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Biomedical subjects

Z Kalapesi

Publications and source records attributed to Z Kalapesi.

8 recordsLinked to original sources
PubMed1982

Ventilatory response to 100% and 15% O2 during wakefulness and sleep in preterm infants.

To examine the ventilatory response to 100% and 15% O2 during wakefulness and sleep, we studied eleven preterm infants birthweight 1770 +/- 102 g; gestational age 32 +/- 1 weeks; postnatal age 31 +/- 5 days) on two occasions each. Wakefulness (W) was present around feeding time and was defined by open eyes for more than 2 min plus presence of purposeful movements. Rapid eye movement (REM) and non-rapid eye movement (N-REM) sleep were defined using electroencephalogram (EEG), electrooculogram (EOG), electrocardiogram (ECG), and body movements. During 100% O2 breathing, immediate (30 s) decreases of 28, 39 and 37% followed by late (5 min) increases in ventilation (Ve) of 42, 49 and 27% were observed during W, REM and N-REM sleep (P greater than 0.05 between states). PaCO2 decreased significantly towards the end of 5 min of breathing 100% O2 in W, REM and N-REM sleep (P greater than 0.05). Average duration of apnea following sudden administration of 100% O2 was 8.5, 11.1 and 8.8 s during W, REM and N-REM sleep (P greater than 0.05 between states). During inhalation of 15% O2, there was a late decrease in ventilation of 19 and 23% during wakefulness and REM sleep, and a sustained increase in Ve of 17% during N-REM sleep (P less than 0.05). PaCO2 at the end of hypoxia (5 min) was significantly decreased in N-REM sleep only (P less than 0.05). We suggest that (i) peripheral chemoreceptor activity is qualitatively intact during W and sleep, as reflected by (a) the immediate changes in Ve during inhalation of high and low O2, and (b) apnea following administration of 100% O2. (ii) The late decrease in ventilation with hypoxia is absent in N-REM sleep.

Electroencephalography↗
PubMed1981

The effect of 2% CO2, 100% O2, theophylline and 15% O2 on "inspiratory drive" and "effective" timing in preterm infants.

We studied 20 preterm infants (B.W. 1440 +/- 80 g (S.E.); G.A. 33 +/- 1 wk) to determine the effect of respiratory stimulants and depressants on respiratory output as measured by VE = VT . f, and VE = VT/Ti . Ti/Ttot. These 20 infants were divided in four groups of five infants. Each group received a respiratory stimulant (2% CO2, 100% O2 or theophylline) or'a respiratory depressant (15% O2). VT/Ti is mean inspiratory flow and represents a mechanic translation of neuronal output. Ti/Ttot is a dimensionless number and has been defined as effective timing. Each study consisted of 3-5 min while the infant breathed 21% O2, followed by 5 min breathing 2% CO2, 100% O2 or 15% O2. The effect of theophylline was assessed by 48-72 h after the initial dose. The respiratory stimulants caused an increase in VT with little or no change in f; 15% O2 produced a decrease in f primarily. According to the newer approach, 2% CO2, 100% O2 and theophylline produced an increase in "inspiratory drive" with little or no change in "effective" timing; 15% O2 decreased "effective" timing primarily via an increase in Te. These findings suggest that the paradoxical decrease in ventilation during hypoxia in preterm infants may not be solely dependent on the central depressant effects of O2. At least in part, the mechanism may be due to a direct action of low O2 on elements controlling expiratory time.

Carbon Dioxide↗
PubMed1981

Effect of periodic or regular respiratory pattern on the ventilatory response to low inhaled CO2 in preterm infants during sleep.

We wanted to know whether the ventilatory response to low concentrations of CO2 is measurable in the absence of change in alveolar PCO2, is sleep state dependent, and is dictated by the resting respiratory pattern. Therefore, we gave 11 preterm infants (birth weight, 1,565 +/- 122 g; gestational age, 32 +/- 1 wk; postnatal age, 28 +/- 5 days) 0.5 to 1.5% CO2 after a control period of breathing 21% O2. They were studied on 2 or 3 occasions, the aim being to have 5 infants in each of 2 categories, periodic to regular breathing, and regular to regular breathing, after administration of CO2 in both sleep states (n = 20). In both sleep states, when low CO2 increased ventilation, alveolar PCO2 also increased. The increase in ventilation was primarily due to an increase in breathing frequency if breathing was periodic, and to an increase in tidal volume if breathing was regular. This response was not affected by sleep state. We conclude that changes in respiratory pattern with low inhaled CO2 are fundamentally dependent on whether the baseline respiration is periodic or regular.

Carbon Dioxide↗
PubMed1980

Chemical control of respiratory frequency and tidal volume during sleep in preterm infants.

During a given sleep state, respiration changes from periodic to regular and vice-versa. Because such spontaneous changes occur without changes in electro-encephalogram (EEG), electro-oculogram (EOG), electro-cardiogram (ECG) or body movements, we hypothesized that they are induced by chemical stimuli such as CO2. To test this hypothesis we examined 12 preterm infants in whom spontaneous changes in respiratory pattern were allowed to occur within the same sleep state, and infants in whom such changes were induced by inhalation of 0.3% to 1.2% CO2. Using a nosepiece and a screen flowmeter we measured the respiratory pattern, VE, f, VT, TI, TE, Ttot, VT/TI, TI/Ttot and PACO2. In REM sleep, spontaneous changes from periodic to regular were associated with increase in VE from 0.466 (mean) to 0.530 L/min (P less than 0.5) and CO2 induced changes accompanied by an increase in VE from 0.416 to 0.571 L/min (P less than 0.05). Similarly in N-REM sleep, VE increased from 0.385 to 0.445 L/min (P less than 0.05) during CO2 induced changes, and from 0.420 to 0.454 L/min (P less than 0.05) during CO2 induced changes, and from 0.420 to 0.454 L/min (P less than 0.05) during CO2 induced changes. Increased VE produced both spontaneously or by CO2 administration was associated with decreased VT, decreased Ttot, decreased VT/TI and slight increase in PACO2. We suggest that changes in respiratory pattern occurring within the same sleep state are chemically mediated.

Carbon Dioxide↗