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

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

The influence of hypercapnia, hypoxia and status epilepticus on cerebral cortex concentrations of adenosine, adenine nucleotides and cyclic AMP was studied on lightly anaesthetized (70% N2O) and artificially ventilated rats. Neither hypercapnia (arterial PCO2 about 80 and about 300 mmHg) nor hypoxia (minimal values of 19 mmHg) altered tissue concentrations of AMP, cyclic AMP or adenosine. Bicuculline-induced status epilepticus was accompanied by increased concentrations of cyclic AMP but adenosine concentration did not change. Experiments with ischemia, and those in which tissue hypoxia was exaggerated by unilateral carotid artery ligation, showed that tissue adenosine concentrations were elevated only when AMP concentration rose. It is concluded that the marked increase in cerebral blood flow which occurs in hypoxia and status epilepticus is unrelated to changes in tissue adenosine concentration and that the increase in cyclic AMP during neuronal hyperactivity is triggered by other mechanisms than adenosine accumulation.
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PMID:Adenosine and cyclic AMP in cerebral cortex of rats in hypoxia, status epilepticus and hypercapnia. 21 98

To study the significance of normalization of ventilatory or thermal homeostasis during naloxone reversal, 95 patients were given naloxone after thiopental-N2O-O2-relaxant anaesthesia supplemented with fentanyl (6 microgram/kg/h). If naloxone 0.16 mg was given to combat postoperative apnoea during hypercapnia (end tidal carbon dioxide concentration (ETco2)8%), minute ventilation and respiratory rate were significantly higher during the first minutes as compared to the normocapnic patients. Shivering occurred in 44% in the hypercapnic group, as compared to about 30% if naloxone was given during normocapnia (ETco2 5%). Postoperative pain and restlessness were significantly increased in the hypercapnic group. During normocapnia, untoward reactions were less frequent (40%) if naloxone was given in smaller increments (0.08 + 0.08 mg) rather than in one dose (0.16 mg) (72%). This was mainly due to nausea (8% compared to 32%). The incidence and severity of shivering showed a positive correlation to the duration of anaesthesia (r = 0.42) and to the total amount of fentanyl (r = 0.32), but not to the actual postoperative oesophageal temperature (r = -0.13). The results indicate that though untoward reactions after naloxone reversal are aggravated by naloxone-induced normalization of deranged homeostatic mechanisms, their aetiology probably should be sought in an acute abstinence syndrome.
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PMID:Restlessness and shivering after naloxone reversal of fentanyl-supplemented anaesthesia. 42 15

Changes in pulmonary hemodynamics and acid-base balance were recorded during induction of anesthesia using either intravenous administration of barbiturate (28 patients) or inhalation of N2O-O2-halothane (12 patients). The two types of induction resulted in equal elevations of pressures within the pulmonary circulation. The increase, proportional on the two sides of the heart, was most pronounced immediately before endotracheal intubation. Cardiac index decreased before and during intubation but subsequently increased to levels above control values. Systemic blood pressure increased more during barbiturate than during inhalation induction. Changes in acid-base balance were similar during the two types of induction: arterial blood PCO2 and PO2 increased, pH decreased, and standard bicarbonate remained unchanged. Changes in pulmonary arterial mean pressure and central venous pressure were correlated with changes in PACO2. Pulmonary capillary filtration pressure (i.e., pulmonary capillary wedge pressure minus plasma colloid osmotic pressure) was negative in every patient before anesthesia. During induction of anesthesia, filtration presures became positive in half the patients. Observed changes in circulation may have been caused by hypercapnia alone or by a combination of hypercapnia and vescular reflexes associated with instrumentation during intubation. The increased strain on the heart during induction of anesthesia may lead to cardiac failure in patients with diminished cardiac reserve.
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PMID:Pulmonary hemodynamics during induction of anesthesia. 84 81

The cardiovascular effects of equipotent (minimum alveolar concentration; MAC) doses of halothane versus halothane plus 25% N2O (H25N2O) in spontaneously breathing dogs do not differe except that nitrous oxide increased mean arterial pressure (AP) and decreased arterial oxygen partial pressure (PAO2). When 75% nitrous oxide was added to halothane anesthesia, AP, mean pulmonary artery pressure (PAP), heart rate (HR), cardiac output (CO), stroke volume (SV), total peripheral resistance (TPR), and left ventricular work (LVW) increased and PAO2 and hemoglobin saturation decreased. Arterial oxygen tensions below 80 torr were common at moderate and deep anesthetic levels of halothane plus 75% N2O (H75N2O). The specific contribution of N2O, hypoxemia, hypercapnia, or temporal recovery (or a combination of these) in producing cardiovascular stimulation were not determined.
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PMID:Circulatory effects of halothane and halothane-nitrous oxide anesthesia in the dog: spontaneous ventilation. 111 85

The cerebrovascular response to CO2 has been reported to be preserved during propofol anesthesia, but no comparison with awake control values has been made, and the additional influence of N2O has not been investigated. Using the noninvasive technique of transcranial Doppler ultrasonography, this study investigated the cerebrovascular response to varying levels of PaCO2 while awake and during anesthesia with propofol and propofol/N2O. Seven adults without systemic diseases undergoing nonneurologic surgery were studied. A pulsed-wave Doppler monitor was used to measure the mean middle cerebral artery flow velocity (Vmca) during varying levels of PaCO2 (25-55 mmHg) under the following conditions: 1) awake; 2) propofol 2.5 mg.kg-1 bolus followed by continuous infusion of 150 micrograms.kg-1.min-1; and 3) propofol as in the condition above plus 70% N2O. During the awake study condition, hypocapnia was induced by voluntary hyperventilation, and hypercapnia was induced with rebreathing of 7% CO2 in a closed circuit. During the anesthetized study conditions, hypocapnia and hypercapnia were induced by adjustment of minute ventilation. A minimum of five to six simultaneous Vmca and PaCO2 measurements were obtained under each of the study conditions. Systemic blood pressure was monitored via a radial arterial catheter, and phenylephrine was administered if mean arterial blood pressure decreased below 60 mmHg (phenylephrine was used in three of five patients in the propofol-N2O group). Linear regression and analysis of covariance were used for statistical analysis of Vmca-PaCO2 relationships.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of propofol with and without nitrous oxide on cerebral blood flow velocity and CO2 reactivity in humans. 144 39

The effects of variation of arterial CO2 tension (PaCO2) on the electroencephalogram (EEG) and posterior tibial nerve somatosensory cortical evoked potentials (PTN-SCEP) during opioid/N2O anesthesia have not been well documented. We studied the effects of hypocapnia (PaCO2 approximately 23 mmHg) and hypercapnia (PaCO2 approximately 50 mmHg) during steady-state alfentanil/N2O anesthesia in 16 patients. EEG and PTN-SCEP were recorded continuously, while PaCO2 was altered in 15-min intervals by varying the inspired CO2 concentration. Hypocapnia caused significant increases in power in the delta, theta, and beta bands (P less than 0.01), with the greatest increase observed in the alpha band. Relative power increased in the alpha band but remained unchanged in the delta, theta, and beta bands. Median frequency and 95% spectral edge frequency were unaltered during hypocapnia. In contrast, hypercapnia caused a significant decrease of power in the alpha and beta bands, whereas delta and theta power remained unchanged. This was reflected in a significant decrease of the 95% spectral edge frequency, from 8.9 (6.7-11.6) to 7.0 (5.6-8.6) Hz. All EEG parameters returned to normal upon restoration of normocapnia. There was a significant negative correlation between power in the alpha band and end-tidal CO2 in all patients (r = 0.47 to -0.89). PTN-SCEP latencies and amplitudes were not significantly different from control values during hypocapnia and hypercapnia. It is concluded that variations in PaCO2 within the limits 20-50 mmHg produce substantial changes in the EEG power spectrum, especially in the alpha band (8-12 Hz), but do not alter PTN-SCEP.
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PMID:Influence of changes in arterial carbon dioxide tension on the electroencephalogram and posterior tibial nerve somatosensory cortical evoked potentials during alfentanil/nitrous oxide anesthesia. 190 85

The electroencephalographic (EEG) effects of a new inhaled anesthetic are of interest because of the potential of such agents to produce excitatory (convulsant) activity and because of the potential usefulness of the EEG as an indicator of anesthetic depth and cerebral activity. Accordingly, we examined the EEG in 12 healthy, young male volunteers during desflurane anesthesia. Each subject had a baseline recording and then steady-state exposure to 6, 9, and 12% (0.83, 1.24, and 1.66 MAC) desflurane in O2 alone, and to 3, 6, and 9% desflurane in O2 with 60% N2O. The sequence of doses and the presence of N2O were randomized. We used mechanical ventilation to maintain normocapnia at each dose level. We also tested the effects of hypercapnia secondary to spontaneous ventilation. Additionally, at 1.24 MAC, subjects' lungs were hyperventilated to a PCO2 of 25.8 +/- 0.7 mmHg and exposed to rhythmic, loud clapping to attempt to provoke excitatory phenomena. Finally, after at least 6 h exposure to desflurane, we repeated measurements at 0.83 and 1.66 MAC to assess possible tolerance. Four channels of EEG were monitored visually, and at each dose, a quantitative EEG analysis was performed. Desflurane produced EEG changes comparable to those observed with equipotent levels of isoflurane. No epileptiform activity was seen. Desflurane significantly suppressed EEG activity; prominent burst suppression was seen at 1.24 MAC and higher. Substitution of N2O for 0.42 MAC desflurane reduced the degree of EEG suppression relative to the equipotent administration of desflurane and O2. Quantitative EEG measures for the early doses and for the later, repeated exposures did not differ.
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PMID:The electroencephalographic effects of desflurane in humans. 200 Oct 21

Diabetes has been reported to impair vasodilatory responses in the peripheral vascular tissue. However, little is known about vasodilatory function in the diabetic brain. We therefore studied, in the N2O-sedated, paralyzed, and artificially ventilated rat, the effects of chronic hyperglycemic diabetes on the cerebral blood flow (CBF) responses to 3 acutely imposed vasodilatory stimuli: hypoglycemia (HG) (plasma glucose = 1.6-1.9 mumol ml-1), hypoxia (HX) (PaO2 = 35-38 mm Hg), or hypercarbia HC) (PaCO2 = 75-78 mm Hg). In addition, we evaluated the somatosensory evoked potential (SSEP) and plasma catecholamine changes in rats exposed to acute glycemic reductions. Diabetes was induced via streptozotocin (STZ, 60 mg kg-1 i.p.). All results in diabetic rats were compared to those obtained in age-matched nondiabetic controls. The animals were studied at 6-8 weeks (HG experiments) or 4-6 months (HG, HX, and HC experiments) post-STZ. Values for CBF were obtained for the cortex (CX), subcortex (SC), brainstem (BS), and cerebellum (CE) employing radiolabeled microspheres. Up to three CBF determinations were made in each animal. In 6-8 week diabetics vs. controls, CBF increased to a lesser value in the CX, SC, and BS (p less than 0.05). Thus, in the diabetics, going from chronic hyperglycemia to acute hypoglycemia, CBF values (in ml 100 g-1 min-1 +/- SD) increased (p less than 0.05) from 89 +/- 22 to 221 +/- 57 in the CX, from 82 +/- 21 to 160 +/- 52 in the SC, and from 79 +/- 34 to 237 +/- 125 in the BS. In controls, going from normoglycemia to acute hypoglycemia, the CBF changes (p less than 0.05) were 128 +/- 27 to 350 +/- 219 (CX), 117 +/- 11 to 358 +/- 206 (SC), and 130 +/- 29 to 452 +/- 254 (BS). CBF changes and absolute values in the CE were similar in the two groups. At 4-6 months post-STZ, a complete loss of the hypoglycemic CBF response was found in the CX, SC, and CE. In the BS, a CBF response to hypoglycemia was seen in the diabetic rats, with the CBF increasing from 114 +/- 28 (hyperglycemia) to 270 +/- 204 ml 100 g-1 min-1 (p less than 0.05), compared to a change from 147 +/- 36 (normoglycemia) to 455 +/- 299 ml 100 g-1 min-1 (p less than 0.05) in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic hyperglycemic diabetes in the rat is associated with a selective impairment of cerebral vasodilatory responses. 205 Jul 55

The build-up and clearance of halothane in rat brain have been measured non-invasively by 19F NMR spectroscopy using a surface coil placed on the intact scalp. When the halothane supply (3% in O2/N2O, 33/66%) was turned off, the 19F signal decreased exponentially to approximately 50% of the initial value, with a time constant, in normal rats, of 8.6 +/- 0.7 min (mean +/- SEM, n = 16), followed by a decay slower by at least one order of magnitude. The time constant of the rapid decay (tau), which was found to be specific for brain, was reduced in hypoxic/hypercapnic (5% O2/5% CO2) rats to 2.9 +/- 0.2 min (p = 0.001, n = 4), in rats infused with physostigmine (20 micrograms/kg/min i.v.) to 5.7 +/- 0.3 min (p = 0.005, n = 6) and increased in rats injected with pentothal (40 mg/kg i.p.) to 10.7 +/- 1.6 min (p = 0.2, n = 5). Based on the theory of exchange of inert gas at the lungs and tissues developed by Kety, the rapid exponential decay of the 19F signal was used to calculate relative cerebral blood flow (CBF). Assuming the cortical CBF in a normal rat to be about 130 mL min-1 100 g-1, the following CBF values (means +/- SEM) were obtained: controls 130 +/- 10, hypoxia/hypercapnia 390 +/- 59, hypercapnia 220 +/- 25, physostigmine 195 +/- 26, pentothal 105 +/- 23 mL min-1 100 g-1. These values are in good agreement with published values obtained with established methods.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Non-invasive determination of cerebral blood flow changes by 19F NMR spectroscopy. 251 56


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