Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect on CO2 storage and elimination of variations in the slope and intercept of the ventilatory response to CO2 curve was examined. Theoretical and experimental results show that although CO2 elimination rate following a transient ventilatory disturbance is decreased at low ventilatory response slopes, this decrease can be compensated by elevated PCO2 intercepts, or thresholds. Conversely, high CO2 elimination rate following a ventilatory disturbance due to a high ventilatory response slope can be off-set by a depressed PCO2 threshold. The results suggest that elevated thresholds which often accompany depressed ventilatory response slopes may be part of a compensatory mechanism for minimizing transient hypercapnia and acidosis.
 ...
PMID:Transient CO2 elimination and storage as functions of the ventilatory response to CO2. 49 46

The influence of regional alveolar oxygen and carbon dioxide tensions on the distribution of lung blood flow and gas exchange was studied in unanaesthetised sheep. Right apical lobe (RAL) hypoxia, induced by administering nitrogen or nitrogen/oxygen mixtures to the lobe, stimulated a prompt, graded and well sustained reduction in lobar blood flow. Maximum hypoxia was accompanied by an approximate 65% reduction in perfusion, a significant fall in RAL carbon dioxide tension and output, a reversal of lobar oxygen flux and an average 13 Torr fall in arterial oxygen tension. The reduction in perfusion and gas exchange persisted in the face of elevated systemic oxygen tensions produced by giving pure oxygen instead of air to the remainder of the lung (RL). Mild RAL hypercapnia potentiated the hypoxia-induced change in perfusion and gas exchange. During lobar hypoxia RL blood flow and gas exchange increased to maintain total pulmonary gas exchange at an essentially constant level. RAL hyperoxia did not significantly alter the distribution of perfusion or gas exchange.
 ...
PMID:Regional alveolar gas composition and lung function in sheep. 49 47

We measured cerebral blood flow using both the radioactive microsphere technique and the cerebral venous outflow technique in dogs anesthetized with chloralase. The effect of sympathetic stimulation on cerebral blood flow was observed during both normocapnia and prolonged hypercapnia using both blood flow techniques. The increase in blood flow with hypercapnia was the same with both methods. During hypercapnia the venous outflow method showed a 38% decrease and microspheres an 18% decrease in cerebral blood flow with sympathetic stimulation. At normal CO2, stimulation caused a decrease in cerebral venous flow: no change was observed with the microsphere method. Analysis of the blood flow patterns to extracerebral tissues and evaluation of extracerebral arterial reference samples failed to prove the existence of axial streaming and subsequent skimming of microspheres within the cephalic circulation. It is concluded that direct electrical stimulation of the sympathetic innervation of the cerebral vessels is capable of reducing cerebral blood flow even during a profound hypercapnic vasodilation.
 ...
PMID:Sympathetic modulation of hypercapnic cerebral vasodilation in dogs. 49 41

One subject was exposed for six days to increasing levels of CO2, rising at a constant rate from 0.03 to 3.0% CO2 within a 15-h period followed by 9 h of air breathing. To assess acid-base parameters, arterialized capillary blood was taken from a finger twice daily (at 8 a.m. and 11 p.m.) at times corresponding to the beginning and end of the intermittent exposure to CO2. Venous blood samples were obtained on alternate days at the same times. Urine specimens were collected twice daily. The subject was on a liquid diet. Resting respiratory minute volume (VE), oxygen consumption (VO2), carbon dioxide excretion (VCO2), alveolar carbon dioxide and oxygen tension (PACO2) and PAO2) were measured twice daily. PACO2 and PAO2 were also determined at the end of breath-holding twice daily; CO2 tolerance tests and lung function tests were also carried out. In contrast to the effects of chronic exposure to 3% CO2, the CO2 tolerance tests showed an increased sensitivity (increase of slope) and breath-holding PACO2 did not change, indicating that acclimatization to CO2 did not develop. The ventilatory response to CO2 was not sufficient to prevent CO2 accumulation in the body; this accumulation was eliminated during the nightly air-breathing periods on the fourth and fifth days, indicated by higher values of PaCO2 and PACO2. The known renal response to hypercapnia, consisting of an increased excretion of titratable acidity, ammonia, and hydrogen ion excretion, occurred but was interrupted after the first day and was triggered again on the fourth and fith days when accumulated CO2 was released from body CO2 stores. The second renal response was associated with a marked calcium excretion, which suggests that bone CO2 stores were involved.
 ...
PMID:Effect of intermittent exposure to 3% CO2 on respiration, acid-base balance, and calcium-phosphorus metabolism. 50 20

A recent report (J. Appl. Physiol. 38: 382-388, 1975) suggests that negative blood-gas CO2 partial pressure (PCO2) differences exist in the dog during hypercapnia, as mean expired PCO2 exceeded arterial PCO2 by more than 10 Torr when the CO2 fraction in inspired gas (FICO2) was 0.1. We have reinvestigated this problem in anesthetized dogs breathing spontaneously room air or hypercapnic mixtures (FICO2 = 0.05 or 0.10). During steady state, arterial blood samples were analyzed with electrodes, care being taken to keep the electrode temperature within +/- 0.2 degrees C at the actual aortic temperature of the animal. Respired gas was measured at the tracheostomy by a sensitive low-noise respiratory mass spectrometer. During room air breathing, the arterial-end-expired PCO2 difference, P(a-E')CO2, averaged +5 Torr and decreased to +0.9 Torr and to +0.1 Torr with FICO2 = 0.05 and 0.1, respectively. Hypoxia (FIO2 = 0.10) had no apparent effect on the P(a-E')CO2 difference. We ascribe the decrease in P(a-E')CO2 with hypercapnia to the diminishing effects of alveolar dead space, whereby end expired PCO2 approached arterial PCO2. We then conclude that in blood-gas equilibration lungs, PCO2 in end-capillary blood comes close to alveolar PCO2, and that the negative blood-gas PCO2 differences reported earlier are probably caused by deficiencies in the techniques used.
 ...
PMID:Arterial-expired PCO2 differences in the dog during acute hypercapnia. 51 9

The steady-state arterial CO2 tension (PaCO2) was examined during control and intravenous CO2 loading in awake dogs unencumbered by any breathing apparatus. The dogs inhaled air while undergoing intravenous CO2 loading, and we estimated the gain, delta VA/delta PACO2. CO2 was introduced into the systemic venous blood via a membrane gas exchanger in a femoral arteriovenous shunt circuit, and the extracorporeal blood flow was maintained constant at 0.5 l/min. A total of 11 experiments were performed in 3 dogs comprising 93 control observations and 83 CO2 loading observations. Intravenous CO2 produced a significant increase in the steady state PaCO2, a finding consistent with our previous study in tracheostomized awake dogs. We conclude that intravenous CO2 produces hypercapnia in the awake dog with an intact airway unencumbered by external respiratory apparatus.
 ...
PMID:Arterial PCO2 response to intravenous CO2 in awake dogs unencumbered by external breathing apparatus. 51 11

A marked increase in the prostaglandin E (PGE) content in the cerebrospinal fluid (CSF) and the arterial blood of cats was observed under conditions of 3-minute hypocapnia. During 30-minute hypocapnia a restoration of the initial PGE level was seen. The PGE content in CSF increased while in the arterial blood it decreased comparatively to the control under conditions of 3-minute hypercapnia. In 30-minute hypercapnia the PGE amount in the CSF and the blood dropped in comparison with 3-minute hypercapnia being below the basal level in the blood. It is suggested that in hypocapnia PGE should limit its constrictive effect on the cerebral vessels while under conditions of hypercapnia they are to promote the realization of the cerebral vessel reaction to CO2.
 ...
PMID:[Variations in prostaglandin E content in the arterial blood and cerebrospinal fluid under conditions of hypo- and hypercapnia]. 51 23

Net base and mineral balances were evaluated in a group of male 350 g Wistar rats exposed to 10% carbon dioxide in air for 10 days with a view to identifying the source of net base subject to retention during renal compensation of sustained respiratory acidosis. In response to hypercapnia, the rate of renal net acid excretion rose but insignificantly. However, a rise in whole body net base concentration from about 215 mmol/kg to about 250 mmol/kg came about by ongoing gastrointestinal absorption in the weight-losing animal, absorbed net base being distributed to extracellular and non-extracellular compartments of the body, presumably including bone. During an 8-day recovery period, a small decrement in whole body net base concentration was observed.
 ...
PMID:Balance of net base in the rat: adaptation to and recovery from sustained hypercapnia. 53 94

Conscious rabbits were exposed to atmospheric air or to 6% CO2 in air at ambient temperatures (Ta) of 5, 20 and 35 degrees C. Measurements were made of rectal temperature (Tre), metabolic rate (MR), respiratory frequency (f), tidal volume (VT), and minute volume (VE). CO2 exposure did not affect Tre at any Ta and only affected MR at 35 degrees C when it caused an increase. At each Ta hypercapnia caused an increase in VT and a decrease in f. At 5 degrees C VE was increased by CO2, at 35 degrees C VE decreased, and at 20 degrees C the results were variable. The data were examined in the light of theories relating to the relative contributions of inputs from brain stem and from pulmonary stretch receptors, in response to body temperature and CO2 partial pressure. It was concluded that hypercapnia stimulates an increase in VT via the brain stem, whereas at the same time removing a hypocapnic drive which, along with central thermal inputs, stimulates f.
 ...
PMID:Responses of conscious rabbits to CO2 at ambient temperatures of 5, 20, and 35 degrees C. 53 44

We measured ventilatory responses to CO2 (delta VI/delta PCO2) and transient hypoxia (delta VI/delta SaO2) during reductions of brain blood flow (BBF) to 70% and 50% of control in unanesthetized goats. Increase in inspiratory volume per change in CO2 tension (delta VI/delta PCO2) was measured during rebreathing with sampling of both arterial and cerebral venous blood; increase in inspiratory volume per fall in arterial oxygen saturation (delta VI/delta SaO2) was assessed by the transient N2 inhalation method. Delta VI/delta SaO2 did not significantly change at 70% BBF, but was depressed at 50% BBF. Delta VI/delta PCO2 increased (0.94 +/- 0.18 to 1.29 +/- 0.24 l . min-1 . Torr-1) at 70% BBF if arterial CO2 tension were used to represent the CO2 stimulus but was unchanged if venous CO2 tension were used. At 50% BBF, delta VI/delta PCO2 was depressed (0.38 +/- 0.13 l . min-1 . Torr-1) for both representations of the CO2 stimulus. Brain ischemia increased blood pressure and heart rate but blunted the increase in BBF caused by hypercapnia. We conclude that 1) moderate brain ischemia (70% BBF) does not affect chemosensitivity to hypoxia and CO2, 2) delta VI/delta PCO2 may not be accurately determined from PaCO2 during brain ischemia because cerebrovascular reactivity to CO2 is depressed, and 3) severe brain ischemia (50% BBF) blunts delta VI/delta SaO2 and delta VI/delta PCO2, probably as a consequence of hypoxic depression of the respiratory neurons.
 ...
PMID:Effects of graded reduction of brain blood flow on chemical control of breathing. 53


<< Previous 1 2 3 4 5 6 7 8 9 10