PubMed Health⌕ Search

Biomedical subjects

M Weis

Publications and source records attributed to M Weis.

At least 55 records · Page 3Linked to original sources

The continuing challenge of cardiac transplant arteriosclerosis.

Coronary arteriosclerosis of the graft, a manifestation of CAV, continues to limit the long-term success of cardiac transplantation. It is characterized by vascular injury induced by a variety of noxious stimuli, including the humoral and cellular immune system response to the allograft, ischemia-reperfusion injury, viral infection, immunosuppressive drugs, and classical risk factors. The proliferative and obstructive vascular lesions are thought to develop through repetitive endothelial injury followed by repair response. T lymphocytes, macrophages and neutrophils migrate to the subendothelial area via the activity of endothelial adhesion molecules, and, in turn, produce various cytokines and growth factors which cause progression of the process. Development of anti-endothelial antibodies may progress CAV in specific settings. Intravascular ultrasound studies reveal a dual morphology with donor-transmitted or de novo focal, noncircumferential plaques in proximal segments and/or a diffuse, concentric pattern of intimal proliferation observed in distal segments. In addition to the morphological alterations, functional endothelial and smooth muscle cell alterations may occur independently and transiently. The use of cyclosporine A levels > 3 mg/kg/day, HMG-CoA-reductase inhibitors and calcium antagonists has been shown to decrease the progression of CAV. Strategies for blocking T-cell costimulation and expression of adhesion molecules, cytokines and antiendothelial antibodies, as well as, antiproliferative drugs, methods to augment endogenous nitric oxide bioavailability and newer immunosuppressive regimens may be protective to endothelial injury and subsequent development of CAV. Revascularization procedures have an established, but very limited role in the setting of significant focal lesions. The ethical dilemma surrounding retransplantation, however, is considerable because of the scarcity of donor hearts.

Animals↗

Cardiac allograft vasculopathy: a review.

Cardiac allograft vasculopathy (CAV) remains a troublesome long-term complication of heart transplantation. It is manifested by a unique and unusually accelerated form of coronary disease affecting both intramural and epicardial coronary arteries and veins.CAV is characterized by vascular injury induced by a variety of noxious stimuli, including the immune system response to the allograft, ischemia-reperfusion injury, viral infection, immunosuppressive drugs, and classic risk factors such as hyperlipidemia, insulin resistance, and hypertension. The obstructive vascular lesions are thought to progress through repetitive endothelial injury followed by repair response. The role of major histocompatibility complex donor-recipient differences in the pathogenesis of CAV has not yet been completely elucidated. Intracoronary ultrasound studies reveal a dual morphology with donor-transmitted or de novo focal, noncircumferential plaques in proximal segments and/or a diffuse, concentric pattern observed in distal segments. A lack of correlation between microvascular and epicardial vessel disease suggests discordant manifestations and progression of CAV. Apoptosis and loss of functional vascular remodeling have to be considered as important mediators of clinically relevant CAV. Strategies for blocking T-cell costimulation and expression of adhesion molecules may help prevent chronic rejection in clinical transplantation. 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors and antiproliferative drugs may slow progression of CAV by various effects. Methods to augment endogenous nitric oxide bioavailability as well as newer immunosuppressive regimens may be protective. Balloon angioplasty has a limited role in the treatment of focal lesions. Experiences with coronary stenting, coronary artery bypass grafting, and transmyocardial laser revascularization are limited. Retransplantation has a worse outcome than initial transplantation.

Animals↗

[Heart transplantation--state of the art today].

In spite of pharmacological progress, end stage congestive heart failure is still associated with a decrease in quality and expectation of life. Heart transplantation remains the last therapeutic option for these patients. While the one year survival rate has increased over the last few years up to 84%, a major problem remains the significant lack of donors. Therefore, the criteria for the selection of candidates for cardiac transplantation have to be kept quite tight: Evidence of poor outcome without transplantation is associated with ejection fractions below 20 to 25%, cardiac indices less than 2.01/min/m2, left ventricular filling pressure above 20 mm Hg and a enddiastolic diameter of > 80 mm. There are, however, also quite important functional parameters indicating the need for heart transplantation, e.g. the maximal oxygene uptake being less than 10 ml/kg/min or below 50% of the age-appropriate value. Elevated pulmonary vascular resistance above 4 to 5 Wood units without a significant decrease during application of prostaglandin derivatives or inhalation of NO represents a contraindication for orthotopic heart transplantation; alternatively, a heterotopic transplantation can be considered. Since there is a significant shortage of suitable donor organs, the donor criteria have been broadened, e. g. the accepted donor age was increased to 60 years. Based on these extended criteria, a careful donor evaluation including cardiac history, cardiac examination, ECG and echocardiogram has to be performed. Coronary angiography in older donors is suggested, but in many cases not possible due to circumstances. Further precondition for a good graft function is a sophisticated donor management until the time of explantation. Hypovolemia and hypocalemia, hypothermia, hypoxia and rapid lost of circulating triiodothyronine (T3) have to be detected and balanced. The cardioplegic solution used might not only have an impact on the immediate postoperative performance of the graft, but also on the long term outcome, particularly with regard to graft vessel disease. There are generally two types of solutions: Those with intracellular and those with extracellular electrolyte concentrations. In addition, the potassium concentration might be of some importance. Potassium seems to damage endothelial cells and trigger subsequent immunological reactions. Therefore, high potassium concentrations in the cardioplegic solution might correlate with the incidence of graft vessel disease during the long term follow-up. The surgical technique for orthotopic heart transplantation developed at the beginning of the sixties by Lower and Shumway has been used unchanged for the last 30 years. The only alteration recently introduced is the separate direct anastomosis of the pulmonary and systemic veins in order to improve the atrial function. Until recently the commonly employed immunosuppressive strategy after heart transplantation consisted of the standard drugs cyclosporin, azathioprin and prednisolon. Some transplant-units use additionally induction therapy with antibody preparations. Many centers, however, abolished this regimen due to significant short and long term side effects. Promising new, more specific antibodies (which are chimerized or humanised) could revive the induction concept. The most thoroughly tested novel immunosuppressive agent is tacrolimus (FK506). It has been demonstrated to be 10 to 100 times more potent than cyclosporin A in in vitro and in vivo models. It binds to a different binding protein (FK-binding-protein) than cyclosporin (cyclophilin), but has a similar mechanism of action inhibiting the expression of T-cell-activator genes for certain cytokines. First non-randomised studies after heart transplantation performed at the University of Pittsburgh revealed that significantly more tacrolimus than cyclosporin patients were free of rejection. In order to confirm these observations, we performed a prospective randomised controlled clin

Clinical Trials as Topic↗

Variations of segmental endothelium-dependent and endothelium-independent vasomotor tone after cardiac transplantation (qualitative changes in endothelial function).

Endothelial dysfunction is a common phenomenon after cardiac transplantation. However, qualitative differences in endothelial vasoregulation at different coronary segments and at different postoperative times have rarely been explored. To uncover the functional variations of endothelium responses we infused the endothelium-dependent vasodilator acetyl-choline (50 micrograms) followed by the endothelium-independent vasodilator 3-morpholinosydnonimine (SIN-1) (1 mg; 16 patients) or nitroglycerin (0.3 mg; 14 patients) sequentially into the left coronary artery. We investigated the responses of 120 nonstenotic coronary segments (proximal and distal left anterior descending and right circumflex coronary arteries) in 30 patients with quantitative angiography (group 1: 13 patients, 12 +/- 1 months after cardiac transplantation; group 2: 17 patients, 55 +/- 3 months after cardiac transplantation). Continuous-flow measurement was performed to exclude significant reduction of microvascular response influencing epicardial dilation. Five responses to acetylcholine administration followed by nitrates were observed. On the one end of the spectrum, segments dilate to acetylcholine administration with no further dilation to exogenous nitric oxide, indicating completely preserved endothelial function. On the other end, segments constrict to acetylcholine with no change after endogenous nitric oxide, reflecting a defective endothelial and defective smooth muscle function. The different patterns of coronary vasomotor lone responses to endogenous nitric oxide followed by exogenous nitric oxide represent different degrees of endothelial function after cardiac transplantation. In addition, the functional assessment of endothelial integrity shows qualitative time-dependent differences between proximal and distal coronary parts. The existence of coronary segments with functioning endothelium indicates that the latter is not diffusely disturbed in all cardiac transplant recipients and that the endothelial damage is perhaps not irreversibly lost.

Acetylcholine↗

Chromatin condensation during apoptosis requires ATP.

The processes leading to morphological changes of the chromatin in cells that undergo apoptosis are presently unclear. We have recently shown that chromatin fragmentation and the nuclear morphological changes typically seen in apoptosis were reproduced in an in vitro system comprised of isolated rat thymocyte nuclei incubated in the presence of a lysate from Fas/APO-1-stimulated JURKAT cells [Chow, Weis, Kass, Holmström, Eriksson and Orrenius (1995) FEBS Lett. 364, 134-138]. Using this in vitro system, we now report that the presence of ATP is necessary for chromatin condensation, its movement to the nuclear periphery and apoptotic body formation. In clear contrast, chromatin cleavage into high-molecular-mass and oligonucleosomal-length DNA fragments induced by lysates derived from Fas/APO-1-activated JURKAT cells did not require the presence of ATP. The induction of these morphological changes by ATP could not be substituted by the analogues, adenosine 5'-[beta, gamma-methylene]triphosphate and adenosine 5'-[alpha, beta-methylene]-triphosphate, AMP, cAMP and UTP. However, adenosine 5'-[gamma-thio]triphosphate, and to a lesser degree GTP and ADP, could partially replace ATP in inducing nuclear apoptotic morphological changes. It is concluded that ATP is essential for the morphological changes occurring in nuclei during apoptosis, but not for DNA fragmentation.

Adenosine Triphosphate↗

Peroxidase-catalyzed oxidation of 3,5-dimethyl acetaminophen causes cell death by selective protein thiol modification in isolated rat hepatocytes.

In this study we used a peroxidase model system (glucose/glucose oxidase and horseradish peroxidase) to investigate the effect of extracellularly generated reactive metabolites of 3,5-Me2-acetaminophen on cell viability and on cellular thiol levels. Incubation of hepatocytes with 3,5-Me2-acetaminophen in the presence of glucose/glucose oxidase and horseradish peroxidase caused a concentration-dependent loss of cell viability. Loss of viability was associated with decreased protein thiol levels. Addition of the reducing agent DTT, but not catalase, during the incubation restored cellular protein thiol levels and arrested the cell killing. Protein thiol depletion occurred selectively to the mitochondrial and microsomal fractions and was specific for a very limited number of protein bands. The data suggest that the oxidative modification of individual protein cysteine residues within the latter two organelle fractions is critically involved in the mechanism of toxicity.

Acetaminophen↗

Autonomic cardiac abnormalities in alcohol-dependent patients admitted to a psychiatric department.

Standardized heart rate analyses were performed in 60 drug-free patients with alcohol dependence, who were admitted consecutively to a psychiatric department, and in 60 healthy normal matched subjects. The procedure included time and frequency derived measurements of heart rate variability (HRV). The investigations were carried out 3 weeks after admission and treatment on a closed ward to avoid autonomic hyperexcitability during withdrawal or relapse. The patients showed a significantly increased heart rate (p < 0.05), a significant reduction in the coefficient of variation while resting (p < 0.01) and a significant decrease of the high frequency power of spectral analysis (p < 0.01) compared with the normal subjects. Cardiovascular autonomic dysfunction was found in 12 of the patients, but in only one of the normal subjects (p < 0.01). The results indicated moderate parasympathetic (vagal) alteration in alcohol-dependent patients treated in a psychiatric department. This may have implications for psychotherapeutic or psychopharmacological treatment strategies and prognosis in such patients with alcohol dependence.

Adult↗

Time course of endothelial function in epicardial conduit coronary arteries and in the microcirculation in the long-term follow-up after cardiac transplantation.

BACKGROUND: Endothelial dysfunction has been reported in epicardial conduit coronary arteries and in the microcirculation after cardiac transplantation. It has been assumed that endothelial dysfunction may precede hemodynamically relevant transplant vasculopathy. In this study the long-term course of endothelial function was investigated in conduit coronary arteries and in the microcirculation after cardiac transplantation. METHODS: Patients were stratified according to time after transplantation (group I, up to 2 years after transplantation; group II, 2 to 4 years after transplantation; group III, more than 4 years after transplantation). Changes of the diameter of proximal, mid and distal segments of the left anterior descending coronary artery and the circumflex branch of the left coronary artery were investigated after endothelium-dependent and endothelium-independent stimulation with acetylcholine (ACh, 50 and 100 micrograms i.c.) and nitroglycerin 0.3 mg i.c. Coronary flow changes were assessed endothelium-dependently (ACh 50 and 100 micrograms i.c.) and endothelium-independently (dipyridamole 0.56 mg/kg i.v.) utilizing an 8 F Judkins-style Doppler catheter. RESULTS: Application of 50 micrograms/100 micrograms ACh resulted in a reduction of coronary artery diameter in proximal, mid and distal vascular segments of the left anterior descending coronary artery and the circumflex branch of the left coronary artery. The vasoconstrictive effect did not differ significantly between groups I,II and III. Nitroglycerin 0.3 mg i.c. increased coronary artery diameters in groups I, II and III. ACh (50 micrograms/100 micrograms) increased coronary flow index by 217 +/- 70%/236 +/- 110% (P < 0.05 vs. baseline) in group I, 113 +/- 26%/77 +/- 22% (P < 0.05 vs. baseline) in group II and 108 +/- 26%/109 +/- 21% (P < 0.05 vs. baseline) in group III. Dipyridamole increased coronary flow index by 296 +/- 78% (P < 0.05 vs. baseline) in group I, by 63 +/- 16% (P < 0.05 vs. baseline and vs. group I) in group II and by 113 +/- 30% (P < 0.05 vs. baseline and vs. group I) in group III. CONCLUSION: A constant vasosonstrictor response to ACh was observed in epicardial coronary arteries after cardiac transplantation indicating endothelial dysfunction independent of the time course. Endothelial dysfunction in these vessels may not be an early indicator of hemodynamically relevant transplant vasculopathy. Endothelium-dependent and endothelium-independent flow reserves decreased 2 years after transplantation and remained constant thereafter.

Acetylcholine↗

Is diurnal variation of mood associated with parasympathetic activity?

18 patients with distinct improvement of mood in the evening and 18 patients without, both suffering from major depression and equally treated with tricyclic antidepressants (TCA), and an age- and sex-matched group of 18 normal control subjects underwent a standardized heart-rate (HR) analysis (HRA) in the morning (08:00) and 12 h later in the evening (20:00). The battery of cardiovascular reflex tests included the determination of HR variability (HRV) while resting and during deep breathing, and a spectral HRA. The depressed patients with diurnal variation of mood showed significantly decreased HR and significantly increased HRV parameters while resting and during deep respiration in the evening. On the contrary, patients without diurnal changes of mood just showed a significant HRV increase during deep respiration in the evening. No statistically significant changes of these parameters were detected in the healthy subjects. It is not known if the observed changes of HR parameters representing increment of parasympathetic tone are intrinsically related to the mood swings or if this rhythm just becomes visible under the circumstances of depression. Also, the impact of TCA treatment upon the results remains to be elucidated.

Adult↗

Does bright-light therapy influence autonomic heart-rate parameters?

30 inpatients suffering from major depression (DSM-III-R), who did not fulfill the criteria of seasonal affective disorder (SAD), were treated with either doxepin or amitripytyline as monotherapy and supportively with bright light for 14 days. From days 15 to 19, bright light was replaced by dim light. 18 drug-free control subjects underwent an analogous sequence of bright- and dim-light applications. Phototherapy was applied between 06:00 and 07:30. Heart-rate (HR) analysis was performed in the patients and control subjects before and after the 5th session of bright and dim lights, respectively. 12 patients (40%) experienced improvement of mood during bright-light therapy (group I) while 18 (60%) did not (group II). Patients of group I, who reached significantly higher scores in the seasonal pattern assessment questionnaire than patients of group II, showed an increase of the coefficient of HR variation (HRV) during deep breathing as well as an increment of the high-frequency (HF) peak of spectral analysis exclusively after the bright-light sessions. Patients of group II did not show a significant alteration of these parameters, neither under the conditions of bright-light treatment nor under dim light. The control subjects experienced an increment of the HF power exclusively after bright light. The results suggest that a distinct subgroup of patients with non-SAD major depression shows a more pronounced light-associated increment of parasympathetically controlled cardiac functions than the other depressed patients and the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Involvement of multiple proteases during Fas-mediated apoptosis in T lymphocytes.

The mechanism of Fas antigen-mediated apoptosis is at present unclear. We show here that the 100,000 x g supernatant from cell lysates prepared from anti-Fas-stimulated JUR-KAT T cells, induces chromatin fragmentation in isolated nuclei with concomitant morphological changes typically seen in apoptosis. The formation of this apoptotic nuclei promoting activity (ANPA) in JURKAT T cells after Fas antigen ligation was blocked by the serine protease inhibitors, TPCK and DCI, and by the interleukin 1-beta-converting enzyme inhibitor, VAD-FMK. In addition, chromatin degradation and morphological changes mediated by the ANPA in isolated nuclei were inhibited by TPCK, but not by DCI or VAD-FMK. These results suggest that Fas-mediated apoptosis in T cells involves the activation of a cascade of proteases.

Antigens, Surface↗

Identifying delirious states and autonomic cardiovascular dysfunction associated with amitriptyline treatment by standardized analysis of heart rate.

Ninety-one patients treated with amitriptyline and 60 normal control subjects underwent a standardized heart rate analysis in supine posture. Tests included the determination of time- and frequency-derived measurements of heart rate variability. The patients differed significantly from the control subjects in all parameters investigated. Two-thirds of the patients treated with a tricyclic antidepressant (TCA) reached values that met the criteria for cardiovascular autonomic neuropathy. Our results provide evidence that heart rate analysis might be a more sensitive tool in diagnosing amitriptyline-associated anticholinergic delirium than determination of TCA plasma levels. Further research is needed to elucidate what implications the TCA-associated alteration of autonomic cardiovascular function might have for patients.

Adult↗

Cellular events in Fas/APO-1-mediated apoptosis in JURKAT T lymphocytes.

In the present study we investigated the Fas-mediated cellular events using the human leukemic T cell line, JURKAT. Ligation of the Fas receptor with a monoclonal antibody (IgM) resulted in the rapid (within 3 h) induction of apoptosis and was characterized by a sequence of distinct morphological and biochemical events. Thus, plasma membrane blebbing, condensation of the chromatin, and formation of high-molecular-weight (HMW) DNA fragments were the earliest events observed (by 45 min). They were followed by cleavage of DNA into oligonucleosomal-length fragments (laddering pattern) and the formation of apoptotic bodies, and finally, rounding of the apoptotic cells and complete cleavage of DNA into oligonucleosomal-length fragments occurred. The mitochondria remained structurally intact up to the stage of oligonucleosomal-length DNA cleavage, and the ability of the cells to exclude trypan blue was not compromised throughout the time course of the experiments. In contrast to many other model systems, apoptosis in JURKAT cells after anti-Fas treatment did not require the presence of extracellular Ca2+ or Mg2+ and was only partially inhibited by Zn2+. In addition, Fas-mediated apoptosis was unaffected by the presence of free radical scavengers or inhibitors of protein phosphatases, protein kinases, and nitric oxide synthesis. However, the serine protease inhibitors, N-tosyl-L-phenylalanine chloromethyl ketone (TPCK) and 3,4-dichloroisocoumarin (DCI) prevented anti-Fas-induced apoptosis in JURKAT cells. Low concentrations of these inhibitors blocked oligonucleosomal-length, but not HMW, DNA fragmentation. The latter required a higher concentration of TPCK or DCI to block. In addition, low concentrations of DCI also prevented Fas-mediated plasma membrane blebbing. In summary, our results suggest that proteolysis plays a central role in Fas-mediated apoptosis and that distinct proteolytic enzymes are involved in HMW DNA fragmentation, and oligonucleosomal-length DNA fragmentation, as well as in plasma membrane blebbing.

Antibodies↗

Amelioration of endotoxin-induced acute lung injury in pigs by HWA 138 and A 80 2715: new analogs of pentoxifylline.

We have evaluated the potential therapeutic effects of the xanthine derivatives HWA 138 (1-(5 hydroxy-5-methylhexyl)-3-methylxanthine) and A 80,2715 (1-(5 hydroxy-5-methylhexyl)-3-methyl-7-propylxanthine) on acute lung injury in endotoxemic pigs when administered following the septic insult. Salmonella abortus equi endotoxin (LPS) was given as a continuous intravenous infusion of 2 micrograms/kg/h over a period of 8 h. 1 h after the start of the LPS infusion the animals received a bolus injection followed by continuous infusion of A 80,2715 (3 mg/kg + 1.5 mg/kg/h; n = 6), HWA 138 (3 mg/kg + 1.5 mg/kg/h; n = 6), or saline (LPS control; n = 6). Treatment with A 80,2715 or HWA 138 inhibited the LPS-induced increases in the pulmonary artery pressure (p < .05; ANOVA) and in lung wet/dry weight ratio (p < .05), and ameliorated the LPS-induced deterioration in lung mechanics (decreased lung dynamic compliance (p < .05); increased peak airway pressure (p < .05)). Xanthine treatment, however, failed to significantly improve arterial PO2 and did not affect peripheral leukopenia. The results of this study suggest a potential therapeutic role for HWA 138 and A 80,2715 in attenuating endotoxin-induced acute lung injury.

Animals↗