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Biomedical subjects

H Kritz

Publications and source records attributed to H Kritz.

At least 37 records · Page 2Linked to original sources
PubMed1997

Prostaglandin E1 decreases human arterial accumulation of radiolabeled apo B-containing lipoproteins in vivo.

OBJECTIVE: An increased apo B-containing lipoprotein influx and cholesterol ester accumulation in arteries are well-known events in human atherogenesis. In vitro and experimental animal studies have provided evidence of a beneficial effect of PGE1 on both vascular apo B-containing lipoprotein accumulation and cholesterol ester content. METHODS: We examined the effect of PGE1 (administered via an intravenous portable infusion pump at a rate of 5 ng PGE1 kg-1.min-1 for 5 days a week, 6 h daily, over a total of 5 weeks) in ten patients (eight males, two females) on 123I-apo B-containing lipoprotein accumulation into the large arteries in vivo. Apo B-containing lipoprotein isolation was carried out by immunoaffinity chromatography and radiolabeling with the iodine monochloride method. 123I-apo B-containing lipoprotein accumulation was imaged and quantified by means of special computer software before and after 5 weeks of PGE1 therapy. RESULTS: PGE1 led to a significant decrease in maximal arterial apo B-containing lipoprotein retention. The mean decrease in the carotid and femoral arteries in type I lesions amounted to between 16.9% and 30.4%, and in type II lesions between 22.4% and 30.7%, 20 h after injection of radiolabeled apo B-containing lipoprotein. The type of arterial apo B-containing lipoprotein kinetic curves, however, remained unchanged. CONCLUSION: These findings indicate that PGE1 decreases the apo B-containing lipoprotein influx in the large arteries and the vascular cholesterol content, suggesting that PGE1 may lead to regression of lipid-rich lesions in human in vivo.

Alprostadil↗
PubMed1997

Chloroquine minimizes sampling artefacts for radioimmunological determination of thromboxane B2 in plasma.

Chloroquine is known to inhibit platelet activation by various mechanisms including arachidonic acid liberation from membrane phospholipids. We therefore examined the influence of chloroquine in addition to the conventional EDTA/acetylsalicylic acid cocktail on thromboxane B2-plasma values. In 11 healthy volunteers the influence of venous occlusion, needle diameter and EDTA (+ acetylsalicylic acid + chloroquine) was examined. In 27 healthy adults, 51 patients with clinically manifested coronary heart disease as well as in 31 patients with peripheral vascular disease parallel samples drawn in the presence of chloroquine showed lower thromboxane B2 in all these three groups of patients, especially in conditions associated with platelet activation and high thromboxane B2-values. These findings suggest that the routine addition of 10 mM chloroquine to the conventional stabilization cocktail can strongly be recommended.

Adult↗
PubMed1997

[Imaging of early carotid artery atherosclerotic lesions with 111In-labeled polyelonalhuman IgG (HIG)].

AIM: To assess the value of scintigraphy with 111In-HIG for diagnosis and evaluation of the stage and the clinical extent of carotid artery disease in humans a prospective clinical comparative trial of scintigraphy vs. sonography was performed. METHODS: 58 patients (38 male, 20 female; mean age 60 +/- 7 years) with hyperlipidemia and ultrasonographically detectable carotid artery lesions were studied. After i.v. injection of 18.5 MBq 111In-HIG, anterior scintigraphic images of the neck were acquired. Real time two-dimensional B-mode ultrasonography of the left and the right carotid arteries was performed. RESULTS: 111In-HIG-scintigraphy as compared to the morphological gold standard (ultrasonography) had a sensitivity of 70-73%, specificity of 33-41% and a positive predictive value of 77-82% for detecting carotid atherosclerotic lesions. There was, however, no significant correlation between scintigraphy and ultrasonography. CONCLUSION: However, the data provide evidence that the two imaging techniques are visualizing different aspects of atherogenesis. On the one hand a functional one reflecting the activity of the disease (111In-HIG) and on the other hand the morphological one resembling the extent of the disease (ultrasonography).

Aged↗
PubMed1997

[Multi-drug management after myocardial infarct].

Since the results of studies done with angiotensin-converting-enzyme(ACE)-inhibitors, systemic thrombolysis and primary percutaneous transluminal angioplasty (PTCA) have been published, post-myocardial infarction therapy has changed dramatically. In most european countries systemic thrombolysis as early as possible is the standard therapy. Cardiologists prefer more and more immediate revascularisation if the technical standard of the hospital is allowing an acute intervention. Pharmacological therapy is done initially with beta-blockers and platelet aggregation inhibitors, if necessary intravenously, since the results of the e.g. GUSTO- and the AIRE-study are known. If left ventricular dysfunction exists or develops, ACE-inhibitors are given after the third day post myocardial infarction.

Adrenergic beta-Antagonists↗
PubMed1997

[Acetylsalicylic acid after myocardial infarct].

There is no doubt about the positive influence of acetylsalicylic acid on vascular disease. The antithrombotic therapy with acetylsalicylic acid is a fundamental of secondary prevention of vascular events, especially in nonfatal myocardial infarction, instable angina pectoris, stroke and in patients with amaurosis fugax. Clinical studies done since 1990 about the effect of a low-dose therapy confirmed the experimental results, which showed that 25-50 mg acetylsalicylic acid per day are enough, to suppress platelet function as far as necessary, without influencing the protective function of prostacyclin synthesis. Side-effects can be reduced to a minimum with a reduced dosage. The wide-spread use of a low-dose acetylsalicylic acid therapy in primary prevention especially in patients at high risk has to be reevaluated in further studies.

Aspirin↗
PubMed1996

The prostacyclin stimulating plasma factor activity improves thromboresistance only if vascular PGI2-production is intact.

PGI2 is important in regulating platelet vessel wall interaction (1). In perfusion chamber experiments the amount of PGI2 formed was inversely related to the amount of platelets deposited (2). In 1978 a plasma factor was described which stimulates vascular PGI2-production (3). In later years, this activity has been monitored in different patient groups (for review see 4). Interestingly, it has been found that diseases associated with an increased bleeding tendency such as uraemia (5) or hepatic failure (6) were associated with an increased PF-activity while others with an enhanced thrombophilia sometimes show an absence of PF-activity (7). Recently, the PGI2 stimulating plasma factor has been purified and cloned (8). It was the aim of these experiments to assess whether PF-activity plays a role in local hemostasis regulation under in-vivo flow conditions and whether this is dependent on the presence of an intact PGI2-formation.

Adult↗
PubMed1996

Passive smoking and platelet thromboxane.

While active smoking is known to enhance platelet thromboxane production, no data on passive smoking is available yet. The influence of single and repeated exposure to passive smoke for 60 minutes in a 18 m3 room was assessed in non-smokers as compared to sex and age matched smokers. All the evaluated measures (malondialdehyde, plasma thromboxane B2, 11-dehydro-thromboxane B2, serum thromboxane B2, conversion of exogenous arachidonic acid to thromboxane B2 and to hydroxy-5, 8,10-heptadecatrienoic acid) were higher in smokers than non-smokers at baseline, immediately and 6 hours after passive exposure to cigarette smoke. Repeated exposure of non-smokers rendered their platelets more activated becoming close to the behaviour of smokers. These results indicate that passive smoking may activate thromboxane A2 release from the platelets, contributing to the development of hemostatic imbalance.

Adult↗
PubMed1996

[Differential diagnosis of diseases of the Achilles tendon. A clinico-sonographic concept].

Ultrasound of the Achilles tendon is a suitable means of differentiating various diseases of the tendon and the surrounding tissue. Different forms of degenerative disease (tendinitis, peritendinitis or bursitis, fibroosteitis, and Haglund's disease) can be discriminated from rheumatic and metabolic diseases. Congenital and developmental abnormalities can also be detected. Tendon degeneration mainly occurs in the ventral part of the medial third of the tendon ("critical zone"). Immature tissue in this area leads to temporary [correction of temorary] instability of the tendon with a high risk of rupture ("vulnerable phase"). With sonography, lesions of the Achilles tendon are visible early in the course of the disease.

Achilles Tendon↗
PubMed1996

Prostaglandin E1 increases binding of 123I-low-density lipoprotein to the human liver in vivo.

Previous in vitro radioligand binding data have shown that prostaglandin E1 (PGE1) increases the number and the binding affinity of low-density lipoprotein (LDL) receptors of the human liver. Experimental data in normo- and hypercholesterolaemic rabbits have confirmed these findings, showing a significant increase in LDL-binding to the liver in vivo after prolonged PGE1 therapy. METHODS. This study aimed to confirm the experimental and animal data in human in vivo. 123I-LDL binding to the liver was quantified in vivo in patients suffering from peripheral vascular disease, seven of them with heterozygous familial hypercholesterolaemia (HC) and five with normal total plasma cholesterol, after PGE1 administration (5 ng.kg-1.min-1; 6 h daily for 5 days/week for 5 weeks). LDL uptake by the liver was quantified by single photon emission computer tomography (SPECT). RESULTS. The amount of LDL trapped by the liver in normocholesterolaemics (45.6%) was significantly higher than in hypercholesterolaemics (22.0%). PGE1 induced an increase in liver LDL binding, which was more pronounced in HC (+38.2%) than in normocholesterolaemic patients (+8.11%).

Aged↗
PubMed1996

Prostaglandin E1 decreases circulating endothelial cells.

Prostaglandin E1 (PGE1) has been claimed to have cytoprotective effects and also to decrease thrombogenicity. The effect of intraarterial (i.a.) and intravenous (i.v.) administration of PGE1 on the number of circulating endothelial cells (CEC) was investigated in patients with peripheral vascular disease (PVD). Patients with hyperlipoproteinemia and also smokers exhibited higher numbers of CEC. PGE1 significantly (p < 0.01) decreased CEC. In parallel, plate let survival was prolonged (r = 0.82). This effect lasted for more than a month after stopping PGE1-therapy. The observed decrease in CEC reflects the decreased thrombogenicity and improved haemostasis achieved after PGE1.

Alprostadil↗
PubMed1996

Prostaglandin I2-mediated upregulation of 125I-LDL-receptor binding by isradipine in normo- and hypercholesterolemic rabbits in vivo.

The in-vivo low-density lipoprotein (LDL)-uptake by the liver was monitored during the initial 60 minutes after injection of radiolabelled LDL. LDL-uptake by the liver as evidenced by the liver/blood pool ratio in normocholesterolemic male New Zealand white rabbits (44.2 +/- 3.1% of whole body activity) was almost double as compared to the ones fed a 1% cholesterol enriched diet (22.5 +/- 3.3%). The blood disappearance of 125I-LDL was significantly faster in normocholesterolemic animals. A 4-week treatment with the dihydropyridine calcium channel blocker isradipine resulted in a significantly enhanced LDL-binding by the liver, both in normo- and hypercholesterolemic animals to a comparable extent. A concomitant acetylsalicylic acid (ASA) treatment completely abolished the benefit induced by isradipine while ASA alone was ineffective. Similarly, 125I-LDL disappearance from blood was improved by isradipine, while ASA neutralizes this effect. Again, ASA alone did not change the kinetics. Plasma cholesterol and high-density lipoprotein (HDL) cholesterol remained unchanged. Isradipine significantly enhanced vascular prostaglandin(PG)I2-generation while concomitant ASA treatment or ASA application alone almost completely depressed PGI2-formation. It is concluded that the improved LDL-binding by the liver is due to an enhanced PGI2-formation evoked by isradipine.

Animals↗
PubMed1996

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.

Adolescent↗
PubMed1996

MRI in assessment of the systemic manifestations of rheumatological disease.

Magnetic resonance imaging (MRI) has emerged as complementary imaging modality to conventional radiography. The same diagnostic rules that are used in the interpretation of the routine radiographs should be applied to the analysis of MR images with the macroscopic spread of the disease as a main diagnostic clue. MRI has been shown to be a sensitive tool in detecting early arthritic changes and erosions, inflammation in periarticular tendons and tendon sheaths, and in juxtaarticular bursae. MRI plays a pivotal role in diagnosis of arthritis of the craniocervical junction and its complications. It also has been used effectively to detect insufficiency fractures and osteonecrosis. MRI may be important in diagnosing early arthritis, in specifying the differential diagnosis of rheumatic disease, and in selecting subgroups of patients to provide tailored therapeutic regimens.

Arthritis, Rheumatoid↗
PubMed1996

Low cholesterol and cancer.

PURPOSE: The relation between plasma cholesterol (CH) concentration and mortality is complex. The plasma CH concentration correlates positively with mortality from coronary heart disease, but some studies have shown a negative relation with death from cancer. If these two relations reflect causal mechanisms that are reversible by changing the plasma CH concentration, the benefits of lipid reduction for heart disease might be offset by an increased mortality from cancer. Different aspects between lipid metabolism and cancer, as well as new insights into this interesting field, are discussed. METHODS: The literature was searched using MedLine through 1966 and January 1996. RESULTS: There is no evidence from the data available at present that the association between low CH and a higher risk of cancer is causal. CONCLUSION: This issue should not affect the advice on health matters offered by doctors, especially to patients with other risk factors for cardiovascular disease. The possibility that hypercholesterolemia (HC) drugs can induce a reduction of tumor-cell growth makes them potentially useful as an adjuvant to chemotherapy and ultimately increases the probabilities in the prevention and treatment of cancer.

Animals↗
PubMed1996

Imaging of atherosclerosis (Part I).

Atherosclerosis is the leading cause of morbidity and mortality in the Western World. Standard imaging techniques such as angiography, ultrasonography and computed tomography are still not effective in detecting atheromatous plaques in their early stages of development, when the lesions are most metabolically active and therapeutic interventions could beneficial. These techniques identify morphological changes such as increased wall thickness, decreased luminal diameter or related haemodynamic changes such as turbulence of blood flow. Unfortunately, all these phenomena occur when the plaque has evolved and encroaches on the lumen. There is a need for non-invasive methods that could assess the presence and the extension of atherosclerotic disease in its early stages, when the lesions are in their metabolically most active stage but still do not narrow the diameter of the lumen. Part I of this article presents an overview of the diagnostic procedures angiography, sonography, computed tomography and magnetic resonance tomography in imaging atherosclerotic lesions. Part II will concentrate on the diagnostic possibilities of scintigraphic imaging and positron emission tomography.

Animals↗