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Biomedical subjects

N H Edelman

Publications and source records attributed to N H Edelman.

At least 73 records · Page 4Linked to original sources
PubMed1984

Correlation between ventilation and brain blood flow during sleep.

The relationships between brain blood flow (BBF) and ventilation (VI) were studied during sleep in 13 goats. Unilateral BBF was continuously measured with an electromagnetic flow probe; total and regional BBF were assessed by the radioactive microsphere technique in four animals. Interacting changes in VI and BBF occurred during both slow wave (SWS) and rapid eye movement (REM) sleep. During SWS, significant decreases in VI and increases in arterial PCO2 occurred compared to wakefulness. BBF during SWS correlated linearly with arterial CO2 tension (PaCO2); nd the relationship was similar to that for awake goats breathing CO2. During REM sleep, VI was significantly less than both the awake (W) and SWS states due principally to a decrease in tidal volume. BBF during REM sleep was significantly and substantially increased compared with both the W and SWS states; this increase was shared by all brain areas. The increase in BBF during REM sleep was greater than that predicted from changes in PaCO2. In five goats provided with chronic sagittal sinus fistulae, arteriovenous oxygen difference was measured in separate studies and found to be significantly lower during REM sleep compared with W; brain O2 consumption was similar in magnitude in the REM and W states. Thus, the high BBF of REM sleep was also unexplained by an increase of brain metabolic activity. We conclude that, during SWS, increases in BBF are explained by hypoventilation and hypercapnia. In contrast, during REM sleep, BBF is substantially in excess of that expected from PaCO2 or brain metabolism. It is postulated that this excess of BBF during REM sleep could reduce the central chemoreceptor pH relative to that present in SWS. The combination of reduction of sensitivity to CO2 and lower tissue PCO2 during REM sleep makes it likely that the output of the central chemoreceptors during this state is less than that during SWS and wakefulness. This may contribute to the low tidal volume and respiratory irregularities of this sleep period.

Animals↗
PubMed1983

Sleep deprivation decreases ventilatory response to CO2 but not load compensation.

Because sleep is known to reduce ventilatory drive, and sleep deprivation is a common accompaniment to ventilatory failure, we tested ventilatory response to carbon dioxide (delta V1/delta PCO2) and response to an inspiratory flow resistive load (change in delta P100/delta PCO2 with load) after both a normal night of sleep and after 24 hours of sleep deprivation in 13 healthy volunteers. Sleep deprivation was associated with a significant decrease in delta V1/delta PCO2 from 2.51 +/- .36 to 2.09 +/- .34 L/min/mm Hg (p less than 0.02). However, load compensation was preserved during sleep deprivation. Since many acutely-ill patients are sleep deprived, an associated reduction of ventilatory drive may play a role in progressive respiratory insufficiency.

Adult↗
PubMed1982

Brain hypoxia and control of breathing: role of the vagi.

Vagally mediated reflexes play an important role in the generation of respiratory responses to various stimuli. This study examined the role of vagally mediated mechanisms in the generation of the respiratory responses to progressive brain hypoxia secondary to carboxyhemoglobinemia (HbCO 0-55%) in six unanesthetized goats. Ventilation, respiratory cycle timing, and the lung inflation reflex were measured before and during CO inhalation in intact and bilaterally vagotomized animals. Our results indicate that vagal reflexes contribute a small magnitude of the hyperpnea caused by carboxyhemoglobinemia. Furthermore, in contrast to that reported for CO2 inhalation, the tachypneic nature of the ventilatory response to CO is not a vagally mediated phenomenon. CO inhalation had a biphasic influence on the strength of the lung inflation reflex measured as the ratio of inspiratory time during occlusion (TIoccl) to inspiratory time of the preceding spontaneous breath (TIspont). At HbCO levels of 35%, TIoccl/TIspont was enhanced, whereas at HbCO levels of 55% of ratio fell to unity, indicating abolition of the reflex. After vagotomy, this ratio was unity at all levels of carboxyhemoglobinemia.

Animals↗
PubMed1982

beta-Aminopropionitrile prevents bleomycin-induced pulmonary fibrosis in the hamster.

beta-Aminopropionitrile (beta APN), an agent that prevents collagen accumulation in tissues, was evaluated for its ability to prevent excess collagen formation in bleomycin-induced pulmonary fibrosis in the hamster. Two groups of animals received a single endotracheal dose of bleomycin; one of these was injected with beta APN twice daily for 30 days. A third group received endotracheal saline and a fourth group received saline and beta APN. After 30 days, we measured pressure-volume curves of saline-filled lungs, collagen content, and degree of fibrosis. Endotracheal bleomycin increased collagen content, decreased lung volume, and produced fibrosis and a mortality rate of 51%. The administration of beta APN to bleomycin-treated animals prevented excess collagen accumulation and diminished total protein, reversed volume diminution, produced less fibrosis, and improved the mortality rate to 24%; beta APN alone had no effect on lung mechanics or collagen content. The biochemical, functional, and structural features of bleomycin-induced lung fibrosis are amenable to control with beta APN.

Aminopropionitrile↗
PubMed1982

Ventilatory response to isocapnic hypoxia in parents of victims of sudden infant death syndrome.

Ventilatory response to progressive isocapnic hypoxia was measured in 14 parents of victims of sudden infant death syndrome (SIDS) and 12 matched control parents. Controls had a value for a measure of ventilatory responsiveness (parameter A) of 200.8 +/- 46.4, while SIDS parents had a significantly lower value of 64.4 +/- 16.2 (P less than 0.01). Since degree of hypoxic ventilatory drive is a hereditary characteristic, it is concluded that a relatively low ventilatory responsiveness to hypoxia might have been present in the SIDS victims.

Carbon Dioxide↗
PubMed1981

Endorphins and the control of breathing. Ability of naloxone to restore flow-resistive load compensation in chronic obstructive pulmonary disease.

Since narcotic drugs profoundly depress breathing, we tested whether endogenous opioids influenced control of breathing in chronic obstructive pulmonary disease (COPD), reasoning that the stress of chronic dyspnea might cause elaboration of "endorphins." In 14 patients with COPD (but without respiratory failure) and eight normal controls, we measured ventilation, mechanical lung function, respiratory sensitivity to carbon dioxide, and the increase in respiratory effort elicited by an increase in resistance to breathing; each measurement was performed before and after administration of the opiate antagonist naloxone. Before naloxone, increased resistance to breathing enhanced respiratory effort in all controls, but seven of 14 patients with COPD had no response. After naloxone, these seven patients had load responses. Furthermore, the respiratory effort elicited by the resistance also increased after the drug was given to the patients who had had a response. These data suggest that endorphin elaboration minimizes the stress of chronic airway obstruction.

Aged↗
PubMed1981

Role of carotid chemoreflex in respiratory acclimatization to hypoxemia in goat and sheep.

The role of the carotid body chemoreflex in the ventilatory acclimatization to chronic hypoxia was studied in the unanesthetized goat and sheep. The time-cours of changes in ventilation, PCO2, pH and PO2 of arterial blood and cisternal fluid (CF) were measured before and following exposure to a simulated altitude of 3660-5000 m, with and without intact carotid sinus nerves. At sea level, after section of carotid sinus nerves most animals hypoventilated chronically, and developed mild arterial hypoxemia and hypercapnia. Upon exposure to acute hypoxia, all of the intact animals hyperventilated and CF pH increased from 7.310 to 7.380 whereas after chemodenervation, the increase in ventilation was small and delayed, and CF pH decreased from 7.285 to 7.143. During exposure of the intact animals to chronic hypoxia, hyperventilation accompanied by decreases in arterial and CF P CO2 reached its peak in two days; these changes partially subsided during the next few days. Partial compensation of respiratory alkalosis occurred during the first day. In contrast, several chemodenervated animals died during chronic hypoxia; the survivors showed either a small decrease or an increase in Pa CO2. Thus, an intact peripheral chemoreflex drive during hypoxia is necessary for ventilatory acclimatization which raises the arterial and presumably tissue PO2 in spite of alkalosis. The new proposal is that a central tissue metabolic acidosis resulting from a direct effect of acute hypoxia is partly compensated as hypoxia is prolonged. This central compensation decreases ventilatory drive and hence opposes the ventilatory acclimatization during chronic hypoxia initiated by the peripheral chemoreflexes.

Acclimatization↗
PubMed1981

The effect of positive end-expiratory pressure ventilation (PEEP) on cerebral blood flow and cerebrospinal fluid pressure in goats.

The effect of cerebral blood flow (CBF) and cerebrospinal fluid pressure (CSFP) of mechanical ventilation with positive end-expiratory pressure (PEEP) at 5, 10, and 15 cm H2O was studied in 23 paralyzed, ventilated goats which were divided into three treatment groups. Group I received no volume expansion agent to counteract the hemodynamic effects of PEEP. Group II received normal saline to maintain a constant arterial blood pressure (BP), and Group III received a mannitol solution for BP maintenance. In all three groups there were similar increases in central venous pressure (CVP) of approximately 2.5 times the zero PEEP level at 15 cm H2O PEEP (P less than 0.001). In Group I, BP fell an average of 32 per cent, cardiac output fell 47 per cent and cisternal CSFP increased 40 per cent above zero PEEP levels at 15 cm H2O PEEP (P less than 0.01). CBF in this group was decreased 18 per cent when compared with the zero PEEP baseline at 15 cm H2O PEEP (P less than 0.008). In Group II animals there were no significant changes in BP or cardiac output (CO) at any of the PEEP levels. CSFP in this group, at 15 cm H2O PEEP, increased 84 per cent above the baseline zero level and CBF decreased 32 per cent at 15 cm H2O PEEP when compared to the zero PEEP level (P less than 0.008). In Group III there were no significant reductions in BP or CO. Unlike Groups I and II, no significant changes in CFSP were observed at any level of PEEP. In addition, CBF in this group did not change significantly from the zero-PEEP baseline level any level of PEEP. Thus, when PEEP therapy is associated with substantial decreases in BP and CO, CBF may decrease as well. Maintenance of BP and CO by volume expansion with a crystalloid solution resulted in a greater reduction in CBF than in the untreated group but maintenance of BP and CO by mannitol infusion resulted in maintenance of CBF at the baseline, pre-PEEP level. The authors conclude that brain interstitial fluid pressure is an important variable in the determination of cerebral blood flow during ventilation with PEEP.

Animals↗
PubMed1981

Hypoxic arousal in intact and carotid chemodenervated sleeping cats.

To determine whether the carotid chemoreceptors or hyperpnea are required for arousal from sleep by hypoxia, 14 sleep-deprived cats were studied during slow-wave (SWS) and rapid-eye-movement (REM) sleep. Rapid hypoxia was produced by inhalation of 5% O2 in N2 or 6% CO in 40% O2 by intact cats and 5% O2 in N2 after carotid body denervation. Preliminary studies identified a period of SWS unassociated with spontaneous arousals. In 69 studies during SWS unassociated with spontaneous arousals, arterial O2 saturation (SaO2) values at arousal were: 47.1 +/- 1.5% (mean +/- SE) (5% O2, intact); 48.9 +/- 1.4% (6% CO, intact); and 49.9 +/- 2.0% (5% O2, denervated). During SWS associated with spontaneous arousals, SaO2 values at arousal were 71.6 +/- 1.8% (5% O2, intact). Arousal from REM occurred at significantly lower values: 31.7 +/- 3.9% (6% CO, intact) and 43.5 +/- 2.3% (5% O2, intact). During both SWS and REM, inhalation of 5% O2 by intact animals caused a substantial increase in ventilation while 6% CO did not. We conclude that more severe hypoxia is required for arousal from SWS when studies are done in a period unassociated with spontaneous arousals than from SWS associated with spontaneous arousals. Hypoxic arousal does not appear to require activation of the carotid bodies or hyperpnea.

Animals↗
PubMed1981

Respiratory flow-resistive load compensation during sleep.

We studied ventilation, arterial blood gas tensions, and the ventilatory and airway occlusion pressure responses to hypercapnia of eight cats during wakefulness, quiet (slow-wave) sleep, and active (rapid-eye-movement) sleep. Responses to hypercapnia were measured before and during added airway resistance. Ventilation decreased, and arterial PCO2 increased during both slow-wave and rapid-eye-movement sleep. Unloaded ventilatory and airway occlusion pressure responses to hypercapnia decreased during slow-wave and rapid-eye-movement sleep as well. Flow-resistive loading caused awake cats to increase their occlusion pressure response to hypercapnia, thereby preserving their ventilatory responses. In contrast, during both slow-wave and rapid-eye-movement sleep, cats showed no augmentation of the occlusion pressure response and concomitant decrease of the ventilatory response to hypercapnia with the load. Thus, sleep was associated with loss of flow-resistive load compensation. It is postulated that, in an appropriate setting, this phenomenon could serve a protective function by decreasing the chances for progression from partial to complete upper airway obstruction during sleep.

Airway Resistance↗
PubMed1981

Prevention of bleomycin-induced pulmonary fibrosis in the hamster by cis-4-hydroxy-l-proline.

We investigated the effect of the proline analogue cis-hydroxyproline on pulmonary fibrosis produced by intratracheal administration of bleomycin in hamsters. Two groups of animals received a single dose of bleomycin; one of these groups was also injected with cis-hydroxyproline twice daily for 30 days. Control animals received intratracheal saline. Lungs were examined on day 30. In the bleomycin group, the collagen content of lungs was 131% of the control value (p less than 0.05). Administration of cis-hydroxyproline decreased collagen accumulation to 114% of the control value (p less than 0.05). Pressure-volume curves were significantly shifted downward and to the right of control in the bleomycin group; this shift was partially prevented by cis-hydroxyproline. Morphometric studies showed that alveolar walls comprised 15% of the lung parenchyma in the control group and 19% in the bleomycin group (p less than 0.05). Administration of cis-hydroxyproline significantly decreased alveolar walls to 16% of the lung parenchyma (p less than 0.05). We conclude that cis-hydroxyproline partially prevents the chemical, structural, and functional changes of bleomycin-induced pulmonary fibrosis in the hamster.

Animals↗
PubMed1980

Ventilatory control in parents of victims of sudden-infant-death syndrome.

Since a defective ventilatory-control mechanism may have a role in the sudden-infant-death syndrome (SIDS), and hereditary factors influence the degree of ventilatory drive, we measured ventilatory responsiveness to carbon dioxide with and without increased airway resistance in 12 parents of SIDS victims and 12 control parents matched for age and size. Ventilatory response (delta VI/delta PCO2) and "respiratory drive" (delta P100/delta PCO2) were measured both with and without added resistance to inspiratory flow. SIDS parents had significantly lower ventilatory response with added resistance (P less than 0.05) and without it (P less than 0.01) and significantly lower respiratory drive with added resistance (P less than 0.001) and without it (P less than 0.05). Control parents had significantly increased respiratory drive when the resistance was added (P less than 0.005), whereas SIDS parents did not. The data suggest that a low ventilatory response to carbon dioxide and a diminished compensatory response to increased airway resistance may increase a potential parent's risk of having a child susceptible to SIDS.

Adult↗