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Biomedical subjects

M E Schlaefke

Publications and source records attributed to M E Schlaefke.

9 recordsLinked to original sources
PubMed1987

Transcutaneous monitoring as trigger for therapy of hypoxemia during sleep.

Based on results on central chemosensitivity in cats, paired stimuli were applied for therapy to infants with central respiratory insufficiency of various degrees. An unspecific respiratory stimulus, e.g. light for 1 s, was followed by a jet of either O2 or 2% CO2 in O2 for 1.5 s. The unspecific and the chemical stimuli were interspaced by 0.5 s. The combined stimulation was repeated every 10 s. The program was triggered by using threshold values of transcutaneous pO2. In infants with intratrachial tubes or tracheostoma we used the end tidal pCO2 for triggering the stimulation. The method could prevent hypoxemia during sleep in non-ventilated subjects with sleep apnea syndromes or in infants with severe hypoxemia during sleep after being rescued from Sudden Infant Death Syndrome (SIDS). In patients with Ondine's Curse Syndrome (OCS) with its CO2 insensitivity, paired stimuli were used in order to condition the chemical function of the respiratory system. Polysomnograms from 310 clinically healthy infants including healthy siblings of SIDS victims revealed instability of arterial pO2 and low CO2 sensitivity during sleep within the second month and the fourth to ninth month of life, respectively. These data challenge the described method as a potential preventive or therapeutic measure to defeat SIDS and sleep apnea syndromes in conjunction with disturbed chemical regulation of respiration.

Arousal↗
PubMed1983

Role of chemical afferents in the maintenance of rhythmic respiratory movements.

In seven anesthetized cats central chemosensitivity was eliminated (cold block) and peripheral chemoreceptors were either stimulated or eliminated (sectioned) to test whether nonchemical vagal afferents can maintain rhythmic ventilation and to determine the relative contribution of the carotid and aortic chemoreceptors to ventilatory drive without central chemosensitivity. Elimination of all chemical afferents invariably induced apnea, whereas ventilation was reduced from 533 to 159 ml X min-1 during cold block of central chemosensitivity and to 478 ml X min-1 after sectioning both sinus nerves. Cold block with only the aortic chemoreceptors and vagal afferents intact produced apnea in four of six cases tested. Stimulation of peripheral chemoreceptors during cold block remained effective and interrupted apnea in three of the four cats with only aortic chemoreceptors intact. We conclude that the nonchemical vagal respiratory afferents alone are unable to maintain rhythmic ventilation. Respiratory rhythm generation is, under the conditions of our experiments, critically dependent on sufficient afferent input from chemical afferents. Of these, central chemosensitivity plays the major role, followed by carotid body and, least importantly, by aortic afferents.

Afferent Pathways↗
PubMed1979

Elimination of central chemosensitivity by coagulation of a bilateral area on the ventral medullary surface in awake cats.

Breathing and respiratory response to CO2 were observed in 6 awake cats and 1 control before and after bilateral coagulation of the formerly described area S (Schläfke and Loeschcke, 1967) on the ventral medullary surface under hyperoxic conditions. Ventilation decreased, PCO2 rose and CO2 response was almost or completely abolished in 4 cats, and moderately reduced in 2 cats. Inhalation of CO2 had an inhibitory effect on ventilation in two cases. In some instances the respiratory frequency was increased by CO2. Periodic breathing as well as spontaneous hyperventilation elicited by 'arousal' indicate parallels to the Pickwickian or Ondine's curse syndrome. No respiratory changes were produced by a lesion on the pyramidal tract medial to the area S. It is concluded that central chemosensitivity can be eliminated within the superficial layer of the area S. The loss of CO2 response seems to be correlated with complete destruction of the superficial nerve cells located within the area S (Petrovický, 1968) and degeneration within the ventral part of the nucleus paragigantocellularis.

Animals↗
PubMed1979

Respiratory response to hypoxia and hypercapnia after elimination of central chemosensitivity.

Central respiratory drive responding to pH changes was eliminated by bilateral coagulation or cold block of area S (intermediate area) on the ventral medullary surface in 7 anaesthetized cats. Arterial pH, PCO2, and PO2 (4 cats) and the respiratory response to hypoxia and hypercapnia (6 cats) were observed before and after coagulation. After coagulation in hyperoxia the arterial pH dropped from 7.30 to 7.09, the arterial PCO2 was elevated from 4.80 kPa to 8.17 kPa (6 cats). Ventilation increased by 477 ml at a PCO2a of 6.58 kPa when PO2a was reduced from 39.5 kPa to 8.5 kPa before coagulation, after coagulation ventilation increased by 241 ml (4 cats). The peripheral chemoreceptors guaranteed spontaneous breathing even in hyperoxia. The data reveal that the loss of respiratory homeostasis by elimination of the S areas is due to the loss of central chemosensitive drive with concomitant reduction of peripheral chemoreceptor effect.

Animals↗
PubMed1973

'Specific' and 'non-specific' stimuli in the drive of respiration.

In decerebrate and awake cats it was shown that central chemosensitivity can be blocked by cooling or coagulating bilaterally a formerly described area on the ventral medullary surface of cats, called area S. Such a procedure is followed by apnoea under the condition that vagi and sinus nerves are cut. With either vagi, sinus nerves, or central chemosensitivity intact respiration can be influenced by noise, touch, and electrical stimulation of dorsal roots, femoral nerves, and pontine reticular formation. With vagi, sinus nerves, and central chemosensitivity blocked, these "non-specific" stimuli are not able to influence respiration. In the described experiments vagi, sinus nerves, and central chemosensitivity were essential for the activity of the respiratory centres and were therefore called "specific".

Animals↗