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Query: UMLS:C0020440 (hypercapnia)
7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were conducted on cats under nembutal anesthesia; a study was made of pulse activity of bulbar respiratory neurons, electrical activity of the diaphragm and of the intercostal muscles; pO2, pCO2, pH, arterial blood oxygen saturation were determined in combined action of hypoxia and hypercapnia. When hypoxic gaseous mixture was given for respiration the developing hypocapnia disturbed the discharge rhythmic activity of the respiratory neurons, the respiration acquiring a pathological character of the Cheyne--Stokes type. After addition to the hypoxic gaseous mixture of 2% CO2 the gaseous composition of the arterial blood approached the initial values; this addition prevented the development of hypercapnia and disturbances of rhythmic discharge activity of the respiratory neurons. Addition of 5% CO2 to the hypoxic gaseous mixture produced a negative effect: at first it intensified and then depressed the pulse activity of the respiratory neurons, caused metabolic and respiratory acidosis, and promoted asphyxia.
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PMID:[Combined effects of hypoxia and hypercapnia on the functional state of the respiratory center]. 0 Jan 3

The cerebral haemodynamic effects of CT 1341 also called Alfatesin, an anaesthetic steroid, were studied in the cat by means of the Xenon 133 isotopic clearance method to measure the cerebral blood flow. The injection or intravenous drip of Alfatesin in animals whose arterio PCO2 was kept unchanged induced a cerebral blood flow diminution, the importance of which was proportional to the injected dose. The cerebral blood flow fall was partly due to a cerebral arterio vasoconstriction evidenced by direct observation of the cortex vessels and by a diminution of the intracranial presure. During a deep anaesthesia induced by Alfatesin with recurrent burst suppression, there was a loss of cerebral blood flow autoregulation while the CO2 cerebral vascular reactivity was maintained. This last result accounts for the increase in cerebral blood flow parallel to the hypercapnia that could be observed among animals breathing freely.
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PMID:[Study of the effects of Alfatesin on cerebral blood flow in cats]. 0 57

The combined effect upon cerebral blood flow (CBF) of an elevation of cerebrospinal fluid pressure (CSFP) and changes in respiratory CO2 was studied in nine baboons under chloralose anesthesia. The animals were mildly hyperventilated and provided with increasing amounts of CO2 in O2-air. Arterial CO2 tensions (PaCO2) increased from 17 to 58 mm Hg. Internal carotid blood flow (ICBF) was measured at normal CSFP and at hydrostatically maintained 50 mm Hg CSFP. It was found that: 1) end-tidal CO2 may be used as a substitute for arterial PaCO2 determinations; 2) this elevation of CSFP has little effect on ICBF during hypercapnia and normocapnia; however, 3) during hypocapnia the ICBF is reduced an additional 20% when CSFP is elevated; that is, ICBF is reduced 50% from normal when end-tidal CO2 is reduced to 2% at this elevated level of CSFP. Caution should be exercised during hyperventilation therapy particularly if the elevated CSFP or intracranial pressure (ICP) is not reduced to approach normal levels; in these conditions, the combination of decreasing PaCO2 and elevated ICP may reduce CBF below critical levels and thus lead to cerebral hypoxia.
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PMID:Effects of hyperventilation, CO2, and CSF pressure on internal carotid blood flow in the baboon. 0 53

The variations in pressure of the cerebrospinal fluid was studied in 20 patients before and after induction of anesthesia with alfatesine (0.1 ml/Kg). 14 patients received no other complementary drug (group 1); in the six other cases, 1 g. of acetylsalicylic acid was administered as an analgesic complement (group II). All of the patients spontnaeously ventilated an O2 - N2O 50 p. 100 mixture. The C.S.F. pressure fell by 39 p. 100 on the average (p. less than 0.001) in group I and did not vary in group II. This fall is essentially related to cerebral vasoconstriction, therefore to the fall in cerebral blood flow caused by Alfatesine. In group II hypercapnia was noted in all of the patients; it abolishes the cerebral vasoconstriction due to Alfatesine; the cerebral blood flow did not fall neither did the C.S.F. pressure.
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PMID:[Impact of alfatesine anesthesia on cerebrospinal fluid pressure in man]. 0 9

Seventy-four patients aged 14 months to 71 years, classified as ASA I and II were anesthetised with Ethrane for surgical interventions of mean duration 117 minutes. With the exception of 5 patients who were directly anesthetised with Ethrane, the others received Ethrane after induction with Penthiobarbitone. Maintenance of anesthesia was ensured with 1 to 4p. 100 concentrations of Ethrane and 33p. 100 oxygen and 66p. 100 nitrous oxide. Tracheal intubation was facilitated by injection of 1 mg/kg of succinylcholine. Induction with enflurane is rapid with no phenomena of excitation or irritation of the ear passages. The cardiovascular apparatus is stable with no arrythmia but an increase in heart rate of 11 to 50p. 100 is noted and in 41p. 100 of the cases hypotension of 35p. 100 of the intitial value. During spontaneous ventilation, a type of rapid and superficial respiration is observed with a flow volume of 5.3 ml/kg for an average frequency of 25/min. The arterial blood gases show slight hypercapnia. Myorelaxation is significant and better than that obtained with halothane. Coming round poses few problems apart from agitation in adolescents. Response to simple orders appears at 13 minutes. Trembling and rigidity occur in 41p. 100 of the cases for 5 to 30 minutes. From the hepatic point of view, no lastin enzyme changes were noted and no renal toxicity was demonstrated. Ethrane appears to be a good anesthetic agent but the few advantages mentioned means that it does not fulfil ideal conditions.
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PMID:[Clinical evaluation of the new anesthetic "Ethrane"]. 0 15

1. Techniques for the measurement of unidirectional flux rates in fish which require no anaesthesia or surgery are described. 2. Resting values for Cl- uptake at 10 and 17 degrees C were 8-03 +/- 1-11 and 13-52 +/- 0-95 mu-equiv. 200 g-1 h-1 (+/- S.E.), respectively; and for Na+ the rates were 15-49 +/- 0-40 and 26-30 +/- 0-36, respectively. 3. Hypercapnic acidosis caused an increase in Na+ uptake, presumably through Na+/H+ (or NH+4) exchange. It is suggested that this is a compensation mechanism leading to the increase in blood buffering observed in response to hypercapnia. 4. Alkalosis was observed following acute temperature increase and was accompanied by an increase in the rate of Cl-/HCO-3 exchange and also by an increase in Na+/H+ exchange. 5. The role of these branchial ion exchange mechanisms in overall acidbase regulation is discussed.
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PMID:Branchial ion uptake in arctic grayling: resting values and effects of acid-base disturbance. 0 14

During general anesthesia for bronchoscopy, hypoxemia is a major risk, especially in patients with a severe intrapulmonary shunt. With the technique of apnea in pure oxygen, after one hour denitrogentation, and with an intake of 50 liters of oxygen per minute through the bronchoscope, the PaO2 was greater than 400 mm of Hg, but hypercapnia and acidosis occurred. To compensate the latter, five minute sessions of apnea, alternating with two minutes of jet hyperventilation, nevertheless, have the disadvantage of producing a Ventrui phenomena at the proximal end of the bronchoscope, hence a fall in FiO2 which was dangerous in these high risk patients. The authors propose a method so that the Venturi phenomenon, which cannot be prevented, occurs in pure oxygen.
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PMID:[Seeking an ideal protocol for the stability of blood gases during general anesthesia for bronchosopies]. 1 91

It is a clinical impression that less fentanyl is needed for anesthesia during hyperventilation and hypocarbia. If true, it might be due to both increased penetration of fentanyl, a highly lipid-soluble agent, into the brain and increased brain tissue binding. Serum and brain concentrations of fentanyl were determined in dogs anesthetized with halothane during normocarbia, hypocarbia by hyperventilation, and hypercarbia by addition of CO2 to the inspired mixture. Fentanyl, 12.5 micrograms/kg, was injected iv, and serum and brain samples were taken for fentanyl analysis by radioimmunoassay. Brain fentanyl values peaked latest (15--20 min) and were highest during hypocarbia; brain fentanyl values peaked earliest (0--5 min) and were lowest during hypercarbia; values during normocarbia were intermediate in time to peak (10--15 min) and concentration. Thereafter, brain levels declined, but during hypocarbia were significantly higher and during hypercarbia were significantly lower than during normocarbia. Interestingly, serum fentanyl levels were also significantly higher during hypocarbia. The brain--blood fentanyl ratios for each of the three CO2 levels increased for 30 min and thereafter stayed relatively constant. The brain--blood ratios were highest with hypocarbia and lowest with hypercarbia. At 35 min, when clinical analgesia may be considered terminated, hypocarbic brain levels were double those of normocarbia. The authors feel this reflects, to a large extent, higher serum fentanyl concentrations and delayed cerebral wash-out because of decreased blood flow. To a small but unknown extent the higher brain fentanyl levels result from increased brain--blood penetration due to increased lipid solubility, and increased brain tissue binding of fentanyl during respiratory alkalosis.
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PMID:Fentanyl concentrations in brain and serum during respiratory acid--base changes in the dog. 3 75

The ventilatory response to a transient hypercapnia was studied in four awake rabbits maintained in a volume displacement plethysmograph : the increase in inspiratory volume (VI) was associated or not with an increase in inspiratory and expiratory durations (TI and TE). These ventilatory variations were consistent with the activation of the peripheral chemoreceptors by carbon dioxide (short latency of the initial response). After vagal blockade by local anaesthesia, relative ventilatory variations were not significantly different from those previously measured. Central activity seems an important factor reducing inhibitory vagal input and favouring peripheral chemoreceptor afferents.
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PMID:Interaction between vagal and chemoreceptors afferents in ventilatory response to transient hypercapnia (awake rabbits). 8 Jan 70

Cerebral blood flow (CBF) was determined in the rat under 70% nitrous oxide anesthesia and pentobarbital anesthesia. The application of the Fick principle technique of Kety et al. was modified utilizing 133Xe infused intravenously steadily for 30 seconds, at which time the animal was decapitated and the head frozen in liquid nitrogen. A prior femoral artery to femoral vein shunt was led through a polyethylene catheter of 0.13 ml volume. This catheter passed as a coil in a NaI crystal well-counter with the arterial 133Xe concentration curve recorded by a ratemeter-recorder system. The results of the hemispheric blood flow (HBF) were: under 70% nitrous oxide anesthesia in normocapnia (Paco2 38 mm Hg), 86 +/- 15 ml/100 gm per minute; with hypocapnia (Paco2 20 mm Hg), 40 +/- 5 ml/100 gm per minute; with hypercapnia (Paco2 63 mm Hg), 187 +/- 10 ml/100 gm per minute; and with pentobarbital anesthesia (Paco2 38 mm Hg), 41 +/- 8 ml/100 gm per minute.
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PMID:The measurement of cerebral blood flow in the rat. 12 60


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