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Biomedical subjects

J Teichmann

Publications and source records attributed to J Teichmann.

At least 19 recordsLinked to original sources
PubMed1990

[The effect of ganglionectomy and cold exposure on the ventromedial hypothalamic nucleus, blood glucose and liver glycogen in regard to circadian rhythms].

To analyse the importance of the ventromedial hypothalamic nucleus (VMH) for the circadian regulation of the carbohydrate metabolism rats were investigated after bilateral cervical sympathetic ganglionectomy (SCGx) 30 d earlier and exposure to cold (10 degrees C) 72 h earlier. In order to assess the circadian rhythms of nuclear volume oscillations of the VMH, blood glucose, and liver glycogen 4 times a day (light-dark cycle: 14L:10D, light on 05.00 h) rats were sacrificed at midlight and middark as well as 1 h after the onset of the light and dark periods. The circadian curves were calculated in a model-free way by the procedures of locally adjusted polynomial approximation. Ganglion removal and exposure to cold resulted in an increase of blood sugar and of nuclear volume of the VMH, but only of its lateral part. The liver glycogen decreased. Additionally, both the coordination between the circadian curves of the nuclear volume and of the blood glucose as well as of the inverse curves of the liver glycogen was destroyed after SCGx. These results are in agreement with the conviction that the enhanced blood glucose activates the VMH. The augmentation of blood glucose was discussed in connection with influences of the likewise increased thyrotropin-releasing hormone and thyrotropin on the increased plasma levels of catecholamines, with secondary increased plasma levels of glucagon as well as decreased insulin levels after SCGx and exposure to cold. The sympathetic denervation of the pineal gland (SCGx) produced the mentioned desynchronization of the curves. At the present we are not able to explain the approximate restitution of the circadian rhythms after additional exposure to cold.

Animals↗
PubMed1983

Metabolic clearance rates of catechol estrogens in rats.

MCRs of the catechol estrogens 4-hydroxyestradiol (4-OHE2) and 2-hydroxyestradiol (2-OHE2) and of the parent estrogen 17 beta-estradiol (E2) were determined in rats. Long term ovariectomized Wistar rats were infused with the steroids at a constant rate for 3 days via a catheter placed in the abdominal aorta. Blood samples were drawn discontinually by retroorbital puncture, and the serum concentrations of E2, 4-OHE2, and 2-OHE2 were measured by RIA. Steady state was reached within 24 h of infusion. Mean serum MCRs were calculated to be 740 +/- 117 ml/h for E2, 2700 +/- 1000 ml/h for 4-OHE2, and 8300 +/- 1700 ml/h for 2-OHE2. Thus, the MCRs of the catechol estrogens were definitely higher than the MCR of E2 resulting in an apparent ratio of 1:4:11 (E2:4-OHE2:2-OHE2).

Animals↗
PubMed1982

Nitroprusside-hypotension: cerebral blood flow and cerebral oxygen consumption in neurosurgical patients.

The effects of nitroprusside-induced hypotension on cerebral blood flow and cerebral oxygen consumption were investigated in nine patients scheduled for cerebral arterial aneurysm surgery. Anesthesia was maintained with nitrous oxide/oxygen and fentanyl; muscle relaxation was achieved with pancuronium; PaCO2 was maintained at 4.79-5.32 kPa. Mean arterial pressure was reduced to 50 mmHg by nitroprusside infusion after opening of the dura. Measurements were recorded and blood samples were taken 15 min before induction of hypotension, during stable hypotension and 15 min after termination of nitroprusside infusion. Measurements included: cerebral blood flow, using the argon-washin technique, cardiac output (thermodilution), mean arterial pressure and heart rate. Cerebral blood flow averaged 56 +/- 6 min . 100 g before hypotension. Nitroprusside produced hypotension but did not significantly alter cerebral blood flow (61 +/- 7 ml/min . 100 g). Cerebral blood flow remained virtually at preinfusion values upon cessation of infusion (53 +/- 6 ml/min . 100 g). Cerebral oxygen uptake averaged 3 +/- 0.2 ml/min . 100 g before hypotension and did not change significantly during hypotension (3.3 +/- 0.3 ml/min . 100 g) and after termination of hypotension (2.7 +/- -0.3 ml/min . 100 g). In two patients nitroprusside produced a 17 and 20% increase, respectively, in cerebral blood flow with no change in cerebral oxygen consumption, together with a marked increase in cardiac output and heart rate.

Adolescent↗
PubMed1979

[The effects of halothane-, nitroprusside- and trimethaphan-induced hypotension on cerebral blood flow and intracranial pressure (author's transl)].

Arterial hypotension to about 50 mm Hg mean pressure was induced in anaesthetized and artificially ventilated dogs by halothane, nitroprusside, and trimethaphan to study their effects on cerebral blood flow and intracranial pressure during hypotension. During nitroprusside induced hypotension there was a 32% increase in cerebral blood flow above control and a marked decrease in cerebral arteriovenous oxygen content difference indicating luxury perfusion of the brain. Cerebral blood flow remained high even 30 min after termination of hypotension. During halothane and trimethaphan hypotension cerebral blood flow remained unchanged. In all groups epidural pressure did not change substantially during hypotension but increased during recovery from nitroprusside hypotension by a maximum of 72% above control. It is concluded that during and after nitroprusside hypotension loss of cerebral autoregulation occurs which may result in a marked rise in intracranial pressure. Special vulnerability seems to exist shortly after termination of induced hypotension when arterial pressure begins to rise and brain perfusion follows a pressure-flow relationship.

Animals↗
PubMed1978

[Effects of isovolaemic haemodilution on pulmonary gas exchange and haemodynamics (author's transl)].

In experiments on 11 closed chest dogs the behaviour of pulmonary gas exchange and haemodynamics during isovolaemic haemodilution with 6% dextran was studied. The dogs were ventilated artificially (IPPB, PEEP = 0) with room air. After haemodilution a slight increase of arterial PO2 from 86 to 92 mm Hg was found. In another series of experiments an inspiratory O2-concentration of 25% was applied resulting in an increase of arterial PO2 from 106 to 113 mm Hg. In both series a decrease of alveolararterial PO2 gradients was observed. Effective pulmonary capillary blood flow varied in accordance with changes of cardiac output. Thus intrapulmonary shunt is supposed to have remained constant. The changes of pulmonary O2 diffusing capacity could be explained by the effect of haemodilution per se. At the end of the experiments ventilation was changed by adding a positive endexpiratory pressure of 8 cm H2O resulting in a decrease of arterial PO2 and a steep fall of cardiac output. In conclusion, isovolaemic haemodilution leads to only negligible variations of pulmonary gas exchange which should not be of any clinical importance.

Animals↗
PubMed1977

[Pulmonary gas exchange during isovolaemic haemodilution (author's transl)].

In experiments on 6 closed chest dogs the behaviour of pulmonary gas exchange during isovolaemic haemodilution with 6% dextran was studied. The dogs were ventilated artificially using an inspiratory gas mixture containing 25% O2. A slight increase of arterial Po2 values was found. This change was accompanied by a decrease in alveolar-arterial Po2 and Pco2 gradients. The size of effective pulmonary capillary blood flow varied in accordance with the size of cardiac output. The changes of pulmonary O2 diffusing capacity could be explained by the effect of haemodilution per se.

Animals↗