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Biomedical subjects

V Hossmann

Publications and source records attributed to V Hossmann.

At least 37 records · Page 2Linked to original sources
PubMed1983

Antithrombin III deficiency in ischaemic stroke.

AT III activity and concentration were measured in 36 patients (mean age 65.5 yrs, range 43-77 yrs) with ischaemic stroke within maximally 48 h of the acute event. In 12 patients (= 33%) AT III activity was reduced below 18.4 IU/ml: 50% of these patients showed normal and 50% reduced AT III concentration of less than 22 mg/dl. In 15 patients AT III activity and concentration were measured in the acute phase on admission to hospital and 12 months later. In the acute phase, AT III activity was reduced when compared with AT III concentration (y = 0.19 chi + 15.5) and did not correlate with the latter. 12 months later, however, AT III activity and concentration correlated significantly (r = 0.92; p less than 0.001) and the regression line was steeper (y = 0.8 chi). During the acute phase of ischaemic stroke, intravascular coagulation is evidently increased and inactive AT III-thrombin complexes are formed, whereby the concentration of active AT III decreases. A patient with progressive stroke and reduced AT III activity of 14.2 IU/ml was therefore substituted with AT III concentrate. The further neurological course was favourable.

Adult↗
PubMed1983

Controlled trial of ancrod in ischemic stroke.

In a randomized, single-blind study, 30 patients with acute ischemic stroke were treated with either low-molecular weight dextran and mannitol alone (group A, mean age, 63.3 +/- 11.8 years, n = 15) or in combination with the viper venom enzyme ancrod (group B, mean age, 67.9 +/- 7.6 years, n = 15). Lowering of plasma fibrinogen levels to 100-130 mg/dL with ancrod resulted in a significant reduction of the apparent blood viscosity, ie, of 37% at a shear rate of 0.03 s-1, compared with only 7% in group A. Fibrin degradation products increased considerably from 3.1 +/- 0.4 to 154.3 +/- 31.6 mg/L on day 3, while plasminogen decreased from 98.2% +/- 2.0% to 79.8% +/- 2.9% in group B. Global coagulation and platelet function tests were not influenced by either treatment. Neurological score improved by 1.1 arbitrary units (AU) in group A and by 2.6 AU in group B. Five patients in group A and two in group B died during the first two weeks. This preliminary study indicated a slightly better outcome in the ancrod treated patients. The beneficial effect may be due to the anticoagulative and fibrinolytic activity of ancrod rather than its effect on blood viscosity.

Ancrod↗
PubMed1981

Norepinephrine release in essential hypertension.

Supine basal plasma norepinephrine was higher in a group of newly diagnosed patients with mild essential hypertension than in age- and sex-matched "laboratory-naive" volunteers. Sympathetic activation by exercise and change of posture increased plasma norepinephrine in both groups, with a tendency toward higher values in the hypertensive patients, but norepinephrine clearance was slower and half-life longer in these patients. Thus the estimate of neuronal norepinephrine release obtained by correction of plasma norepinephrine for individual values of clearance was in the same range in both groups. Plasma norepinephrine was lower in younger "laboratory-adapted" subjects than in the "laboratory-naive" normotensive subjects, but clearance was in the same range in both. Thus, variations in kinetics may contribute to differences in plasma norepinephrine between patients with essential hypertension and matched controls. In contrast, the lower plasma concentration of norepinephrine in "laboratory-adapted" than in "laboratory-naive" controls appears to reflect a lower level of sympathetic activity in the former.

Adult↗
PubMed1981

[Depression of sinus nodal automaticity during permanent atrial pacing for the determination of the sinoatrial conduction time (author's transl)].

In 36 patients sinoatrial conduction time (SACT) was calculated by the continuous-atrial-pacing technique, first described by Narula et al. (9). Using three different stimulation frequencies, it could be shown that the return cycles A2A3 and the postreturn cycles A3A4 both were linearly correlated with rising stimulation frequency. Thus, if the formula given by Narula et al. was used [SACT = (A2A3 - A1A1) : 2] the calculated SACT-values linearly rose, too, which was caused by a stimulation frequency dependent progressive depression of the sinus nodal automaticity. This interfering influence of sinus nodal depression could be corrected by applying a modified formula for calculation of the SACT, i.e. SACTM = (A2A3 - A3A4) : 2. Thus calculation of sinuatrial conduction time by the modified continuous-atrial-pacing technique represents a method widely applicable in routine electrophysiological testing.

Electrocardiography↗
PubMed1980

Effect of intravascular platelet aggregation on blood recirculation following prolonged ischemia of the cat brain.

Reversible complete cerebro-circulatory arrest was produced in normothermic, anesthetized cats for 1 h by clamping the innominate and subclavian arteries, followed by blood recirculation of the brain for 30 min to 4 h. Blood volume of tissue samples was measured by intravenous injection of 125I-albumin and the platelet number by labelling of autologous platelets with 51Cr. The number of platelets trapped in the tissue was determined by subtracting from the total platelet count of the tissue sample those contained in the streaming blood, calculated from the blood volume by 125I-albumin. In sham-operated animals, after recirculation of autologous 51Cr labelled platelets for 60 min, no platelets were entrapped in the brain vasculature and total platelet number and fibrinogen concentration in the venous blood did not change. In animals submitted to complete cerebral ischemia for 1 h the number of trapped platelets increased significantly in the whole brain after 30 min of recirculation, i.e. the period of maximal postischemic vasodilatation and hyperemia, and highest concentrations were found in the border zone with 270 +/- 60 x 10(4) platelets/g tissue and in the brainstem with 240 +/- 70 x 10(4) platelets/g tissue. Blood platelets and fibrinogen concentration in the venous blood decreased significantly from 288 +/- 37 x 10(6)/ml and 299 +/- 50 mg% to 186 +/- 25 x 10(6)/ml platelets and 112 +/- 22 mg+ of fibrinogen, respectively. Platelets were nearly completely washed out of the brain after 4 h of recirculation. The highest increase of platelets was found in the kidney, lung and liver after 30 min of recirculation, indicating that intravascular coagulation following prolonged cerebral ischemia affects the extracerebral organs more than the brain itself.

Animals↗
PubMed1980

The renin--kallikrein--prostaglandin system: plasma active and inactive renin and urinary kallikrein during prostacyclin infusion in man.

Renal prostaglandins are integrated with the kallikrein-kinin and renin-angiotension systems in a vasoactive hormone complex. Prostacyclin potently stimulates renin release from rabbit cortical slices and plasma renin activity rises in response to prostacyclin infusion in man. Prostaglandins also stimulate the production of kallikrein, a potential activator of renin in vivo. To investigate the mechanism of prostacyclin induced renin release, human volunteers were infused with prostacyclin 8ngKg-1min-1 and vehicle alone in random order. Despite a marked increase in plasma active renin during prostacyclin both plasma inactive renin and urinary kallikrein failed to alter from control values. Urinary sodium and volume were increased by prostacyclin. The stimulation of renin by intravenous prostacyclin is not mediated by activation of the kallikrein system.

Adult↗
PubMed1980

Sedative and cardiovascular effects of clonidine and nitrazepam.

Five healthy male subjects, aged 26 to 35 yr, received single oral doses of clonidine 0.3 mg, nitrazepam 20 mg, or placebo double-blind with an interval of at least 1 wk between each treatment. Clonodine induced a maximal fall in systo9lic blood pressure from 104.2 +/- 1.6 to 84.7 +/- 1.4 mm Hg (mean +/- SEM) after 3.5 hr and nitrazepam from 102.9 +/- 1.9 to 90.3 +/- 2.6 mm Hg after 1.0 hr while after placebo blood pressure rose steadily from 102.5 +/- 2.9 to 109.6 +/- 3.5 mm Hg at the end of the 8-hr study. Total sleep time increased from 90.3 +/- 2.5. min after placebo to 256.2 +/0 21.0 min after clonidine (p < 0.001) and 281.0 +/- 40.3 min after nitrazepam (p < 0.001). Stage I sleep increased from 49.7 +/- 11.2 to 76.9 +/- 10.2 min after clonidine and to 76.3 +/- 25.2 min after nitrazepam (p < 0.0), while the greatest increase was observed in stage II: 230.7 +/- 25.6 min after clonidine and 236.6 +/- 35.4 min after nitrazepam compared with only 48.5 +/- 15.8 min after placebo (p < 0.001). Plasma norepinephrine did not change after placebo but fell after nitrazepam from 0.28 +/- 0.04 to 0.14 +/- 0.02 ng/ml after 3 hr (p < 0.05) and after clonidine from 0.23 +/- 0.07 to 0.07 +/- 0.02 ng/ml after 2 hr (p < 0.01). Clonidine and nitrazepam both induced similar hypnotic and hypotensive effects with some evidence that this might be due to a reduction in sympathetic tone.

Adult↗
PubMed1980

[Atrial versus ventricular cardiac pacing in the elderly with respect to hemodynamic data (author's transl)].

The importance of synchronized atrial and ventricular action is well known. Especially in elderly patients the circulation of the brain, the kidneys and the coronary arteries may be diminished by ventricular stimulation. Permanent atrial, atrial triggered ventricular, and bifocal stimulation increases cardiac output by 20-30 percent. From the hemodynamic data the best results during atrial stimulation are obtained at a frequency of 80 to 85 bpm.

Cardiac Output↗
PubMed1979

Interindividual variation in kinetics of infused epinephrine.

1-Norepinephrine was infused continuously for 10 hr into 5 normotensive, male laboratory subjects (mean age, 32.4 +/- 1.9 yr) at a mean rate of 0.06 microgram/kg/min. Mean plasma norepinephrine (NE) rose from the preinfusion level of 0.19 +/- 0.02 microgram/l to a steady state level of 1.22 +/- 0.29 microgram/l. The mean increase in blood pressure was 21.8 +/- 0.9 mm Hg systolic and 14.1 +/- 1.0 mm Hg diastolic. The mean depression in heart rate was 12.7 +/- 1.7 beats/min. The clearance of norepinephrine ranged from 27.9 to 100.0 ml/kg/min (mean. 58.0 +/- 13.8) and was little influenced by acute hemodynamic changes. The volume of distribution ranged widely (0.09 to 0.40 l/kg), the mean value being 13.51 1. The mean norepinephrine half-life was brief, ranging from 1.45 to 2.9 min (mean, 2.09 +/- 0.34 min). There was no evidence of a slowly accumulating high-capacity low-affinity pool of norepinephrine. These results support the use of plasma norepinephrine as an index of sympathetic activity within an individual but not its validity in interindividual comparisons.

Adult↗
PubMed1978

Microsphere analysis of local cerebral and extracerebral blood flow after complete ischemia of the cat brain for one hour.

In normothermic anesthetized cats complete cerebral circulatory arrest for one h was produced and followed by blood recirculation of the brain for 30 min to 4 h. Total and local blood flow of the brain, kidney, heart and liver were measured before and after ischemia using radioactive labelled microspheres. Before ischemia blood flow of the brain was 39.1 +/- 2.3 ml/100 g/min, of the kidney 307.2 +/- 28.3 ml/100 g/min, of the heart 241.1 +/- 32.5 ml/100 g/mmin and of the liver 87.8 +/- 25.6 ml/100 g/min (means +/- SEM). Regional flow rates within the brain varied between 35 and 51 ml/100 g/min. Reactive hyperemia was present in the brain 30 min after the beginning of recirculation following ischemia for 1 h. Local cerebral flow rates increased three to five times above the control flow, depending on the respective region. Mean cerebral blood flow returned to or slightly below normal, 2 to 4 h after ischemia, but there was considerable redistribution of flow rates within the brain. The filter capacity of the brain for microspheres of 15 mu and 50 mu diameter did not change after ischemia indicating that postischemic blood recirculation was not accompanied by an opening of arteriovenous shunts.

Animals↗