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D Erb

Publications and source records attributed to D Erb.

6 recordsLinked to original sources
PubMed1997

[Exercise hemodynamic in hypertension associated with coronary microangiopathy, coronary heart disease and without ischemic syndrome effect of nifedipine].

OBJECTIVE: Is heart function during exercise impaired in hypertensive patients with effort angina and ST-segment depression but normal coronary angiograms? METHODS AND RESULTS: In 12 hypertensive patients (group 1; aged 53 +/- 4 yrs), who had ST-segment depression during exercise, concomitant angina pectoris but normal coronary angiograms, and no LVH, left ventricular function at rest and during exercise was studied by cardiac catheterization and compared with 12 hypertensives with CAD (group 2; aged 56 +/- 5 yrs) and 12 hypertensives without ST-segment depression (group 3; aged 56 +/- 7 yrs) after discontinuation of all cardiac medications. PCWP was normal at rest and pathologically increased at 79.2 +/- 17.9 watts only in group 1 and 2 (30.2 +/- 6 mm Hg; 31.5 +/- 5 mm Hg, respectively) but not in group 3 (18.5 +/- 3 mm Hg; p < 0.001). Repeated measurements during exercise and 30 min after 10 mg nifedipine orally, showed a significant (p < 0.001) and nearly identical fall in MAP, an increase in CI (p < 0.01), and an unchanged HR x SBP in all groups. However there were significant differences in decrease of PCWP (group 1: -41.4%; group 2: -22.9%, p < 0.01; group 3: -25.4%, p < 0.01) with concomitant reduction in ST-segment depression (p < 0.01) in group 1 and 2 (-43.7% and -36% respectively). CONCLUSIONS: ST-segment depression during exercise ECG with concomitant angina pectoris is not a false-positive finding in hypertensive patients with normal angiograms and without LVH but demonstrates myocardial ischemia, resulting in an impaired left ventricular heart function. This seems to be mainly caused by a functional changeable disorder of the coronary vascular bed as heart function is improved after nifedipine.

Coronary Disease↗
PubMed1992

Expression and function of VLA-alpha 2, -alpha 3, -alpha 5 and -alpha 6-integrin receptors in pancreatic carcinoma.

The expression of the VLA-integrins alpha 2, alpha 3, alpha 5 and alpha 6 was studied immunohistochemically in tissue samples from ductal pancreatic cancer, chronic pancreatitis, normal pancreas and in 8 cell lines of ductal human pancreatic cancer. Furthermore, adhesion assays on purified extracellular matrix (ECM)-compounds were used to define the function of alpha 2, alpha 3, alpha 5 and alpha 6 in pancreatic cancer cells. Immunohistochemically, VLA alpha 2 and VLA alpha 6 were moderately to strongly expressed on the basal surface of ductal and acinar cells in normal pancreatic tissue, while centro-acinar cells predominantly expressed VLA alpha 3 and VLA alpha 5. Pancreatic carcinoma showed intense staining for VLA alpha 2 and VLA alpha 6 with a diffuse distribution on the cell surface. The redistribution of VLA alpha 2 and VLA alpha 6 may reflect a loss of spatial arrangement of tumor cells and their ability to interact randomly with extracellular matrix structures during invasion and metastasis. Expression of VLA alpha 3 and VLA alpha 5 in pancreatic carcinoma was heterogeneous, ranging from moderate to weak, and was lost in about 50% of the cells. Two pancreatic carcinoma cell lines (PC 3, PC 44) were further investigated in adhesion assays. Monoclonal antibodies (MAbs) against alpha 2 (GI 9, 10-G-11) were able to inhibit tumor-cell adhesion to collagen IV (59%-72%) in both cell lines. A MAb against alpha 6 (GoH3) inhibited tumor-cell adhesion to laminin (52%-86%) in both cell lines. These results suggest that alpha 2 is a collagen-binding site and alpha 6 a laminin-binding site in pancreatic cancer cells. The anti-alpha 5-MAb SAM I inhibited adhesion of PC3 to fibronectin (76%), being without effect in PC44. Adhesion of both cell lines to fibronectin was almost completely inhibited by RGDS (85%-88%). Thus, alpha 5 is a functionally important fibronectin binding site in some pancreatic carcinoma cells, suggesting further RGD-dependent fibronectin binding sites in other pancreatic carcinoma cells.

Amino Acid Sequence↗
PubMed1992

[Disordered 24-hour blood pressure rhythm in normotensive and hypertensive asthma patients].

Asthmatic patients typically show a nocturnal increase in bronchial obstruction. In 100 asthmatic patients, we investigated if there is also a reduced decline of blood pressure; we used 24-h blood-pressure monitoring. The whole group consisted of 50 hypertensive asthmatic patients (group 1, 48.8 +/- 11 years, 30 females, 20 males), 25 normotensive asthmatic patients (group 2, 49.6 +/- 10 years, 22 females, 3 males) and 25 antihypertensive-treated asthmatic patients (group 3, 50.2 +/- 8 years, 15 females, 10 males). 52% of group 1, 52% of group 2, and 44% of group 3 patients showed no sufficient nocturnal systolic and diastolic blood pressure decline (less than - 15%). When we looked only for systolic blood pressure that was also the case in 82%, 92%, and 64% of the patient groups', respectively. There was no significant difference in daytime blood pressure between hypertensives (group 1) without (142 +/- 9/93 +/- 5 mmHg) and with 142 +/- 12/92 +/- 6 mmHg) sufficient nocturnal blood pressure decline, however, nighttime blood pressure (135 +/- 14/84 +/- 5 mmHg versus 123 +/- 14/72 +/- 6 mmHg) was significantly (p less than 0.0001) different. This was also true for the normotensive asthmatic patients (group 2). The results cannot be explained by differences in heart rate, degree of asthma, or in anti-obstructive medication.

Asthma↗
PubMed1991

Impaired left ventricular function during exercise in hypertensive patients with normal coronary arteriograms.

Patients with left ventricular hypertrophy (LVH) often exhibit manifestations of myocardial ischemia. In 17 hypertensive patients (group 1, mean age of 56 +/- 4 years, 10 females, 7 males) with ST-segment depression during the exercise electrocardiogram (ECG) and effort angina and normal coronary arteriograms, the left ventricular function at rest and during exercise was studied by heart catheterization. The results were compared with 17 hypertensive patients (group 2, mean age of 56 +/- 6 years, 6 females, 11 males) with coronary artery disease (CAD). The normal pulmonary wedge pressure at rest (group 1, 8.9 +/- 3 mm Hg; group 2, 8.9 +/- 3 mm Hg) was pathologically increased (p less than 0.001) in both groups (group 1, 27.1 +/- 5 mm Hg; group 2, 28.8 +/- 7 mm Hg) even at a work load of 50 W with a further increase at 75 W to 31 +/- 4 and 29.7 +/- 4 mm Hg, respectively. Cardiac output was normal. There was no significant correlation between ST-segment depression, pulmonary wedge pressure, LVH, and Holter ECG. Hypertensive patients without CAD may reveal a disturbed pump function due to ischemia even at low work loads, which does not differ significantly from patients with CAD. This may provoke subendocardial fibrosis and thereby contribute to the development of heart failure.

Blood Pressure↗