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T Berndt

Publications and source records attributed to T Berndt.

12 recordsLinked to original sources
PubMed2001

Role of HSP70i in regulation of biomaterial-induced activation of human monocytes-derived macrophages in culture.

The functioning of an implant depends on the material properties and the wound-healing process. The latter is led by an inflammatory reaction guided mainly by monocyte/macrophage activity. This in vitro study investigated human monocytes/macrophages in culture from 2 h to 10 days on silicone, polyurethane, teflon and TCPS. Analysis of cytokine release by ELISA showed that maturing macrophages have different capacities to produce cytokines TNFalpha, IL10, IL8 and GM-CSF. The long culture-mature macrophages on all polymers produced comparable low levels of TNFalpha, IL10 and IL8. Monocytes/macrophages on polyurethane and teflon, and those on silicone only in long culture-time produced high GM-CSF amounts, where as those on TCPS exhibited low levels of GM-CSF. FACS analysis revealed that HSP70i was highly inducible after short time culture yet this high level was maintained in long culture-mature macrophages on TCPS only, whereas on other polymers the mature macrophages showed a high reduction in HSP70i level, which demonstrated a high stress-response by cells on TCPS. Accordingly, CLSM-analysis revealed low nuclear NF-kappaB in cells on TCPS and high nuclear NF-kappaB in mature macrophages on silicone and polyurethane, showing a high cellular activation on the latter two polymers. This corresponded also to the high mitochondrial activity by XTT metabolism displayed by the mature macrophages on polyurethane >/= silicone > teflon > TCPS. These data show a correlation of (1) cytokines (TNFalpha, GM-CSF) and HSP70i, (2) NF-kappaB and HSP70i by monocytes/macrophages after contact with polymers. Thus, HSP70i might be a useful molecular candidate for exploring biomaterial-induced inflammatory reaction.

Journal Article↗
PubMed1997

Release of a stable cardiodepressant mediator after myocardial ischaemia during reperfusion.

OBJECTIVE: The aim of this study was to investigate whether cardiodepressant mediators are released after myocardial ischaemia during reperfusion. METHODS: Using a double heart model, the effect of the reoxygenated coronary effluent of an isolated guinea pig heart on a sequentially perfused second heart was studied under control conditions and after 10 min ischaemia of the first heart. Investigation of the modulating role of known autacoids took place by using free radical scavengers, an NO synthase inhibitor and adenosine receptor antagonists. In order to identify the chemical nature of cardiac metabolites, the coronary effluent was also subjected to different chemical treatment modes. RESULTS: No haemodynamic changes were observed during sequential perfusion under control conditions. After 10 min of global ischaemia in heart I, a marked decrease in LVP (-22%), LVdP/dtmax (-43%), LVdP/dtmin (-41%) and coronary perfusion pressure (-25%) was measured in heart II during sequential perfusion. The negative inotropic effect was rapid in onset and reversible within 5 min; free radicals, nitric oxide and adenosine were not involved. Storage of the coronary effluent of the first heart up to 24 h, heating, or protease treatment did not modify its cardiodepressant effects on the second sequentially perfused heart. CONCLUSIONS: These results suggest the release--from an isolated heart after ischaemia during reperfusion--of a cardiodepressant mediator which induces a potent reversible negative inotropic effect on a sequentially perfused heart. The mediator is stable and in all probability not a protein.

Adenosine Deaminase↗
PubMed1997

Cardiodepressive mediators are released after ischemia from an isolated heart: role of coronary endothelial cells.

OBJECTIVES: This study was designed to ascertain whether cardiodepressive mediators released after ischemia originate from coronary endothelial cells. BACKGROUND: Endothelial cells modulate myocardial contractility under physiologic conditions. Few data are available describing the role of coronary endothelial cells on myocardial function after ischemia. METHODS: Using a model of sequential perfusion of two isolated rat hearts, the effect of the reoxygenated coronary effluent of heart I was investigated on myocardial contractility of heart II. After 40 min of separate perfusion at constant flow (10 ml/min), the two hearts were perfused sequentially with (group I) or without (control group) preceding ischemia (10 min) of heart I. In groups II and III, the coronary endothelium of heart I was functionally removed by Triton X-100 or hyperkalemic infusion before global ischemia. Endothelial damage was confirmed by functional tests and electron microscopy. RESULTS: Under control conditions no changes were observed in heart II during sequential perfusion. In contrast, after 10 min of ischemia in heart I, a marked reversible decrease in left ventricular pressure, left ventricular dP/dtmax and left ventricular dP/dtmin (-55%, -66% and -70%, respectively) was observed in heart II. Heart rate and coronary perfusion pressure did not change significantly. Selective endothelial damage of heart I before ischemia did not modify the negative inotropic effect observed in heart II. CONCLUSIONS: Cardiodepressive mediators are released after ischemia during reperfusion from an isolated heart and induce a reversible negative inotropic effect in a sequentially perfused heart. It is unlikely that these agents are derived from the coronary endothelium.

Animals↗
PubMed1980

Renal brush border membrane adaptation to phosphorus deprivation: effects of fasting versus low-phosphorus diet.

Alimentary phosphorus deprivation due to a low-phosphorus diet (LPD) elicits a profound antiphosphaturia and an increase in sodium-dependent inorganic phosphate (Pi) uptake by renal cortical brush border membrane (BBM) vesicles. But, in alimentary phosphorus deprivation due to total fasting, high urinary excretion of Pi persists. In the present study, we determined whether low tubular reabsorption of Pi in fasting is due to a diminished capacity of the specific Pi transport system with the renal cortical luminal BBM or whether it is due to a reduced transepithelial reabsorption of Pi because of metabolic conditions occurring in proximal tubule cells during fasting. Sodium-dependent Pi transport in compared with fasted rats or rats fed a normal phosphorus diet. Sodium-dependent uptake of D-glucose was significantly lower in LPD rats, compared with fast animals or animals fed a normal diet. Thus, in contrast to LPD, fasting does nt elicit an increase in Pi transport and a decrease in D-glucose transport across the isolated renal BBM. The same differences in BBM transport of Pi were present also in thyroparathyroidectomized rats. Further experiments demonstrated that the adaptation of renal function and the renal BBM transport to LPD are overridden by a subsequent period of total fasting. Results of the present study show that fasting both prevents and reverses the renal response of rats to alimentary phosphorus deprivation. The differences in Pi excretion between fasted rats, LPD rats, and LPD rats subsequently fasted are attributed, at least in part, to specific adaptive changes in sodium-dependent Pi transport across the luminal BBM, rather than to alterations in other cellular (metabolic) components of transepithelial Pi reabsorption in the proximal tubule.

Animals↗
PubMed1978

Nephron heterogeneity of phosphate reabsorption.

Previous micropuncture studies in rats have demonstrated that fractional phosphate delivery (FDP%) from superficial distal nephrons is higher than in urine. To determine whether this apparent reabsorption could be accounted for by a lower FDP% from the deep nephrons, FDP% was determined in free-low micropuncture from deep nephrons (DN) (ascending limb of the loop of Henle in the papilla), superficial nephrons (SN) (distal tubules in the cortex), and urine (duct of Bellini). In six acute thyroparathyroidectomized (TPTX) rats, FDP% in DN was significantly less than SN. The urinary fractional phosphate excretion (FEP%) was significantly less than in the SN, but not significantly different from the DN. In six chronic TPTX rats, FDP% in DN was significantly less than in SN. The urinary FEP% was significantly less than the FDP% in the SN, and significantly less than the FDP% in the DN, evidence which favors phosphate reabsorption in the terminal nephron. We conclude that in TPTX rats, which are conserving phosphate, deep nephrons reabsorb phosphate more avidly than superficial nephrons.

Animals↗
PubMed1977

Phosphate transport in superficial and deep nephrons in phosphate-loaded rats.

We tested the hypothesis that greater phosphate delivery from deep nephrons than from superficial nephrons contributes to the addition of phosphate to the collecting system during phosphate loading. In the first group of eight anesthetized Munich-Wistar rats infused with phosphate and parathyroid hormone (PTH), fractional delivery of phosphate (FDP%) from superficial distal tubules was 56 +/- 6%, significantly less than the amount appearing in the urine, 67 +/- 6% (P less than 0.01). In the second group of six rats, we determined whether this addition of phosphate could be accounted for by a higher FDP% from the deep nephrons. Free-flow micropuncture collections were taken from deep nephrons (ascending limb of the loop of Henle in the papilla), superficial nephrons (distal tubules in the cortex), and urine (duct of Bellini). The FDP% to the ascending limb of the loop of Henle in deep nephrons was 78 +/- 10%, significantly greater than to the distal convoluted tubules in superficial nephrons, 51 +/- 6% (P less than 0.005), and the fractional excretion of phosphate in urine, 72 +/- 10% (P less than 0.05). Although a difference between FDP% in superficial and deep nephrons due to reabsorption in the ascending limb of the loop of Henle cannot be ruled out from the present data, other studies indicate that this interpretation is unlikely. We conclude that greater phosphate delivery by deep nephrons contributes to the addition of phosphate to the collecting system of phosphate-loaded rats.

Animals↗
PubMed1976

Left anterior descending coronary artery obstruction. Clinical, electrocardiographic, and angiographic correlates.

Seventy-six patients with severe (greater than 80%) occlusive left anterior descending coronary artery disease by coronary angiography were examined for the electrocardiographic characteristics of this disease in the presence (group A 59 patients) or the absence (group B 17 patients) of anterior wall asynergy (akinesis or dyskinesis). The incidence of clinically documented anterior myocardial infarction in these two groups of patients was examined. The collateral circulation to the left anterior descending coronary artery was also examined in the groups of patients with and without anterior wall asynergy. Thirty-eight of 59 (64%) patients with anterior wall asynergy (group A) showed electrocardiographic signs of anterior myocardial infarction, 17 per cent showed probable electrocardiographic signs of anterior myocardial infarction and 19 per cent showed no electrocardiographic signs. None of the 17 patients without anterior wall asynergy (group B) showed electrocardiographic signs of anterior myocardial infarction. In group A 74.6 per cent had documented clinical evidence of previous anterior myocardial infarction. Collateral filling of the distal left anterior descending coronary artery was seen in 71 per cent of group A and 100 per cent of group B patients. There was a significantly higher incidence (P = 0.02) of collateral filling in the patients without electrocardiographic evidence of definite anterior myocardial infarction (93% of 28 patients), than in those who showed definite electrocardiographic evidence of anterior myocardial infarction (66% of 38 patients).it is concluded that severe occlusive left anterior descending coronary artery disease with anterior wall myocardial asynergy is usually associated with electrocardiographic signs of anterior myocardial infarction, whereas equally severe left anterior descending coronary artery disease without anterior wall asynergy is rarely associated with electrocardiographic abnormalities of anterior myocardial infarction. Severe left anterior descending coronary artery obstruction without electrocardiographic and angiographic evidence of anterior myocardial infarction is usually associated with collateral circulation to the left anterior descending coronary artery and collateral circulation to the left anterior descending coronary artery is present less frequently when obstruction is associated with anterior myocardial infarction.

Adult↗
PubMed1975

Occult atrial septal defect in adults.

Two patients are described who presented with congestive heart failure and were found to have an atrial septal defect with a pulmonary blood flow approximately twice the systemic blood flow. Most of the usual clinical signs of atrial septal defect were absent, and the diagnosis was established by right heart catheterization and radioisotopic angiography. Both patients had hypertension and coronary artery disease. Atrial septal defect in the adult patient may not be recognized because of associated cardiac disease, including coronary artery disease and hypertension, or pulmonary disease which may obscure the usual clinical signs of a septal defect. Radioisotopic angiography and right heart catheterization should be considered in any patients with heart disease or congestive failure of obscure cause even if the usual diagnostic signs of atrial septal defect are absent.

Cardiac Catheterization↗
PubMed1975

Evaluation of portable radionuclide method for measurement of left ventricular ejection fraction and cardiac output.

Seventeen patients with coronary artery, valvular, or myopathic heart disease were studied to determine correlations of the cardiac output and ejection fraction when comparing the results obtained with a portable probe technique using 113mIn with those obtained with standard methods (cineangiographic, Fick, and dye dilution). With ejection fractions ranging from o.10 to 0.85, the coefficient of correlation was 0.90 when comparing cineangiographic and radionuclide techniques. Cardiac output determinations by the radionuclide technique also correlated well with standard methods (r equals 0.88). The radionuclide method shows promise as an accurate, safe, and simple method in the evaluation of cardiac function at the bedside.

Angiocardiography↗