Search PubMed⌕ Search

Biomedical subjects

F Dienstl

Publications and source records attributed to F Dienstl.

At least 55 records · Page 3Linked to original sources
PubMed1988

Short latency somatosensory evoked potentials and brain-stem auditory evoked potentials in coma due to CNS depressant drug poisoning. Preliminary observations.

In patients in coma due to severe CNS depressant drug overdose the central somatosensory conduction time (CCT) after median nerve stimulation is prolonged and N20 is dispersed. Brain-stem auditory evoked potentials demonstrate delayed interpeak latencies (IPLs) I-III, III-V and I-V. This was observed in 4 out of 5 patients investigated after intake of an overdose of amitriptyline (2 cases), barbiturates, meprobamate and nitrazepam (one case each). Toxic levels of drug overdose were related to prolonged CCT and IPLs, whereas normal CCT and IPLs were found at therapeutic drug plasma levels. CCT, IPLs and dispersion of N20 decreased during the course of coma. All patients were successfully treated. It appeared that SSEP and BAEP investigations could make a distinction between a 'toxic' and a 'therapeutic' coma level in severe drug overdose. It further appeared that normalization of CCT and IPLs preceded clinical improvement.

Adult↗
PubMed1987

New aspects of the kinetics of isoenzyme CK-MB during myocardial infarction: discontinuous release?

Intermittent liberation of the serum marker myoglobin is found in acute myocardial infarction, and the ST segment of the electrocardiogram also shows a phasic rise and fall. We therefore measured the serum marker CK-MB at close intervals of time and recorded an oscillation in the serum level. The peaks are not as high as in the serum myoglobin time curve, and it is not easy to decide if they represent the intermittent liberation of the serum marker. It was possible to distinguish between a "high release" and a "low release" group of patients: the former having a maximum CK-MB value of greater than 100 U/l and the latter of less than 100 U/l. Most patients showed 2-3 "initial peaks" within the first 8 h. The highest of these immediately preceded the climb to the definitive maximum value. We conclude that the small size of the peaks in the CK-MB time curve is due to a different mechanism of enzyme release.

Adult↗
PubMed1987

The antihypertensive effect of lisinopril compared to atenolol in patients with mild to moderate hypertension.

In a multicenter, parallel, double-blind study, lisinopril was compared with atenolol in the treatment of mild to moderate essential hypertension. Four hundred ninety patients were randomized to a once-a-day treatment with lisinopril 20 mg or atenolol 50 mg for 4 weeks, and the doses of lisinopril or atenolol were increased up to 80 mg or 200 mg, respectively, at 4-week intervals if sitting diastolic blood pressure (SDBP) was not well controlled. Hydrochlorothiazide (HCTZ) 12.5 or 25 mg was added after 12 weeks, if necessary, and titrated upward after 4 weeks to a maximum dose of 25 or 50 mg/day. Lisinopril and atenolol reduced SDBP to a similar extent. All reductions from baseline in sitting diastolic and systolic blood pressure were significant (less than 0.01). Lisinopril produced a significant (less than 0.01) greater reduction in sitting systolic blood pressure (SSBP) than atenolol. Addition of HCTZ caused further blood pressure reductions (p less than 0.01). Five patients (1.7%) on lisinopril and four (2.0%) on atenolol developed skin rashes during weeks 1-12. Two patients (0.7%) on lisinopril 80 mg developed proteinuria (greater than 1 g/day). Cough occurred more often with lisinopril (4.5%), and elevated triglycerides occurred more often with atenolol (2.0%).

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

Impact of thromboischemic reentry mechanism of coronary thrombosis and microembolism in acute myocardial infarction.

It has been suggested that the thromboischemic reentry mechanism (TRM) is responsible for washing platelet aggregates out of the coronary vessels during the early phase of acute myocardial infarction (AMI). This might account for the observation of Schwartz, who reported the presence of multiple microthrombi in the subendocardial blood vessels following AMI but found only a few thrombotic occlusions in the main coronary arteries. This washing-out of the vessel (due to reperfusion waves) intermittently releases myoglobin into the serum and is responsible for the "staccato phenomenon." We examined a group of 177 patients with a mean age of 66.1 years, whose sudden death was definitely of cardiac origin. Infarction was confirmed in 84.7% of the subjects (fresh infarct: 23.7%; fresh infarct with scarring: 25.9%; scarring alone: 35.0%; no change in myocardium: 15.2%). In other words, 49.7% of all postmortem subjects (88 cases) showed fresh infarction. Opening the coronary arteries longitudinally revealed only 7 thrombi in these 88 cases, i.e., 7.9% of all fresh infarcts. These observations confirm those of Roberts (8.5%) and Friedmann (4%).

Arterial Occlusive Diseases↗
PubMed1986

Water intoxication in the course of an acute schizophrenic episode.

In the course of a schizophrenic episode a woman drank a large amount of tap water. She was found nearly unconscious in her room and was admitted to the clinic. Very low sodium and potassium values in the serum were indicative of water intoxication. During hospitalization she also suffered from several convulsive seizures. After replacement of electrolytes she recovered within 12 to 17 h. This case report demonstrates that water intoxication should also be considered in cases of suspected poisoning with other substances such as drugs. In all these cases an electrolyte status is indicated.

Acute Disease↗
PubMed1986

Acute myocardial infarction: an episodic event of several coronary spasms followed by dilatation?

Acute myocardial infarction (AMI) can no longer be considered as a single event, but as a series of episodes. In most of the cases, the initial event may be the induction of a severe spasm of the coronary artery by vasoconstrictive substance released from aggregated platelets. These spasms are followed by dilatation, which is caused by substances set free from the ischemic tissue. Dilatation then results in a washing-out of vasoactive mediators (as well as myoglobin) and platelets, which is reflected as a peak in the blood myoglobin concentration-time curve. The local depletion of vasodilative metabolites allows a further contraction of the coronary vessel. A new accumulation of platelets then stimulates another spasm. This vicious circle (thrombo-ischemic re-entry-mechanism) is repeated several times and can be interrupted by the systemic administration of thrombolytic drugs (streptokinase).

Coronary Vasospasm↗
PubMed1986

New perspectives on the function of coronary artery spasm in acute myocardial infarction: the thromboischemic reentry mechanism. A review of 10 years research on the pathophysiology of AMI.

Research during the last ten years into the pathophysiology of acute myocardial infarction (AMI) has made it gradually clearer that this is a phasic event. A number of independent authors have made this conclusion quite obvious. The authors of this review suggest that the alternating sequence of coronary spasm and dilatation should be described as the "thromboischemic reentry mechanism," which itself leads to waves of reperfusion, producing characteristic episodic changes in some of the parameters of AMI. The spasms are brought about by substances let loose from aggregating platelets. Metabolites released during the concomitant ischemia lead the vessel from spasm to dilatation. Following thrombolytic treatment, the 'staccato' signs of myoglobinemia disappear, because of the withdrawal of the spasmogenic products of the platelets. It could also be shown that the concentration of myoglobin in the serum as a result of the dilating effect of calcium antagonists is twice the mean maximum value that the myoglobin time curve would show without such treatment.

Animals↗
PubMed1985

Pathological findings in coronary arteries associated with sudden death in Austria.

50 witnessed sudden cardiac deaths in the age group between 20-50 years have been studied at autopsy. The most remarkable findings were a high percentage of stenosis and arteriosclerosis of the descending branch of the left coronary artery and a large amount of three vessel disease. It is clear that severe stenosis and sclerosis of the coronary arteries are not essentially related to sudden cardiac death, but a high number of vessels with moderate stenoses and sclerosis has been found. The severity of vessel disease has been evaluated by a coronary score, which takes the haemodynamic effects of the injured coronary arteries on the myocardium into account. We also noted that patients below 35 years of age who died of sudden cardiac death showed a very low coronary score.

Adult↗
PubMed1983

[Type, number and mode of distribution of cases of poisoning at the University Department of Internal Medicine, Innsbruck].

In the course of one year 357 patients were treated in our department for poisoning, nearly always with suicidal intent. Altogether 249 patients were admitted to the wards for 24 hours or longer, and 108 of these (44.6%) were taken into the intensive care unit. Apart from myocardial infarction (276 patients/year), poisoning is the most common reason for admission to the intensive care unit. The age distribution showed a maximum between 15 and 20 years. Only one case proved fatal, representing a mortality rate of 0.3%.

Adult↗
PubMed1983

Myoglobinemia in the early phase of acute myocardial infarction.

Close-meshed determinations of plasma myoglobin, creatine kinase, and its isoenzyme MB were carried out in nine patients admitted to the clinic less than 4 hours after the onset of symptoms in the course of acute myocardial infarction (AMI). Myoglobin clearly appears earlier (mean 2 hours and 30 minutes) in the plasma than creatine kinase (mean 4 hours and 15 minutes) and isoenzyme MB (mean 5 hours and 30 minutes after the onset of symptoms). During the first hours of AMI plasma myoglobin shows multiple peaks in all patients. Because this pattern is observed only with myoglobin but not with creatine kinase, it appears that myoglobin mirrors the early course of the necrosis more distinctly than creatine kinase. Plasma myoglobin was also found elevated after intramuscular injections and a high voltage accident. Myoglobinuria was not detectable after myocardial infarction.

Adult↗