Search PubMed⌕ Search

Biomedical subjects

M Vogt

Publications and source records attributed to M Vogt.

At least 145 records · Page 8Linked to original sources
PubMed1991

Coronary vascular changes in the progression and regression of hypertensive heart disease.

Coronary hemodynamics (blood flow, coronary reserve, myocardial oxygen consumption) were analyzed in both experimental and clinical hypertension. Significantly reduced coronary reserve was found in hypertensive patients with left ventricular hypertrophy. Medial hypertrophy of small coronary vessels associated with a marked increase in the wall thickness/radius ratio was considered sufficient to explain the impaired coronary flow in hypertensive left ventricular hypertrophy. After long-term pharmacotherapy, there was normalization of both medial hypertrophy and coronary reserve. This small-vessel abnormality correlates well with clinical findings in hypertensive heart disease (angina and electrocardiographic changes despite normal coronary arteriogram). Moreover, this structural adaptation of the small vessels may carry the inherent risk of an impaired oxygen supply to the hypertrophied myocardium. Thus, late cardiac failure of the hypertrophied heart in hypertension may be attributed, in part, to this microcirculation disorder. Conversely, reversal of left ventricular hypertrophy and of hypertrophy of vascular smooth muscle by specific pharmacotherapy can be considered a possible rational approach to the prevention of cardiac failure in hypertensive patients. Controlled clinical trials are needed to confirm these findings with regard to prevention of heart failure, and pharmacotherapeutic studies are necessary to define the optimal drug regimen for reversal of vascular smooth muscle hypertrophy.

Adult↗
PubMed1991

Phlebosclerosis: disorder or disease?

Morphological examinations were performed in a total of 318 subjects (168 men and 150 women). Electron microscopic and immunohistological examinations were added in selected cases. Phlebosclerosis is a fibrotic degeneration of the venous wall that is regularly found in non-varicose veins of aged persons. Although its incidence is age-related, no correlation exists between degree and age. Marked degrees may occasionally occur already below the age of twenty. Both sexes and all the superficial leg veins (various levels of the long saphenous vein and minor venous branches) are likewise affected. The intima of the superficial leg veins is predominately involved, but media and adventitia may also be affected. Although the morphological appearance is similar to that of arteriosclerosis, localization, progression and clinical consequences are different. Phlebosclerosis of superficial leg veins is a disorder of little direct clinical consequence, but may have an indirect influence on the wall contractility. In the deep leg veins, however, a distinct phlebosclerosis of the intimal layer may be responsible for the development of thrombosis. As a secondary alteration, phlebosclerosis may complicate varicose veins (fibrous degeneration of wall areas with tortuosity, ectasia and smooth muscle atrophy). These lesions may further impair the already deficient reflux function. However, phlebosclerosis is no prerequisite but a late sequel of varicosis.

Adult↗
PubMed1990

[Typical nosocomial infection with an unusual cause: Hafnia alvei. Report of 2 cases and literature review].

The route of infection and the course of two typical nosocomial infections are described in two patients infected with a rare gram-negative bacterium. Both patients underwent cardiovascular surgery. They were placed close to each other in the intensive care unit for several days and suffered from pneumonia and from wound infection respectively. In both patients bacterial culture grew Hafnia alvei. Successful antibiotic treatment was achieved with Netilmicin and Imipenem. Urinary tract, respiratory tract and wound infections are the most frequent nosocomial infections according to the literature. Risk factors are duration of stay in the intensive care unit, shock, poor general condition and advanced age.

Aged↗
PubMed1990

[Disseminated histoplasmosis as the first manifestation of HIV infection].

A 29-year-old man who had been abroad for several years (mainly Mexico) fell ill with fever (up to 39.8 degrees C), night sweats, weight loss of 10 kg in 6 months (height 181 cm, weight 50.5 kg) and abdominal pain. Computed tomography of the abdomen revealed many enlarged abdominal lymph nodes. Serological tests were positive for HIV antibodies. Fine-needle biopsy of one of the enlarged lymph nodes revealed numerous macrophages with round inclusions, typical for Histoplasma capsulatum. Disseminated histoplasmosis was confirmed by direct antigen demonstration in serum and urine. The patient's serious clinical condition clearly improved and lymph node enlargement regressed after starting specific i.v. treatment with amphotericin B (initially 20 mg/dl, then 50 mg/dl). Although complete cure of the histoplasmosis in connection with the HIV infection is not to be expected, the patient has remained without symptoms for four months on 50 mg weekly of amphotericin B i.v., later changed to imidazole derivatives (400 mg ketoconazole or 200 mg itraconazole, respectively.

Adult↗
PubMed1990

[Recurring oral aphthae, genital ulcers, erythema nodosum, arthralgias].

A 37-year-old Turkish patient suffered from recurrent oral aphthosis, genital ulcers, skin lesions and inflammatory eye disease. Because of typical history, physical findings and absence of laboratory abnormalities Morbus Behçet was diagnosed. Under treatment with prednisone and azathioprine his symptoms disappeared and there was no recurrence of Behçet disease for three months.

Adult↗
PubMed1990

Disorders of coronary microcirculation and arrhythmias in systemic arterial hypertension.

Arterial hypertension is associated with an increased cardiovascular mortality and an increased risk of sudden cardiac death. Therefore, the prevalence of ventricular arrhythmias, identified on 24-hour ambulatory electrocardiographic monitoring, was analyzed in 54 patients (aged 56 +/- 10 years) with arterial hypertension and normal coronary angiograms with respect to left ventricular muscle mass, mass-to-volume ratio, systolic wall stress and coronary microangiopathy. Ventricular ectopic beats (VEBs) were assessed according to a score (modified Lown classification: 1 = no VEB, 2 = less than 30 VEB/hour, 3 = greater than 30 VEB/hour, 4 = polymorphic VEB, 5 = bigeminys, 6 = couplets, 7 = nonsustained ventricular tachycardia). Coronary blood flow was measured by the gas chromatographic argon method. Coronary reserve was determined by measuring coronary resistance before (Rcor) and after (Rmin) administration of intravenous dipyridamole (0.5 mg/kg body weight) (Cor Res = Rcor/Rmin). The frequency (p less than 0.05) and severity (p less than 0.025) of VEBs was higher in normotensive than in hypertensive patients. Although the score of VEBs did not correlate with left ventricular muscle mass (r = 0.20, difference not significant), a slight correlation with mass-to-volume ratio (r = 0.32; p less than 0.05) and systolic wall stress (r = 0.30; p less than 0.05) was found. Hypertensives with a severely reduced Cor Res (less than 2.0) had a significantly higher score of VEBs than those with a nearly normal Cor Res (greater than 3.0) (5.0 +/- 1.5 vs 3.5 +/- 1.7; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1990

Blood rheology as a contributing factor in reduced coronary reserve in systemic hypertension.

The influence of blood fluidity on coronary reserve in patients with essential hypertension and normal coronary arteries was examined. The coronary reserve, expressed as the ratio of coronary vascular resistance under resting conditions to the coronary vascular resistance after administration of dipyridamole, was 4.1 +/- 1.5 in 10 normotensive patients with normal coronary arteries, whereas the mean value was only 2.4 +/- 0.8 in 35 hypertensive patients. When compared with the normotensive control group the 35 hypertensive patients had significantly higher levels of hematocrit (45.9 +/- 3.7 vs 42.3 +/- 3.6; p less than or equal to 0.01) and plasma viscosity (1.39 +/- 0.07 vs 1.32 +/- 0.06 mPas; p less than 0.01). Plasma fibrinogen (291 +/- 67 vs 251 +/- 25 mg/dl) and whole blood viscosity at a shear rate of 2 s-1 (7.77 +/- 1.1 vs 7.21 +/- 1.28 mPas) and at a high shear rate of 100 s-1 (4.23 +/- 0.57 vs 3.91 +/- 0.64 mPas) demonstrated a trend without statistical significance toward higher values in hypertensive patients. When the hypertensive group was further divided according to the coronary reserve (less than 2.5, severely impaired coronary reserve; greater than 2.5 less than 3.8, moderately impaired coronary reserve), the parameters of blood fluidity clearly correlated inversely with coronary reserve. This suggests a major importance of rheologic abnormalities on impaired coronary reserve in hypertensive patients.

Angina Pectoris↗
PubMed1990

Coronary microangiopathy and cardiac hypertrophy.

Even in the absence of coronary heart disease, coronary vasodilator reserve is frequently impaired in hypertensive patients. To study, whether the reduced coronary reserve is due to the degree of left ventricular hypertrophy or is a consequence of primary vascular alterations, coronary reserve was determined in 54 hypertensive patients with angina pectoris and angiographically normal coronary arteries. Twelve normotensive persons were studied for control purposes. Coronary blood flow was measured quantitatively by the gas chromatographic argon method. Coronary reserve was determined by measuring coronary resistance before and after dipyridamole (0.5 mg (kg body weight)-1 i.v.). Left ventricular muscle mass was determined by ventriculography. In hypertensive patients, minimal coronary resistance was markedly increased by 124% and coronary reserve significantly reduced by about 38% compared with healthy normotensives. Hypertensives and normotensives did not differ with respect to myocardial oxygen consumption per unit weight myocardium (11.9 +/- 2.3 vs 11.4 +/- 2.4 ml O2 100g-1 min, n.s.) and resting coronary flow (92.1 +/- 20.8 vs 91.4 +/- 18.9 ml min-1. 100 g, n.s.). No significant correlation was found between minimal coronary resistance and coronary reserve and left ventricular muscle mass and between coronary reserve and diastolic wall stress. Accordingly, the reduced coronary regulation capacity in hypertensives does not parallel the degree of left ventricular hypertrophy and is not due to an increased myocardial oxygen consumption under resting conditions. Consequently, the impaired coronary reserve in hypertensive patients seems to be the consequence of primary microvascular lesions, which are independent of the process of left ventricular hypertrophy.

Angina Pectoris↗
PubMed1990

[Congenital malaria--a rare neonatal infection].

Tropical diseases are rare in childhood in European countries, but tourism and an increasing number of immigrants from countries with endemic malaria may lead to a higher incidence. Our report is about a 24 year old german pregnant who was infected with malaria tropica in Togo during the last trimester of pregnancy. Twenty days after delivery by Caesarean section one of the geminies showed symptoms of florid infection: irritability, fever, haemolytic anaemia, hepato-splenomegaly, and thrombocytopenia. Both placenta and peripheral blood smear revealed plasmodium falciparum in the erythrocytes.

Animals↗
PubMed1989

Membrane proteins of synaptic vesicles and cytoskeletal specializations at the node of Ranvier in electric ray and rat.

Binding sites for antibodies against membrane proteins of synaptic vesicles have been shown to be enhanced at nodes of Ranvier in electromotor axons of the electric ray Torpedo marmorata and sciatic nerve axons of the rat, using indirect immunofluorescence and monoclonal antibodies against the synaptic vesicle transmembrane proteins SV2 and synaptophysin (rat) or SV2 (Torpedo). In the electric lobe of Torpedo, vesicle-membrane constituents occurred at higher density in the proximal axon segments covered by oligodendroglia cells than in the distal axon segments where myelin is formed by Schwann cells. Antibody binding sites were enhanced at nodes forming the borderline of the central and peripheral nervous systems. Filamentous actin was present in the Schwann-cell processes covering both the nodal and the paranodal axon segments as suggested by the pattern of phalloidin labelling. Furthermore, in rat sciatic nerve, Schmidt-Lanterman incisures were intensely labelled by phalloidin. A similar nodal distribution was found for binding sites of antibodies against actin and myosin. Binding of antibodies to tubulin was enhanced at nodes in Torpedo electromotor axons. The apparent nodal accumulation of constituents of synaptic vesicle membranes and the presence of filamentous actin and of myosin are discussed in relation to the substantial constriction of the axoplasm at nodes of Ranvier.

Animals↗
PubMed1989

[Regression of hypertrophy following nitrendipine: effect on systolic and diastolic function].

The purpose of the present study was to determine whether an antihypertensive treatment with the dihydropyridine nitrendipine can induce regression of severe hypertensive hypertrophy and, whether alterations in systolic and diastolic ventricular function do occur. Eleven patients (age 49 +/- 11 years) with hypertensive hypertrophy were treated with nitrendipine (10-40 mg/day) for 12 months. Before and after therapy left ventricular hypertrophy, systolic, and diastolic function were measured by M-mode, two-dimensional- and digitized M-mode echocardiography. Systolic blood pressure dropped from 185.5 +/- 19.8 to 164.1 +/- 15.6 mm Hg (p less than 0.05). Left ventricular muscle mass was reduced from 234.5 +/- 51.2 to 201.5 +/- 37.9 g/m2 (p less than 0.05). Systolic wall stress (257.2 +/- 50.5 vs 245.2 +/- 44.4 x 10(3) dyn/cm2) and fractional shortening (34.9 +/- 6.1 vs 37.1 +/- 5.4%) remained nearly unchanged. The peak rate of left ventricular internal dimension change during diastole (MLVD), as an index of rapid early diastolic filling was increased (13.1 +/- 3.0 vs 16.5 +/- 3.7 cm/s; p less than 0.01), the relaxation time index, as an index of isovolumic relaxation, remained nearly unchanged (76 +/- 35 vs 64 +/- 24 ms; n.s.). A long-term treatment with nitrendipine regressed hypertensive left ventricular hypertrophy in proportion to blood pressure reduction. While systolic function remained unchanged as a consequence of an unaltered systolic wall stress, i.e. afterload, diastolic filling was markedly improved due to changes in left ventricular geometry through reduction in mass to volume ratio. Since relaxation time index remained nearly unchanged, factors contributing to the phase of isovolumic relaxation were not essentially affected by regression of left ventricular hypertrophy.

Adult↗
PubMed1989

[Treatment of myocardial and coronary effects of arterial hypertension].

The hypertensive damage to the target organ "heart" comprises the sum and interactions of the cardiac organ manifestations of arterial hypertension such as myocardial hypertrophy and disease of large and small coronary arteries. As the prognosis of arterial hypertension is determined, to a considerable extent, by these cardiac complications, the aim of treatment of hypertensive heart disease is reversal of the myocardial hypertrophy in order to prevent later progression to hypertensive failure. A further goal of therapy is reversal of hypertensive small coronary disease in order to improve the coronary reserve. While the evidence that regression of hypertrophy can be induced by suitable antihypertensive drugs (calcium channel blockers of the dihydropyridine type, ACE inhibitors, and sympathicolytic substances) is practically conclusive, clinical evidence of reversal of hypertensive small coronary disease has yet to be provided. Moreover, we do not know at present to what extent the prognosis of hypertensive heart disease can be improved by reversal of hypertrophy. Once the stage of hypertensive heart failure is reached, the principles of medical management of heart failure with digitalis, diuretics, and ACE inhibitors apply.

Antihypertensive Agents↗
PubMed1989

Growth factor independence and indefinite growth ("immortalization") appear simultaneously after crisis in murine myelocytes expressing v-myc.

In murine myelocytes doubly infected with the v-myc virus and the v-Ha-ras virus, or the v-myc virus and the v-abl virus, the emergence of growth factor-independent cells is a rare event which coincides with crisis in the cultures. All growth factor-independent cells which emerge from crisis are also "immortalized", i.e., able to grow indefinitely. We wanted to determine whether the v-abl gene plays a role in the immortalization of the growth factor-independent cells. Therefore we infected murine myelocytes with v-myc virus and a v-abl mutant virus coding for a temperature-sensitive tyrosine kinase. Growth factor-independent cell clones were isolated and their properties at the nonpermissive temperature analyzed. We observed that 4 hr after the shift to the nonpermissive temperature the expression of both the genomic and subgenomic viral v-myc transcripts decreased significantly, followed by a loss of the viability of the cells. However, several variants emerged which were able to grow at the nonpermissive temperature and showed elevated expression of v-myc. The results suggest: 1) that v-abl plays a role in the immortalization of the cell clones by maintaining a critical level of v-myc expression; 2) that rare genetic changes leading to constitutive v-myc expression independent of v-abl tyrosine kinase activity can also lead to immortalization in this model system, and 3) that immortalization and growth factor independence occur in post-crisis cells and are associated with constitutive expression of v-myc.

Animals↗
PubMed1988

Release of 3H-dopamine and analogous monoamines from rat striatal tissue.

1. The release of previously accumulated 3H-dopamine (DA) from minces of striatal tissue prepared from the brains of pargyline-pretreated rats was evaluated by superfusion with a physiological buffer solution in a six-chamber apparatus with silver toroid electrodes to provide electrical field stimuli. The identity of released tritium as 3H-DA was demonstrated chromatographically and 3H-DA taken up was found in a synaptosomal subcellular fraction. 2. Release of 3H-DA previously accumulated at 0.3 microM was found to be linearly dependent on stimulus intensity between 1 and 10 V (for 60 sec); 5 V was selected as a standard stimulus. 3. Release of 3H-DA did not occur from minces of rat liver, nor was there release of previously accumulated labeled urea or leucine from striatal tissue by electrical stimulation, 50 mM KCL, or 0.1 mM (+)-amphetamine. When 3H-DA was taken up in the presence of cocaine (1 mM) or benztropine (100 microM), electrically induced release of 3H-DA was markedly reduced, while spontaneous efflux was much less altered. 4. Release of 3H-DA was also induced by depolarizing concentrations of K+, as well as by Rb+ or NH4+, and by veratridine. Electrical release and that induced by 50 mM K+ or 100 microM veratridine was blocked by the omission of Ca2+ (with EDTA added) and that induced by veratridine was blocked by tetrodotoxin (30 microM).

Amines↗