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Biomedical subjects

V Fencl

Publications and source records attributed to V Fencl.

At least 37 records · Page 2Linked to original sources
PubMed1986

Acid-base effects of altering plasma protein concentration in human blood in vitro.

We altered the concentration of plasma proteins in human blood in vitro by adding solutions with [Na+], [K+], and [Cl-] resembling those in normal blood plasma, either protein-free or with a high concentration of human albumin. After equilibrating the samples with a gas containing 5% CO2-12% O2-83% N2 at 37 degrees C, we measured pH, PCO2, and PO2; in separated plasma, we determined the concentrations of total plasma proteins and albumin and of the completely dissociated electrolytes (strong cations Na+, K+, Mg2+ and anions Cl-, citrate3-). With PCO2 nearly constant (mean = 35.5 Torr; coefficient of variation = 0.02), lowering plasma protein concentration produced a metabolic alkalosis, whereas increasing plasma albumin concentration gave rise to a metabolic acidosis. These acid-base disturbances occurred independently of a minor variation in the balance between the sums of strong cations and anions. We quantified the dependence of several acid-base variables in plasma on albumin (or total protein) concentration. Normal plasma proteins are weak nonvolatile acids. Although their concentration is not regulated as part of acid-base homeostasis, hypoproteinemia and hyperalbuminemia per se produce alkalosis and acidosis, respectively.

Acid-Base Equilibrium↗
PubMed1985

Endogenous opioids and ventilatory responses to hypercapnia in normal humans.

Though administration of opioid peptides depresses ventilation and ventilatory responsiveness, the role of endogenous opioid peptides in modulating ventilatory responsiveness is not clear. We studied the interaction of endogenous opioids and ventilatory responses in 12 adult male volunteers by relating hypercapnic responsiveness to plasma levels of immunoactive beta-endorphin and by administering the opiate antagonist naloxone. Ventilatory responsiveness to hypercapnia was not altered by pretreatment with naloxone, and this by itself suggests that endogenous opioids have no role in modulating this response. However, there was an inverse relationship between basal levels of immunoactive beta-endorphin in plasma and ventilatory responsiveness to CO2. Furthermore, plasma beta-endorphin levels rose after short-term hypercapnia but only when subjects had been pretreated with naloxone. We conclude that measurement of plasma endorphin levels suggests relationships between endogenous opioid peptides and ventilatory responses to CO2 that are not apparent in studies limited to assessing the effect of naloxone.

Adult↗
PubMed1985

Endogenous opioids and ventilatory responses to hypoxia in normal humans.

We studied the putative role of endorphins in modulating hypoxic ventilatory responsiveness. In 12 healthy men, minute ventilation (VE)and mouth occlusion pressure (P0.1) responses to progressive isocapnic hypoxia were determined before and after the intravenous administration of the opioid antagonist naloxone (10 mg) or placebo. Plasma levels of beta-endorphin were measured before and after hypoxia. Naloxone did not affect the slopes or x-intercepts of the relationships between either VE or P0.1 and arterial O2 saturation. There was no correlation between the baseline plasma level of beta-endorphin and any measure of responsiveness to hypoxia. Plasma beta-endorphin levels were not affected by either short-term hypoxia or naloxone alone; however, when hypoxia followed naloxone administration, mean +/- SD beta-endorphin increased from 8.0 +/- 8.9 pg/ml to 20.2 +/- 16.6 pg/ml (p less than 0.005). We concluded that endogenous opioids do not have an important modulating influence on hypoxic ventilatory responsiveness in adult human volunteers.

Adult↗
PubMed1984

Naloxone does not affect ventilatory responses to hypoxia and hypercapnia in rats.

Ventilatory responses (tidal volume, respiratory frequency, and minute ventilation) to steady-state hypoxia and steady-state hypercapnia were measured plethysmographically in awake unrestrained adult rats, before and after subcutaneous injection of placebo (saline) naloxone in doses up to 5.0 mg/kg. Naloxone did not alter the ventilatory responses to hypoxia or hypercapnia.

Animals↗
PubMed1984

Respiration of chemodenervated goats in acute metabolic acidosis.

In awake goats before and after ablation of carotid bodies (CBx) we studied the effect of acute metabolic acidosis (AMA) produced by intravenous infusion of HCl on composition of arterial blood and CSF, and on ventilatory responsiveness to hyperoxic CO2 rebreathing AMA caused decrease in PaCO2 (breathing air at rest) indicating that alveolar ventilation was increased relative to CO2 production; position of CO2 response curves was shifted toward lower values of PCO2. These changes were similar before and after CBx, though the levels of PCO2 in arterial blood during air breathing at rest, and in expired gas at a given level of ventilation during CO2 rebreathing, were higher after CBx. We conclude that a respiratory adaptation to AMA does occur in goats deprived of peripheral chemoreceptors, and is probably mediated by the central chemoreceptors.

Acidosis↗
PubMed1984

Adrenergic blockade does not change ventilatory response to CO2 in awake resting goats.

Although adrenergic agonists increase resting ventilation and responsiveness to CO2, there are conflicting data about the effect of adrenergic blockade on ventilatory responses. In this study, we investigated the effect of alpha- or beta-adrenergic blockade on the response to hyperoxic CO2 rebreathing in awake goats. In 5 goats, studied before and after intravenous administration of phentolamine or propranolol, there was no difference (compared to control studies) in the mean slope, x-intercept, or ventilation at end-tidal PCO2 (PETCO2) = 70 torr for the CO2 response curves after either drug. When mean inspiratory flow rate (VT/Ti) was plotted against PETCO2, there was also no change in these measurements after propranolol. After phentolamine, there was a slight decrease in the slope and x-intercept, but no change in VT/Ti at PETCO2 = 70 torr. We conclude that acute administration of alpha- or beta-adrenergic blockers does not affect ventilatory response to CO2 inhalation in goats, and suggest that adrenergic activity is not an important modulating influence for CO2 responsiveness in this species.

Animals↗
PubMed1983

Acclimatization to high altitude in goats with ablated carotid bodies.

In awake goats with ablated carotid bodies, we studied resting pulmonary ventilation, CO2 production, composition of arterial blood and cerebrospinal fluid (CSF), and ventilatory responsiveness to hyperoxic CO2 rebreathing at sea level (SL) and after 3 days at simulated high altitude (HA) (PB 446 +/- 5 Torr, equivalent to 4,300 m). At HA, resting pulmonary ventilation was increased, resulting in marked hypocapnia with appropriate base deficit in blood plasma; CSF became more alkaline; CO2-response curves were shifted to lower PCO2 levels, and their slopes were steeper than at SL. Although these changes in regulation of respiration were not demonstrably different from those seen after normal acclimatization to HA with carotid bodies intact, the mechanisms of their initiation and development are probably different.

Acclimatization↗
PubMed1983

Reversal of arterial-to-expired CO2 partial pressure differences during rebreathing in goats.

Whether CO2 partial pressure (PCO2) in expired gas may exceed that in arterial blood has been controversial. We measured arterial PCO2 (Paco2) and end-tidal PCO2 (PETco2) in four awake goats during air breathing and during hyperoxic CO2 rebreathing in various conditions of acid-base balance. During air breathing, Paco2 was slightly higher than PETco2; i.e., the mean (+/- SE) difference, Paco2 - PETco2, was positive by + 2.36 +/- 0.53 Torr (P less than 0.001). In contrast, during CO2 rebreathing with the same techniques of measurement, this difference was always negative (mean +/- SE = -11.63 +/- 0.22 Torr, P less than 0.001), and it widened as Paco2 increased with rebreathing. Magnitude of the negative difference during rebreathing was too great to be accounted for by incorrect assumptions or measurement error, even if reasonable contributions from all known sources of error were concurrently invoked. We conclude that during hyperoxic CO2 rebreathing in goats, PETco2 exceeds Paco2.

Animals↗
PubMed1979

Composition of cerebral fluids in goats adapted to high altitude.

We explored the ionic composition of cerebral interstitial fluid (cISF) in six unanesthetized goats at sea level (SL) and again after 5 days at a simulated high altitude (HA) of 4,300 m. By measuring net transependymal fluxes of HCO3-, Cl-, and lactate during ventriculocisternal perfusions with lactate-free artificial cerebrospinal fluid (CSF) with various [HCO3-] and [Cl-], we determined [HCO3-] and [Cl-] in the inflowing perfusate that produced zero flux, which are estimates of the concentrations of these ions in cISF. Ventilatory acclimatization to HA was established in the goats with alkaline shift in cisternal CSF pH. At SL zero flux of HCO3- and of Cl- occurred when [HCO3-] and [Cl-] in the perfusate were equal to those in CSF. At HA Cl- flux again was zero when [Cl-] in perfusate and in the goat's own CSF were equal; however, for HCO3-, zero flux occurred at HA when [HCO3-] in perfusate was significantly lower than in CSF. Mean transependymal washout of lactate was 16 times larger at HA than at SL. We conclude that at SL [HCO3-] and [Cl-] in CSF were the same as in cISF. In goats adapted to HA [Cl-] in cISF and in CSF were again equal, whereas [HCO3-] in cISF was lower and [lactate] presumably higher than in CSF. The fluid surrounding the central chemoreceptors appears to be more acidic in goats acclimatized to HA than at SL despite the alkalosis in cisternal CSF. This may contribute to ventilatory acclimatization to HA.

Acclimatization↗
PubMed1976

Alkaline shift in lumbar and intracranial CSF in man after 5 days at high altitude.

In six healthy male volunteers at sea level (PB 747-759 Torr), we measured pH and PCO2 in cerebrospinal fluid (CSF), and in arterial and jugular bulb blood; from these data we estimated PCO2 (12) and pH for the intracranial portion of CSF. The measurements were repeated after 5 days in a hypobaric chamber (PB 447 Torr). Both lumbar and intracranial CSF were significantly more alkaline at simulated altitude than at sea level. Decrease in [HCO3-] IN lumbar CSF at altitude was similar to that in blood plasma. Both at sea level and at high altitude, PCO2 measured in the lumbar CSF was higher than that estimated for the intracranial CSF. At altitude, hyperoxia, in comparison with breathing room air, resulted in an increase in intracranial PCO2, and a decrease in the estimated pH in intracranial CSF. With hyperoxia at altitude, alveolar ventilation was significantly higher than during sea-level hyperoxia or normoxia, confirming that a degree of acclimatization had occurred. Changes in cerebral arteriovenous differences in CO2, measured in three subjects, suggest that cerebral blood flow may have been elevated after 5 days at altitude.

Acid-Base Equilibrium↗
PubMed1976

Ventilatory response to carbon dioxide in humans.

Testing ventilatory responses to CO2 is fraught with difficulties in interpretation and, at present, it can hardly be considered suitable for routine evaluation of patients with pulmonary disease. In spite of the seventy years' work since Haldane's introduction of the CO2 response curve, much remains to be learned about the various components of the regulatory system, and for testing chemosensitivity to CO2 in patients with pulmonary disease, methods more direct than measuring pulmonary ventilation are needed for evaluation of the output of the regulatory system.

Carbon Dioxide↗