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Biomedical subjects

D Klaus

Publications and source records attributed to D Klaus.

At least 37 records · Page 2Linked to original sources
PubMed1988

Noninvasive PtcO2 initial slope index and invasive PtcO2 arterial index as diagnostic criterion of the state of peripheral circulation.

Transcutaneous PO2 (PtcO2), PaO2, PtcO2 arterial index (ARI; PtcO2/PaO2), and the initial slope index (ISI; [delta PO2/min]/starting PtcO2) were measured in 42 healthy volunteers, 12 patients with stable circulation and respiratory insufficiency, and ten patients with insufficient peripheral circulation in cardiogenic shock in order to investigate whether ARI and ISI can be used to detect insufficient circulation. The ISI was measured by placing a PtcO2 electrode on the forearm and interrupting blood flow by inflating a cuff until the PtcO2 dropped to zero. After releasing the cuff pressure, the initial slope of the PtcO2 trace was determined in order to calculate the ISI. In the PtcO2 range between 40 and 100 torr, the ARI and ISI did not depend on the PtcO2 magnitude. In all groups, the ISI behaved similarly to the ARI. We conclude that the noninvasive ISI and invasive ARI are able to differentiate between stable and insufficient peripheral circulation (ISI less than 0.75, ARI less than 0.8; p less than .001).

Adult↗
PubMed1988

[The value of angiotensin-converting enzyme inhibitors in the treatment of hypertension].

Numerous trials have shown the efficacy of ACE-inhibitors in moderate and severe essential hypertension. Their use must be regarded as very promising. They lower peripheral vascular resistance without influencing cardiac index and heart rate. Additionally, they maintain serum potassium and do not effect plasma lipids or provoke diabetes mellitus or gout. In 20-30% of hypertensive patients ACE-inhibitors have to be combined with diuretics and/or calcium antagonists. The addition of beta-blockers is useful in patients with resting tachycardia. In mild hypertension the use of ACE-inhibitors as first-line drugs is indicated in patients with adverse reactions to beta-blockers or diuretics. In bilateral renovascular hypertension, ACE-inhibitors may induce a strong blood pressure fall; in bilateral stenosis they contribute to a deterioration of renal function with reversible renal insufficiency. In renoparenchymal hypertension, ACE-inhibitors may attenuate the progression of renal insufficiency; in addition, proteinuria is lowered. In systolic hypertension in the elderly, one must be aware of a marked first-dose hypotensive effect. ACE-inhibitors decrease exaggerated exercise-induced elevation of blood pressure and heart rate and therefore lower myocardial oxygen consumption. In patients with hypertension and diabetes mellitus, antihypertensive treatment should be initiated for blood pressure levels above 140/90 mmHg, to attenuate the progression of vascular damage in the kidney. In patients with severe left ventricular hypertrophy, ACE-inhibitors reduce left ventricular mass within three months by about 30%. In hypertension and coronary heart disease, recent studies report benefits of ACE-inhibitors on coronary circulation. Presently available ACE-inhibitors and those in preparation do not differ in pharmacodynamic, but in pharmacokinetic properties, concerning the beginning and duration of blood pressure lowering. A hypotensive first-dose effect can be observed in diuretic pretreated patients, in severe (malignant) and renovascular hypertension. ACE-inhibitors should not be used during pregnancy or in patients with autoimmune diseases or those undergoing treatment with immunosuppressive drugs, due to the side effects of neutropenia and proteinuria, which are more often seen under these conditions. Results from long-term studies on the influence of ACE-inhibitor treatment on cardiovascular risk in mild hypertension have not been available until now. In the decision to treat mild hypertension with ACE-inhibitors as first-line drug therapy, the costs of therapy in comparison to cheaper antihypertensives must be taken into account.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

[Differential therapy of exercise hypertension].

Criteria for the diagnosis of exercise hypertension have not yet been established. Published values for blood pressure increase during dynamic exercise in normotensive healthy persons differ greatly dependent on age, sex, heart frequency and load of dynamic exercise. Upper normal systolic values during exercise reach levels between 200 and 230 mm Hg. The incidence of exercise hypertension is therefore reported to range from 1 to 10% of the total population. Follow-up studies show that 10 to 60% of persons with isolated exercise hypertension proceed to chronic arterial hypertension. No results are available on exercise hypertension as a risk factor in contrast to the well-known link between increased systolic and diastolic casual blood pressure and cardiovascular diseases. The development of left-ventricular hypertrophy depends mainly on the average systolic blood pressure during a 24-hour period. Peak values of systolic blood pressure during the day or blood pressure variability are less important. Drug treatment of isolated exercise hypertension is not generally accepted. Non-drug treatment is to be preferred, e.g. weight reduction in overweight, dietary sodium restriction and endurance training. Drug treatment must be considered, if non-drug treatment is unsuccessful and/or risk factors, for example hypercholesterolemia, diabetes, cigarette smoking, or complications of target organs, i.e. coronary heart disease or cerebral infarction, do exist. In antihypertensive treatment of increased exercise blood pressure, the influence of the drugs on the hemodynamic and metabolic parameters must be observed, especially in patients with concomitant coronary heart disease. Increases in blood pressure due to dynamic exercise are better attenuated by antihypertensive drugs than those caused by isometric exercise. The drugs of choice are beta-blockers, preferably beta 1-blockers without ISA. Alternatively, calcium antagonists of the verapamil-type or ACE-inhibitors may be used. In contrast to other antihypertensive drugs, labetalol, calcium antagonists and ACE-inhibitors have no influence on the exercise-induced increase of cardiac index and therefore little effect on the work capacity of the circulatory system.

Antihypertensive Agents↗
PubMed1985

[Regression of left heart hypertrophy in arterial hypertension: principles, experimental and clinical findings].

Left ventricular hypertrophy is the consequence of a structural adaptation of the heart in response to the chronic pressure load, leading to a reduction of the increased systolic wall stress. Studies in spontaneously hypertensive rats have shown, that left ventricular hypertrophy can be influenced by various, but not all antihypertensive agents. Alpha-methyldopa, captopril, beta-blockers and calcium channel blockers resulted in reversal of hypertrophy. Treatment with diuretics, hydralazine or minoxidil did not increase or alter degree of myocardial hypertrophy despite normalization of blood pressure. The biochemical profile after reversal of hypertrophy differs according to antihypertensive therapy, i.e. alpha-methyldopa induces an increase in collagen content, whereas captopril does not alter the collagen content of the myocardium. Adrenergic factors play an important role in modulating the response of the heart. In clinical studies the reduction in cardiac mass does not depend solely on the antihypertensive effect on blood pressure levels. There is only a weak correlation between decrease of left ventricular hypertrophy and fall of blood pressure level, as is shown in 12 patients with essential hypertension, treated with captopril over 6 months. The degree of regression of hypertrophy is influenced by stability of blood pressure control (diurnal variations and response to stress are more important than single casual values), neurohumoral response, presence of associated cardiac diseases, cause and severity of hypertension, genetic factors and age. We studied the regression of left ventricular hypertrophy by M-mode-echocardiography in 12 patients with mild or moderate essential hypertension during a 6-month therapy with captopril (50-75 mg p.d.) and hydrochlorothiazide (50 mg p.d.). In 11 of 12 patients captopril treatment resulted in a reduction of LV-mass of 30.9 +/- 15.1% and wall thickness. Peak systolic and endsystolic wall stress decreased significantly (-29.1% and -27.2%, resp.) after blood pressure reduction, but were still slightly elevated. Ejection fraction increased by 5.4% (p less than or equal to 0.05). 6 hypertensive patients treated for 6 months with metoprolol (150 mg p.d.) and hydrochlorothiazide (50 mg p.d.) do not show significant reduction of LV-mass (-6.5%). Peak and endsystolic wall stress were significantly reduced (-33.1% and -11.5%, resp.) as in captopril therapy. In 34 patients with severe hypertension treated with captopril, hydrochlorothiazide and metoprolol over 30 months, we observed a decline in the Sokolow-Lyon-Index from 4.8 +/- 1.1 mV to 3.8 +/- 0.5 mV after 6 months.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

[Primary hypoaldosteronism, pseudo-hypoaldosteronism and distal tubular acidosis].

Aldosterone deficiency is caused by various defects of aldosterone biosynthesis in the adrenal gland or hyporeninism. The most important symptoms are hyponatremia and hyperkalemia. These electrolyte disturbances are also found in pseudohypoaldosteronism. Pseudohypoaldosteronism type I is characterized by insensitivity of the distal nephron for aldosterone. Hyperabsorption of chloride in the distal nephron leads to pseudohypoaldosteronism type II, which is linked with hypertension, whereas blood pressure in the other mentioned disorders is decreased. Renal tubular acidosis, mainly type 4, with impaired production of ammonia due to hyperkalemia, is frequently observed in hypoaldosteronism and both types of pseudohypoaldosteronism as well. The therapeutic regimen is different: low doses of fludrocortisone in hypoaldosteronism, potassium restriction, sodium bicarbonate and loop diuretics in type I of pseudohypoaldosteronism, and sodium restriction and chloruretic diuretics (thiazide) in type II of pseudohypoaldosteronism. In some cases hyperkalemia requires the use of potassium-binding resins.

Acidosis, Renal Tubular↗
PubMed1984

[Primary hypoaldosteronism and secondary pseudo-hypoaldosteronism].

We observed a 23-year-old man with pronounced hyperkalemia (max. 6.8 mmol/l) and hyponatremia (min. 112 mmol/l), which had been existent for 3 years without complaint except a transitory psychorganic syndrome due to hyponatremia. Physical examination showed no abnormality except hypotension (blood pressure 100/70 mmHg). Renal function tests were normal. Fractional clearance of sodium was significantly increased (0.8%), whereas that of potassium was decreased (2.4%). Plasma renin activity was tripled and rose after furosemide. Plasma aldosterone was lowered and showed no rise after furosemide. Suppression of plasma renin and aldosterone by saline infusion was normal. Pressor dose of angiotensin II was increased (17,9 ng AT II/kg/min). Urinary excretion of aldosterone and its conjugates was below normal, and aldosterone precursors were within normal range. The findings were interpreted as selective primary hypoaldosteronism caused by corticosterone methyl oxidase defect type II. However, neither fludrocortisone (0.5 mg/day) nor sodium chloride (200 mmol/day) led to a normalization of sodium and potassium in plasma. Additional pseudohypoaldosteronism was thus assumed. Aldosterone infusion (3 mg in 1 h) decreased renal excretion of sodium; potassium excretion failed, however, to increase in contrast to its pattern in normal man. These findings resemble additional pseudohypo-aldosteronism of type II. After 8 weeks' application of additional 80 mmol sodium (as sodium bicarbonate) plasma sodium and potassium showed normal values under combined treatment with fludrocortisone (0.1 mg/day) and sodium bicarbonate (80 mmol/day). It is to be assumed that the patient suffers from a reduced aldosterone biosynthesis in the presence of an additional transitory secondary pseudohypoaldosteronism.

Adult↗
PubMed1984

Effect of intraesophageal bile and acid (HCl) perfusion on the action of the lower esophageal sphincter.

We examined the effect of acid and bile on the lower esophageal high pressure zone (LEHPZ) in a combined manometric, pH testing and morphologic study in 12 cats. LEHPZ pressures and swallowing waves (SW) were simultaneously recorded before, during and after perfusion of the esophagus with control fluid, acid (0.1 n HCl) natural bile and a mixture of acid and bile. Endoscopy was performed and biopsies taken before and after the experiments. Bile caused a rise of LEHPZ and SW pressure and mild esophagitis. Acid and bile acid mixture produced a marked progressive decline of LEHPZ and SW pressure (p less than 0.001), incomplete relaxation and severe discoordination of esophageal motility. Continuous pH measurements showed diminished or no clearance and reflux. All acid perfused cats developed necrotic esophagitis and strictures within 4 weeks. LEHPZ pressures returned to almost normal values after this recovering period but peristalsis was still completely discoordinated. Swallowing waves were of exaggerated magnitude and length. From our findings it is evident that bile and acid change LEHPZ competence. Bile and acid seem to have a different effect on motor function of the LEHPZ and esophageal peristalsis.

Animals↗
PubMed1982

[R-wave amplitude during left ventricular volume changes in healthy hearts].

The relationship between R-wave amplitude and left ventricular volume was studied in four tests, each including six normal adults. The means of 10 heart cycles of the R-wave amplitude in surface ECG lead V5 (RV5) and the echocardiographically determined left ventricular enddiastolic dimension (LVEDD) were compared before and during different interventions. After inhalation of 0.3 ml isoamylnitrit, LVEDD was reduced to 7.7%, RV5 to 15.0% below control. During a maneuver of Valsalva, LVEDD decreased to 8.6%, RV5 to 12.9% below control. In both tests heart rates increased markedly. After oral application of propranolol (0.7 to 1.0 mg/kg) LVEDD did not change, whereas RV5 decreased to 8.2% below control. During rapid intravenous infusion of 1 l NaCl 0.9% in 10 to 15 minutes, LVEDD increased to 15.7% above control. R-wave amplitude remained constant. Thus the results of these last two tests let us doubt whether the Brody-effect can be translated without limitation on the in-vivo situation in man.

Adult↗
PubMed1981

[ST-segment depression and R-amplitude changes during bicycle stress test in patients with coronary artery disease (author's transl)].

56 patients were examined with bicycle stress tests. Sensitivity and specificity of ST-segment depression were compared with R-wave amplitude changes. All patients had a coronary angiography because of suspected coronary artery disease (CAD). The specificity of ST-segment depression was 71%, for R-wave amplitude changes 50%. The sensitivity for ST-segment depression was 76% and for R-wave amplitude changes 50%. In addition in 7 patients with angiographically demonstrated CAD repeated stress tests were done. The ST-segment changes were nearly constant in all examinations, whereas the R-wave amplitude in V5 in 5 out of 7 patients changed considerably between decrease and increase. Considering these intraindividual changes, it seems doubtful whether the evaluation of the R-wave amplitude proves to be an improvement of the non-invasive diagnostic procedures of CAD.

Coronary Disease↗
PubMed1980

[Captopril in the treatment of essential hypertension (author's transl)].

The antihypertensive effect of captopril was tested on 19 patients with essential hypertension, WHO grade I or II. In 11 patients blood pressure levels returned to normal over an observation period of 12 weeks at a dose of 3 C 50-150 mg daily (group A). In eight patients with grade II hypertension the absolute blood-pressure reduction was the same, but did not reach normal levels (group B). Although additional intake of propranolol, at a dose of 3 X 40 mg daily, achieved further reduction, normal pressures were still not attained. Initial blood pressure levels were higher and plasma-renin activity lower in patients of group B than of group A. There was a definite rise in plasma-renin activity with captopril, but corresponding to the suppression of plasma-renin in severe hypertension it was less. There was a fall in plasma-aldosterone levels, corresponding to a reduced angiotensin II level as a result of inhibition of the converting enzyme. The fall in plasma-aldosterone activity was less in severe hypertension, although there was the same inhibition of converting enzyme activity in both groups. Normochromic anaemia was noted in three patients, requiring further observation and explanation. No patient developed orthostatic hypotension or reflex tachycardia.

Adult↗
PubMed1978

[Treatment of essential hypertension with a combination of propranolol, spironolactone-thiabutazide and dihydralazine (author's transl)].

In 61 out-patients with essential hypertension, grade I or II, propranolol was administered alone in increasing doses (3 x 40 mg/d or 3 x 80 mg/d) or, if there was insufficient response, with a double or triple combination consisting additionally of spironolactone (50 mg/d)-thiabutazide (5 mg/d) and dihydralazine (3 x 25 mg/d). This treatment schedule achieved normal pressures in 51 patients, in 22 on 40 mg, in 7 on 80 mg propranolol, in 16 after the addition of the diuretic, and in 6 with the triple combination. Four patients had to be excluded from the study because they developed either marked bradycardia or anxiety states or paraesthesias after propranolol (3 x 40 mg/d). On chronic beta-adrenergic blockade the serum potassium level increased slightly, but remained within normal limits. The initial value of plasma-renin activity was highest in the group of those who responded to the propranolol treatment.

Anxiety↗