be the property not only of PGs but also of conventional gastric antisecretory compounds such as H2-receptor antagonists or anticholinergics. This cytoprotection can be demonstrated under conditions excluding any role of gastric secretory inhibition and in the absence of endogenous PGs.

Animals↗