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Biomedical subjects

G Hitzenberger

Publications and source records attributed to G Hitzenberger.

At least 37 records · Page 2Linked to original sources
PubMed1997

[Compliance of the hypertensive patient in medical practice--analysis of an observation study. 2].

In a subgroup of 301 hypertensive patients out of the user--observation study ("Anwendungsbeobachtung") with Renitec und CO-Renitec we studied which compliance-improving methods are effective. We tested the effects of blood pressure self-measurement and of an exclusive conversation with the patients. It could be shown, at least in our approach, that the conversation with the patient resulted in a lighter efficacy than blood pressure self-measurement: > 80% compliance was found in 80% of the patients, compared with only 40% of the patients with standard care.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

[ACE inhibitors from the viewpoint of the clinical pharmacologist].

For treatment of hypertension drugs are desirable which exert a 24 hours lasting blood pressure control. Among the ACE-inhibitors some drugs exist which have this action. The elimination pathway plays a minor role in this respect. Not only the inhibition of Angiotensin II generation but also the decreased inhibition of bradykinin-degeneration plays a crucial role with regard to several endothelial functions controlling the so called remodeling of the cardiovascular system.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

[Therapy of hypertension in general practice with Renitec and Co-Renitec--analysis of an administration study].

In a user-observation study ("Anwendungsbeobachtung") it could be demonstrated that Renitec and Co-Renitec lowered elevated blood pressure but not sufficiently according to the WHO-criteria. It seems that the necessary dose titrations are not carried out in a daily routine. Furthermore it has to be stated that even widespread observation studies are not able to differentiate the properties of a drug. It remains to be considered whether more requirements on observation studies are necessary (regarding exact criteria for their design and increased monitoring) and should be implemented to improve the quality of data, although this would mean more time for the physician. Only under such conditions statements about rare side effects, influences of concomitant diseases and their treatments will be possible.

Aged↗
PubMed1995

Lack of interaction between fluvastatin and oral hypoglycemic agents in healthy subjects and in patients with non-insulin-dependent diabetes mellitus.

Human drug interaction studies in vivo are conducted when in vitro and/or animal interactions suggest clinical relevance. Studies in vitro have indicated that the new, entirely synthetic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor fluvastatin affects the metabolism of the nonsteroidal anti-inflammatory drug diclofenac and the oral hypoglycemic tolbutamide. Diclofenac and tolbutamide are both model substrates of the CYP2C isozymes, suggesting that this enzyme could be involved in the underlying mechanism of interaction. The concomitant use of lipid-lowering drugs with oral hypoglycemic agents has been recommended in patients with non-insulin-dependent diabetes mellitus (NIDDM). Therefore, 2 studies were initiated to explore potential pharmacokinetic and pharmacodynamic interactions between fluvastatin, simvastatin, or placebo and the oral hypoglycemic agents tolbutamide (study I) and glyburide (study II), each in 16 healthy subjects. These compounds were selected because of a demonstrated in vitro interaction with tolbutamide and widespread clinical use of glyburide. A further study (study III) was conducted to investigate the potential pharmacokinetic and pharmacodynamic interactions between fluvastatin and glyburide under therapeutic conditions in 32 patients with NIDDM. Single and multiple coadministration of fluvastatin 40 mg or simvastatin 20 mg increased the mean maximum plasma concentration and area under the concentration-time curve of glyburide by about 20%. The pharmacokinetics of tolbutamide were influenced to only a minor extent. Fluvastatin concentration-time profiles were unaffected by tolbutamide or glyburide coadministration. However, the pharmacokinetic interactions between fluvastatin or simvastatin and tolbutamide and glyburide were not associated with clinically relevant changes in blood glucose and insulin concentrations and, therefore, are not considered to be relevant in therapeutic practice.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1995

Double-blind, placebo-controlled, pharmacokinetic and -dynamic studies with 2 new formulations of piracetam (infusion and sirup) under hypoxia in man.

In a double-blind, placebo-controlled study, pharmacokinetics and pharmacodynamics of 12 g piracetam in 2 different formulations were investigated utilizing blood gas analysis, EEG mapping and psychometry under a transient, reversible, hypoxic hypoxidosis. The latter was induced by a fixed gas combination of 9.8% oxygen (O2) and 90.2% nitrogen (N2, found in 6,000 m altitude), which was inhaled for 23 minutes under normobraic conditions by 18 healthy volunteers. They received after an adaptation session randomized at weekly intervals 12 g piracetam i.v. (250 ml infusion over 30 minutes), 12 g piracetam p.o. (60 ml sirup) and placebo. Blood levels were determined by means of an HPLC at the hours 0, 1, 2, 4, 6, 8 and 24. The 2 formulations showed a very similar time-course, with slightly higher blood levels in the 1st hour after the intravenous than oral administration, and vice versa thereafter. The elimination half-life was 4.3 hours for both formulations, the area under the curve and the clearance value were also almost identical. Evaluation of blood gases, EEG mapping and psychometry were carried out at 0, 2, 4, 6 and 8 hours post-drug. Blood gas analysis demonstrated a drop in SaO2 from 99 to 73 and 70%, in PO2 from 100 to 35 and 33 mmHg, in PCO2 from 36 to 31 and 31 mmHg in the 14th and 23rd minute of inhalation, respectively. pH increased from 7.43 to 7.48 in the respective minutes, while base excess and standard bicarbonate remained stable. EEG mapping exhibited under hypoxia a marked increase of total power, mostly due to an augmentation of delta/theta, and a decrease of alpha activity, which reflects deterioration of vigilance. Both piracetam preparations significantly attenuated this vigilance decrement, with 12 g piracetam i.v. showing its encephalotropic peak effects in the earlier hours, 12 g piracetam sirup in the later hours. At the behavioral level, hypoxic hypoxidosis induced a deterioration of the noo- and thymopsyche, which was mitigated by both piracetam preparations, mostly in the 6th hour. Both formulations were well tolerated.

Administration, Oral↗
PubMed1995

[Refractory hypertension--principles of combination therapy].

"Non response" to treatment of hypertension may have different reasons: it may be "physician-related" ("white coat hypertension"), of "patient related" (poor adherence to prescribed medication, alcohol abuse, obesity) and it may really be a "resistant hypertension". In such cases one should search for a primary disease. If no such disease is found one should--according to the time-factor--wait for several weeks before increasing the dose; later on one should switch to another drug with a different mechanism of action and, if necessary, use a rational combination.

Antihypertensive Agents↗
PubMed1994

Pharmacokinetics of piracetam: a study on the bioavailability with special regard to renal and non-renal elimination.

The basis of this investigation was a trial on the relative bioavailability of a recently developed galenic formulation of piracetam. The open, randomized, single-blind crossover study was performed in 16 healthy male volunteers aged between 20 and 31 years. Under fasting conditions, they were given a single oral dose of 1600 mg piracetam either of the test drug or the reference drug. Blood samples and urine specimens were collected over 24 hours. The quantitative analysis was performed with a high sensitive HPLC-method. The pharmacokinetic analysis was carried out with the PC-based program TopFit. An identical bioavailability of the test drug was found (AUC0-24, AUC0-infinity, Cmax, by comparison to the reference drug. No relevant difference in piracetam excretion between test and reference drug was found, however, in contrast to previous references only about two thirds of the given oral dose could be detected in the urine after administration. A statistically significant difference (p = 0.001) between total clearance and renal clearance was observed. Because an incomplete absorption of the drug in the upper gastrointestinal tract is excluded, an additional extrarenal pathway of piracetam must be discussed; the hypothesis of an exclusive renal elimination of this drug should be overruled.

Administration, Oral↗
PubMed1993

Pharmacokinetics of cyclosporine and multiple-dose diclofenac during coadministration.

Pursuant to anecdotal case reports of a possible drug-drug interaction between cyclosporine and diclofenac, an open, two-period crossover study in 24 healthy male volunteers was undertaken in which a single oral dose of 300 mg cyclosporine was administered alone and on day 8 of multiple oral dosing of 50 mg diclofenac every 8 hours. Serial blood samples were obtained over 48 hours after each cyclosporine dose and over a dosing interval for diclofenac on day 7 (diclofenac alone) and day 8 (coadministration of diclofenac with cyclosporine). The mean pharmacokinetic characteristics of cyclosporine were unchanged during coadministration with diclofenac. Based on area under the curve comparison, lack of a pharmacokinetic interaction was conclusively demonstrated for the extent of cyclosporine absorption. The diclofenac maximum plasma concentration and area under the curve over a dosing interval were significantly increased during coadministration; however, a straightforward interpretation of the statistical results was confounded by pronounced variability in diclofenac pharmacokinetics. The results underscore the need for continued caution when cyclosporine and diclofenac are coadministered.

Administration, Oral↗
PubMed1993

[Reducing blood pressure and modification of coronary risk factors by therapy with doxazosin].

In an open, non-comparative, multicenter trail performed by general practitioners, the efficacy and safety of doxazosin, an inhibitor of postsynaptic alpha 1-adrenoceptors, were studied in 924 patients with mild to moderate hypertension. Under treatment with doxazosin both systolic and diastolic blood pressure decreased significantly from 178.4 +/- 18.2/103.1 +/- 8.6 to 149.1 +/- 12.0/85.6 +/- 7.3 mm Hg; the mean daily dose at the end of the 12 weeks' treatment period was 3.3 +/- 2.6 mg. Heart rate decreased by 5% and body weight by 6%. As compared with baseline values, total cholesterol (255.7 +/- 45.4 vs 232.7 +/- 37.3 mg%), triglycerides (206.3 +/- 97.6 vs 175.2 +/- 70.9 mg%) and blood glucose (101.9 +/- 31.0 vs 97.9 +/- 25.5 mg%) decreased significantly, whilst HDL-cholesterol (47.7 +/- 13.0 vs 51.5 +/- 12.4 mg%) increased. Overall, doxazosin was very well tolerated; only 16% of all patients reported adverse drug reactions. The results of this study confirm the effectiveness of doxazosin as first-line medication in the treatment of hypertension, especially in patients with concomitant metabolic disorders such as hyperlipidemia and diabetes mellitus. Moreover, the patients who appear to benefit most from doxazosin treatment are those who show the highest metabolism-related coronary risk, as calculated according to the Framingham Study equation.

Adult↗
PubMed1992

[Primary and secondary prevention in hypertensive patients. An assessment of current status].

The effect of a long-term treatment with beta-receptor-antagonists after an established myocardial infarction is generally accepted. Beta-receptor-antagonists without intrinsic sympathicomimetic activity should be used, cardioselectivity is of lesser importance, except in patients with special problems (i.e. increased bronchial resistance, decreased peripheral blood flow etc.). Hydrophilic or lipophilic properties do not play any role. For primary prophylaxis in older hypertensives diuretics are the drugs of first line, in patients with high risk for heart- and blood-vessel diseases however beta-receptor-antagonists--eventually in combination with low doses of diuretics-should be chosen.

Adrenergic beta-Antagonists↗
PubMed1992

[The effect of ginkgo biloba special extract (EGb 761, Tebofortan)].

Ginkgo biloba special extract exerts positive effects on hemorheology and platelet aggregation, is a free radical scavenger and possesses PAD antagonistic properties, protects against hypoxia and ischemia, hampers an experimentally induced cerebral edema, has favourable properties on neurotransmitters and enhances cerebral bloodflow. Clinically EGb has proven favourable effects on intellectual deficiency, equilibrium disturbances and peripheral artery occlusions thus being a drug with a clear cut indication for these diseases.

Animals↗
PubMed1991

Antihypertensive effects of isradipine and captopril as monotherapy or in combination.

The antihypertensive effects of isradipine and captopril were studied in 140 patients (70 men) with mild-to-moderate hypertension, aged 26 to 74 years, in a double-blind, randomized, between-patient comparative trial. Initial treatment started with 1.25 mg isradipine twice daily or 12.5 mg captopril twice daily. If normotension was not achieved after four weeks, doses were increased to 2.5 mg twice daily or 25 mg twice daily, respectively. If the maximum dose as monotherapy did not result in normotension, captopril (12.5 mg or, if necessary, 25 mg twice daily) was added to regimens of the isradipine-treated patients or isradipine (1.25 mg or, if necessary, 2.5 mg twice daily) was given in addition to the captopril-treated patients. After 24 weeks of active treatment, systolic blood pressure was significantly reduced (P less than .001) with isradipine (from 168 +/- 18 to 144 +/- 14 mm Hg) and with captopril (from 168 +/- 20 to 143 +/- 10 mm Hg). Diastolic blood pressure also fell significantly (P less than .001) in both groups (isradipine: from 105 +/- 5 to 84 +/- 5 mm Hg; captopril; from 105 +/- 4 to 85 +/- 4 mm Hg). With isradipine as monotherapy, diastolic blood pressure was normalized in 49% of patients compared with 56% with captopril as monotherapy (P = NS). Combining both drugs resulted in an increased rate of normalization (to 87%). The results indicate that combined treatment with a calcium antagonist and an angiotensin-converting enzyme inhibitor is effective in lowering blood pressure and is well tolerated during long-term therapy.

Adult↗
PubMed1991

Evaluation of isradipine and captopril alone or in combination for the treatment of hypertension.

The antihypertensive effects of isradipine and captopril were studied in 231 patients with mild-to-moderate hypertension in a double-blind, randomized, between-patient trial. Treatment was started with 1.25 mg of isradipine or 12.5 mg of captopril twice daily which, if normotension was not obtained, was increased after 4 weeks to 2.5 mg or 25 mg twice daily, respectively. If the maximum dose of each drug alone did not result in normotension, captopril (12.5 mg or, if necessary, 25 mg twice daily) was added to the isradipine regimen, and isradipine (1.25 mg or, if necessary, 2.5 mg twice daily) to the captopril regimen. Following 24 weeks of active treatment, systolic blood pressure (SBP) was significantly (p less than 0.001) reduced by isradipine (170 +/- 17 vs. 153 +/- 17 mm Hg) and by captopril (170 +/- 19 vs. 155 +/- 19 mm Hg). Diastolic blood pressure (DBP) also fell significantly (p less than 0.001) in both groups (isradipine: 106 +/- 5 vs. 93 +/- 8 mm Hg; captopril: 106 +/- 5 vs. 95 +/- 10 mm Hg). After isradipine as monotherapy, DBP was normalized in 49% of patients compared with 52% after captopril monotherapy. Combination of both drugs increased the normalization rate to 84%. The results indicate that combined treatment with a calcium antagonist and an angiotensin-converting enzyme (ACE) inhibitor is effective in lowering blood pressure, and is well tolerated as long-term therapy.

Adult↗
PubMed1990

[Clinical pharmacology of ACE inhibitors].

The main effect of the ACE-inhibitors is a reduction of the peripheral resistance and according to that an increase of blood-flow to the organs. Direct effects on the heart are of minor importance. The exact mechanism of action is not fully understood; the main role plays obviously the inhibition of the angiotensin converting enzyme itself; in addition may be effects on the kallikrein-bradykinin-prostaglandin-system are of importance. The pharmacodynamical effects depend on the plasma-concentration and therefore on the pharmacokinetics. These are different with Captopril and Enalapril: Captopril acts directly whereas Enalapril is a "prodrug". With the nowadays used doses Captopril and Enalapril are widely free of side-effects. With the exception of patients with negative sodium-balance (salt-poor diet and/or treatment with diuretics) or patients with renal insufficiency (sometimes increase of creatinine and potassium). In the first group of patients the first dose of ACE-inhibitors should be administered in the evening before going to bed, in the second group creatinine and potassium must be checked 5 to 7 days after an initiation of treatment.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Influence of vinpocetine on warfarin-induced inhibition of coagulation.

The influence of 14 days of concomitant vinpocetine administration on prothrombin time prolongation of single 25 mg doses of warfarin was investigated. Eighteen male subjects were included in the study. They received 25 mg warfarin the first day. Prothrombin time, warfarin plasma levels and factor VII coagulation time were monitored on days 1-5. Ten mg vinpocetine was administered from day 6 to 24. Another single dose of 25 mg of warfarin was given a second time on day 20. AUC values of prothrombin time, warfarin plasma level and factor VII clotting time curves and appropriate Cmax and tmax plasma levels of days 20-24 were compared with those of days 1-5. The confidence interval limits of the ratio of AUC20-24/AUC1-5 of prothrombin time curves were within the limits of 0.8 and 1.2, so that the formal criteria of equivalent biological activity were met. However, a minute influence probably without clinical implication is likely since both point estimate as well as confidence interval limits were below 1.

Adolescent↗