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Biomedical subjects

V Schulz

Publications and source records attributed to V Schulz.

At least 91 records · Page 5Linked to original sources
PubMed1987

Human corticotropin-releasing hormone in man: dose-response of minute ventilation and end-tidal partial pressures of carbon dioxide and oxygen.

The respiratory stimulant properties of iv injections of 33, 67, and 100 micrograms synthetic human corticotropin-releasing hormone (hCRH) were studied in 12 normal men in a single blind, placebo-controlled trial. All doses of hCRH induced a respiratory stimulation in every subject, and the stimulation was dose dependent. The onset of respiratory stimulation occurred within 15-30 sec after hCRH infusion was started. Initially, there was an increase in tidal volume (VT), followed by an increase in respiratory rate. The maximum minute ventilation (VE) occurred 60-120 sec after starting the injection. The 33-micrograms hCRH dose induced a 35% increase in VE from 6.3 +/- 0.6 (+/- SD) to 9.7 +/- 1.3 liters/min (P less than 0.001) due to a marked increase in VT from 531 +/- 105 to 688 +/- 142 ml (P less than 0.001) and only a slight increase in the respiratory rate from 12.4 +/- 3.0 to 14.3 +/- 3.1 breaths/min (P less than 0.001); heart rate was not altered at this dose. The 100-micrograms hCRH dose increased the VE by 81% to 11.5 +/- 1.5 liters/min, mainly due to an increase in VT. VE was elevated for 5.8, 7.2, or 8.3 min after the end of injection of the three hCRH doses. Increases in VE markedly lowered the end-tidal partial pressure of carbon dioxide (P(ET)CO2; nearly identical with the arterial PCO2 in normal subjects). hCRH (33 micrograms) lowered P(ET)CO2 from 40.3 +/- 1.2 to 37.2 +/- 1.9 mm Hg (P less than 0.001), and 100 micrograms hCRH lowered P(ET)CO2 to 33.4 +/- 1.2 mm Hg. End-tidal partial pressure of oxygen, i.e. the most sensitive parameter for the duration of action of respiratory stimulation, was elevated for 8.5, 10.2, and 14 min after injection of 33, 67, or 100 micrograms hCRH. Sixty-seven micrograms of hCRH was the lowest effective dose for an increase in the heart rate (from 66.4 to 79.0 beats/min; P less than 0.001), and 100 micrograms hCRH markedly increased the heart rate by 20% to a peak value of 83.5 beats/min. Heart rate increased within 90 sec and returned to the control value after 5-10 min. These data suggest that hCRH is a rapidly acting, dose-dependent, and potent respiratory stimulant. Since this hyperventilatory effect of hCRH occurred in every subject after all doses tested, respiratory stimulation may represent specific biological activity of CRH rather than a side-effect.

Adult↗
PubMed1986

Human corticotropin-releasing factor (hCRF) is a potent respiratory analeptic. Physiological and clinical aspects.

During intravenous corticotropin-releasing factor stimulation tests we observed a deepening of the tidal volume in 35 patients. To investigate this presumed respiratory stimulation we measured respiratory parameters in 12 healthy male volunteers in a single-blind placebo-controlled trial. The intravenous 60-s infusion of 100 micrograms of human corticotropin-releasing factor induced a very potent respiratory stimulation in every subject: respiratory minute volume (mean +/- S.D.) increased by 81% from 6.319 +/- 0.577 to 11.464 +/- 1.264 liters per min (P less than 0.001), whereas there was only a slight rise in the mean respiratory rate from 12.4 +/- 3.0 to 14.7 +/- 2.7 breaths per min (P less than 0.001). Mean tidal volume increased from 531 +/- 105 to 809 +/- 175 ml (P less than 0.001). Mean end-tidal partial pressure of carbon dioxide decreased (P less than 0.001) from 40.3 +/- 1.2 to 33.4 +/- 1.2 mmHg, whereas mean end-tidal partial pressure of oxygen increased (P less than 0.001) from 93.2 +/- 5.4 to 113.5 +/- 5.4 mmHg. After 10 to 20 min both end-tidal carbon dioxide and oxygen partial pressures returned to the baseline values. The placebo had no measurable effects. We conclude that human corticotropin-releasing factor is a potent respiratory stimulant. With 100 micrograms the resting respiratory minute volume increases by 81%. These data point to the possible importance of the corticotropin-releasing factor as a useful adjunct in the management of patients with alveolar hypoventilation.

Adult↗
PubMed1986

Hypotensive and antiplatelet actions of motapizone depend on dose and time after ingestion.

Single doses of motapizone 1 to 10 mg were given to 12 healthy subjects. Before and up to 8 h after each dose the blood pressure and heart rate were measured, as well as thrombocyte aggregation "ex vivo" with collagen, ADP and adrenaline. Motapizone produced a dose-dependent reduction in diastolic blood pressure and an increase in heart rate. These effects were demonstrated with individual variations after 1 to 3 mg and as a rule they were very marked after more than 6 mg. With the highest dose (mean 7.7 +/- 2.3 mg) the diastolic pressure fell by an average of 23% 1 h after medication as compared to with the baseline values. At the same time there was marked inhibition of thrombocyte aggregation, which also became apparent after about 3 mg and increased in proportion to the dose. The inhibition of aggregation peaked after 2 h and had disappeared within 8 h. The inhibition of ADP-induced aggregation was particularly marked.

Adult↗
PubMed1986

Inhibition of thrombocyte aggregation by oral motapizone and other drugs.

Ten healthy subjects took single oral doses of placebo, 8.8 +/- 1.8 mg motapizone, 40 +/- 13 mg captopril, 25 mg dihydralazine, 20 mg nifedipine and 4.5 +/- 1.1 mg prazosin in random order, and, as the last preparation 500 mg acetylsalicylic acid. Thrombocyte aggregation induced "ex-vivo" with collagen, ADP and adrenaline was measured before and after 60 min. Immediately before each dose, the "threshold concentration" of each agent was determined in each subject, i.e. the concentration producing about 90% of maximal aggregation. After the preparation had been taken, aggregation was induced with 1-, 2- and 4-times the threshold concentration. Both motapizone and also acetylsalicylic acid caused marked inhibition of aggregation at up to 4-times the threshold concentration; the dose ratio was about 1:50. Motapizone produced greater inhibition of the aggregation induced by ADP and acetylsalicylic acid than of that due to collagen. The inhibitory actions after captopril, dihydralazine, nifedipine and prazosin were weak and did not significantly differ from placebo.

Adult↗
PubMed1985

Hypotensive efficacy of a mixed solution of 0.1% sodium nitroprusside and 1% sodium thiosulphate.

A mixed solution of 0.1% sodium nitroprusside and 1% sodium thiosulphate ('SNP-thiosulphate') was given as i.v. infusion to 80 patients, 30 of whom were hypertensive emergencies and 50 were surgical cases requiring induction of hypotension. This treatment lowered the blood pressure (BP) by an average of 30% of the initial levels in the hypertensive patients and 30-40% of the initial levels in the surgical patients. The mean effective dose in the hypertensive patients was 2.4 micrograms/kg/min compared with about 3 micrograms/kg/min in 40 cases treated with sodium nitroprusside as mono-infusion. For deliberate hypotension in surgical patients the mean doses of SNP, used here in the mixed infusion with thiosulphate, were 1.0 and 2.3 micrograms/kg/min, compared with 1.3-7.5 micrograms/kg/min in 181 patients treated with SNP as monotherapy. In contrast to conventional therapy with SNP, the infusion of SNP-thiosulphate even at extremely high dose rates did not produce toxic concentrations of prussic acid in the blood. In no case was a rise observed in the cellular enzymes as an indirect indication of hypoxic cell damage. SNP-thiosulphate is thus at least as effective at lowering BP as SNP infused alone, and has a substantially lower toxicity risk.

Adolescent↗
PubMed1984

[Treatment of ergotism].

Ergotism occurs in patients so disposed, particularly under ergotamine therapy for migraine. The principal signs are arterial spasms in the legs, or sometimes also the arms, which can lead to gangrene. Intravenous or intra-arterial infusion of sodium nitroprusside or nitroglycerine has proved the only reliably efficacious therapy. The best results have been obtained using nitroprusside: twelve cases are described here. By contrast, nonefficacious measures include, in particular, sympathetic blockade.

Adult↗
PubMed1984

An embryotoxicity study of the fungicide tridemorph and its commercial formulation Calixin.

Tridemorph (N-tridecyl-2,6-dimethylmorpholine), the active ingredient of the commercially formulated fungicide Calixin, is a teratogen in rats and mice. The no-effect level for embryotoxic effects was 27.5 mg/kg for mice and 20.6 mg/kg for rats. By contrast, when Calixin, which contains 83% tridemorph, was administered orally at dose levels of 0.156, 0.722, and 3.909 mg/kg, no embryotoxic effects were observed in two strains of rats. Our extensive investigations, carried out under exposure conditions resembling as closely as possible those reported in another study, did not reproduce the previous findings of teratogenicity of Calixin.

Abnormalities, Drug-Induced↗
PubMed1983

[The therapeutic scope of sodium nitroprusside].

Sodium nitroprusside (SNP) as a monoinfusion was administered to 50 patients for periods of a few hours. A further group of 20 patients received SNP for periods of several days as a combination solution, of SNP mixed with sodium thiosulphate. Infusion of SNP on its own at levels exceeding 2 micrograms/kg/min led to cyanide levels in the blood rising proportional to dosage. Infusion of SNP mixed with thiosulphate showed no such accumulation. This procedure is free of danger and should become the technique of choice when therapeutically administering SNP to lower blood pressure.

Cyanides↗
PubMed1983

Lung metastasis of a meningioma.

UNLABELLED: Case report of a 35-year-old male patient. 1976: operation for a falx-meningioma. 1981: meningioma recurrence and further intracranial meningiomas. HISTOLOGY: 1976 and 1981 endotheliomatous meningioma: no signs of malignancy. Prior to the 2nd operation in 1981 a lung tumor was diagnosed for the first time. HISTOLOGY of the lung tumor: endotheliomatous meningioma, same histology as in cerebral meningiomas.

Adult↗