Biomedical subjects

D B Jennings

Publications and source records attributed to D B Jennings.

At least 55 records · Page 3Linked to original sources

PubMed1984

Acid-base and ventilatory adaptation in conscious dogs during chronic hypercapnia.

Ventilation and cisternal cerebrospinal fluid (CSF) and arterial acid-base balance were measured in awake dogs during air control and from 1 h to 26 days of breathing 5% CO2 in air. Ventilation increased 4-fold during acute hypercapnia and then declined to a minimum at 5-10 days. Between 1-3 days and 16-26 days of hypercapnia ventilation was relatively stable at 2.5 times control. [HCO3-]CSF increased rapidly by 12 h of hypercapnia and in the steady-state [HCO3-]CSF was correlated with PCSFCO2. Between 1 h and 1.5 days of hypercapnia, increase in [HCO3-]CSF was also correlated with increase in [NH3]CSF. Despite increase in [HCO3-]CSF, there was no compensation of [H+]CSF throughout 26 days of hypercapnia. Hydrogen ion may have contributed to the control of ventilation during chronic hypercapnia since ventilation was correlated with [HCO3-]a and [HCO3-]CSF. However, a relationship between ventilation and [H+] of arterial blood and CSF during chronic hypercapnia was relatively poor or absent. Ventilatory adaptation to chronic hypercapnia could not be related to metabolism or to [NH3]CSF. The mechanism(s) by which the increase in PCO2 during chronic respiratory acidosis results in sustained elevation of ventilation remains to be resolved.

Acid-Base Equilibrium↗

PubMed1984

The role of aortic chemoreceptors during acute anemia.

The importance of aortic chemoreceptors in the circulatory and metabolic responses during acute anemia was studied in anesthetized dogs. Data were obtained from nine dogs in which the aortic chemoreceptors were surgically denervated prior to induction of anemia, and from seven sham-operated dogs. Cardiac output (QT), limb blood flow (QL), limb and whole body oxygen uptake (VO2) were determined at normal hematocrit (Hct) and at 30 min of anemia (Hct = 13%) produced by isovolemic dextran-for-blood exchange. At 30 min of anemia, QT was increased from 91 to 186 mL . kg-1 . min-1 (p less than 0.01) and from 99 to 153 mL . kg-1 . min-1 (p less than 0.01) in the sham and denervated groups, respectively. The increase in QT during anemia was less (p less than 0.05) in the aortic-denervated series. Limb flow was also increased during anemia in both groups (p less than 0.01); the mean value of 89 mL . kg-1 . min-1 in the denervated group was less than that of 130 mL . kg-1 . min-1 observed in the sham animals (p less than 0.05). Whole body VO2 decreased (p less than 0.05) in the denervated group at 30 min of anemia; limb VO2 was maintained at the preanemic control value in both groups. The data indicate that during acute anemia the aortic chemoreceptors contribute to the increase in QT.

Acute Disease↗

PubMed1983

PCO2 modulation of ventilation and HCO3- buffer during chronic metabolic acidosis.

Ventilation and acid-base balance were studied in 6 conscious dogs during chronic eucapnic and hypocapnic metabolic acidosis. The dogs had tracheostomas for respiratory studies, exteriorized carotid arteries for obtaining arterial blood and cannulae for sampling cisternal cerebrospinal fluid (CSF). Measurements were obtained on a control diet, and then, during metabolic acidosis induced by adding HCl (7 mmol/kg per day). Initially during metabolic acidosis, PaCO2 was maintained normal by having the dogs breathe 3% CO2 (eucapnia); then the dogs breathed air (hypocapnia). Chronically, arterial and CSF [HCO-3] were related to PCO2. No respiratory compensation occurred during chronic hypocapnic metabolic acidosis since [HCO-3] decreased more than PCO2; consequently, the acidosis worsened. At any [H+], ventilation was related to PCO2. Thus, during hypocapnic metabolic acidosis, ventilation was not increased relative to increase in arterial and CSF [H+]. Modulation of ventilation by PCO2 during severe acidosis may be crucial because stimulation of ventilation by [H+] of arterial blood or CSF would have progressively reduced PCO2 and [HCO-3], resulting in a worsening of the metabolic acidosis.

Acid-Base Equilibrium↗

PubMed1983

Control of respiratory pattern in conscious dog: effects of heat and CO2.

We measured tidal volume (VT) and inspiratory (TI) and expiratory (TE) durations in five conscious tracheostomized dogs breathing air or 5% CO2 in air either at normal (20 degrees C) or elevated (30 degrees C) ambient temperatures. Respiratory frequency ranged between 16 and 333/min due to changes in both TI and TE. During panting TI exceeded TE. During air inhalation instantaneous ventilation (V) spontaneously ranged from 100 to 1,600 ml . kg-1 . min-1. Hypercapnia, heat stress, or both, increased this range of V by increasing maximum V, primarily due to increases in mean inspiratory flow. Under these conditions, changes in TI accounted for more of the spontaneous changes in breath duration. During inhalation of air and 5% CO2, a positive correlation between VT and TI was obtained for TI between 0.13 and 1.05 s; above 1.05 s VT decreased. Heat stress increased VT at a given TI. We suggest that either the decay rate or position of the inspiratory off-switch threshold curve (Clark and von Euler, J. Physiol. London 222: 267, 1972) varies in conscious dogs. Shifts in either the reset (onset) value or decay rate of the curve yield a positive correlation between VT and TI. This modification to the Clark-von Euler model implies that the primary effect of anesthesia on respiratory control is fixation of the inspiratory off-switch threshold curve.

Animals↗

PubMed1982

The effect of body warming on the ventilatory response to CO2 in the awake dog.

Resting awake dogs breathing CO2 lower body temperature and such a change is reported to decrease the ventilatory response to CO2. Therefore, in 6 awake dogs the ventilatory response to CO2, obtained while body temperature was allowed to decrease spontaneously, was compared to the response obtained during warming of their body surface in an attempt to prevent the fall in temperature during hypercapnia. During warming, rectal temperature was maintained 0.5 to 0.7 degrees C higher than when TR was allowed to fall. In warm studies arterial [HCO-3]a was decreased relative to PaCO2 whereas there was a surprisingly large storage of CO2, 17.3 ml CO2/kg . Torr PaCO2. Ventilation was comparable in the dogs during air control of both experiments and before body warming was initiated. Subsequently, there was no consistent effect of warming on either the slope or threshold of the ventilatory response to CO2 with respect to either PaCO2 or pHa. Therefore, producing a higher and more 'normothermic' TR during hypercapnia in awake dogs had no definitive effect on chemical control of breathing.

Animals↗

PubMed1982

Blood-gas CO2 equilibration in lungs of unanesthetized dogs during hypercapnia.

We have reinvestigated the problem of blood-gas equilibration of CO2 in lungs during hypercapnia. Six dogs with chronic tracheostomy and exteriorized carotid artery were subjected in acute experiments to hypercapnic inspired mixtures [CO2 fraction of expired gas (FICO2) = 0.06; 0.08; 0.10]. Expired CO2 partial pressure (PCO2) was continuously measured with a respiratory mass spectrometer and compared with arterial PCO2 determined in blood samples that were collected during apparent steady-state conditions. Particular care was taken in using continuously recorded temperature in the right heart for correction of blood PCO2 measured by CO2 electrodes. In no animal was there a significant difference between arterial and alveolar PCO2. On the average, this difference was -0.1 Torr at FICO2 = 0.06; 0.0 Torr at FICO2 = 0.08, and -0.2 Torr at FICO2 = 0.10. The results are in agreement with the conventional view that PCO2 in pulmonary capillary blood approaches PCO2 in alveolar gas.

Animals↗

PubMed1980

Measurement of total ammonia levels in plasma, whole blood, and cerebrospinal fluid of dogs using an ion-specific electrode.

[NH3] (dissolved NH3 plus NH4+) was measured in cerebrospinal fluid (CSF) and blood of awake and anesthetized dogs using an ion-specific electrode. When oxalate was used as an anticoagulant, plasma [NH3] was increased by 46% in comparison with plasma [NH3] when the anticoagulant was "NH3-free" heparin. As whole blood [NH3] was the same using either anticoagulant, the choice of anticoagulant influenced distribution of NH3 between plasma and red blood cells. In awake animals venous [NH3] was the same as arterial [NH3]; however, following anesthesia plasma [NH3] increased significantly and there was a tendency for venous [NH3] to exceed arterial [NH3]. In some dogs, anesthesia resulted in marked changes in arterial and (or) venous plasma and whole blood [NH3]. Examination of the red blood cell : plasma ratio for [NH3] indicated that ammonia may not be distributed passively between the two compartments. Similarly, calculations of ammonia distribution between CSF and plasma indicated that ammonia is unlikely to be distributed by passive forces between CSF and plasma.

Ammonia↗

PubMed1979

A chronic cannula for obtaining CSF from the cisterna magna of awake dogs.

We have designed a cannula system that can be chronically implanted to end above the dura of the cisterna magna of the dog. During experiments in the awake dog, a screw cap with stylet is removed from the cannula and a spinal needle inserted for the withdrawal of samples of cisternal cerebrospinal fluid (CSF) or for making continuous measurements of pressure. The system can be used for repeated experiments extending over several weeks.

Animals↗

PubMed1979

Body temperature and ventilatory responses to CO2 during chronic respiratory acidosis.

During acute hypercapnia (5% carbon dioxide) in resting conscious dogs, ventilation (Ve) attained a new level above control within 5 min, but rectal temperature decreased gradually to reach a steady state lower than control after 40-60 min. At 2 days of breathing 5% carbon dioxide, Ve remained elevated, as in acute hypercapnia, but Paco2 increased and the threshold of the ventilatory response shifted to a higher Paco2. By 2 days of hypercapnia, rectal temperature (Tr) had returned to normal, reflecting an alteration of hypothalamic temperature control that might be expected to result in enhanced respiratory drive. Surprisingly, despite blood acid-base compensation between 2 and 14 days of hypercapnia, Ve did not decrease, whereas Paco2 decreased to the level observed during acute hypercapnia, and the threshold of the ventilatory response returned to normal. Therefore, at 14 days of respiratory acidosis, acid-based compensation resulting from increase in bicarbonate was not associated with reduced respiratory drive. This result could not be accounted for on the basis of a temperature mechanism because temperature adaptation occurred earlier.

Acidosis, Respiratory↗

PubMed1978

Anemia as a stimulus to aortic and carotid chemoreceptors in the cat.

In cats anesthetized with alpha-chloralose, the activities of aortic and carotid chemoreceptor nerves were measured during a control period and during anemia where the hematocrit was lowered in steps by dextran-for-blood exchange. With anemia there was a sustained nonlinear increase in firing of aortic chemoreceptors. There was a greater firing of aortic chemoreceptors for a given lowering of hematocrit from an initial low blood hematocrit than for a similar decrease in hematocrit from an initial high blood hematocrit. Tonic carotid chemoreceptor firing was independent of blood hematocrit and was only transiently increased at the time of dextran-for-blood exchange. The lack of effect of anemia on carotid chemoreceptor activity appeared to be due to sympathetic nerve activity. Section of the sympathetic nerves to the carotid chemoreceptors resulted in an increase in carotid chemoreceptor afferent activity during anemia in a manner similar to the increase in aortic chemoreceptor activity.

Action Potentials↗

PubMed1976

Ventilation in conscious dogs during acute and chronic hypercapnia.

Minute ventilation was measured in conscious dogs, at rest and during exercise (1 mph), over 60 min immediately following the acute inhalation of 5% carbon dioxide in air and at 2, 4, 7, and 14 days while breathing the same gas mixture in a chamber. The dogs were also studied in the immediate period of air recovery from chronic hypercapnia and 1 day later. Control studies were carried out with the dogs breathing air in the chamber under comparable conditions. A triphasic ventilation change was ovserved in dogs at rest over the 14 days of hypercapnia. After an initial marked increase in ventilation during acute hypercapnia, ventilation returned to control levels by 2 days and then appeared to be elevated above control studies from 4 to 14 days at a time when blood acid-base balance became compensated. When the same dogs were studied during exercise, ventilation was also not different from air control at 2 days of hypercapnia; however during exercise, unlike the resting studies, there was only a tendency for a secondary increase in ventilation at 7 and 14 days of hypercapnia. During the immediate recovery from chronic hypercapnia when the dogs breathed air there was no evidence of hypoventilation either at rest or exercise despite arterial alkalosis. At 24 h of recovery it appeared that dogs while at rest had a slightly reduced ventilatory response to 5% carbon dioxide relative to control studies. The findings provide suggestive evidence that other factors, in addition to acid-base balance, might contribute to the regulation of ventilation during chronic hypercapnia and the recovery from chronic hypercapnia.

Acid-Base Equilibrium↗

PubMed1975

Negative arterial-mixed expired PC02 gradient during acute and chronic hypercapnia.

In resting conscious dogs physiological dead space was calculated using the Bohr equation and measurements of arterial and mixed expired carbon dioxide tension. Whenever dogs inhaled carbon dioxide mixtures (5-10%) that had normal or low oxygen concentrations, the calculated dead space became negative. This paradox was based on the fact that the mixed expired carbon dioxide tension in resting hypercapnic dogs. Under these circumstances carbon dioxide was produced from the lung as measured by gas analyses and blood analyses. By the lung as measured by gas analyses and blood analyses. By reasoning this implies that "alveolar" carbon dioxide tension was higher than pulmonary venous carbon dioxide tension. The negative carbon dioxide gradient persisted at 14 days of chronic hypercapnia and reverted to normal within 10 min of breathing air after chronic hypercapnia. These findings suggest that the exchange of carbon dioxide in the lung cannot be explained solely on the basis of passive diffusion.

Animals↗

PubMed1974