Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Part I of these studies (Artru, 1987) examined how cerebral blood volume (CBV), CSF volume, and brain tissue water and electrolytes determined CSF pressure during 4 h of hypocapnia in sedated dogs. The three groups reported were: hypocapnia (PaCO2 20 mm Hg) with no intracranial mass (group 1), intracranial mass (epidural balloon, CSF pressure 35 cm H2O) but no hypocapnia (group 2), and intracranial mass with hypocapnia used to lower CSF pressure (group 3). It was found that in dogs with an intracranial mass (group 3) the CSF pressure-lowering effect of hypocapnia was sustained for 4 h due to improved reabsorption of CSF, decrease of CSF volume to offset reexpansion of CBV and no increase in the sum of CSF volume and CBV. The present Part II studies (groups 4-8) examine the effects of anesthetics on CSF pressure during conditions like those used for group 3, namely, intracranial mass present and hypocapnia used to lower CSF pressure. When halothane or enflurane were used for anesthesia, the CSF pressure-lowering effect of hypocapnia was not sustained. CSF pressure increased from 17.3 +/- 4.7 and 19.0 +/- 4.1 cm H2O, respectively (mean +/- SD), at 10 min to 50.3 +/- 12.8 and 43.2 +/- 12.8 cm H2O, respectively at 4 h. Increase of CSF pressure was associated with increased resistance to reabsorption of CSF (Ra) and increase in the sum of CSF volume and CBV. With halothane the intracranial volume increase was comprised chiefly of cerebral blood and with enflurane the intracranial volume increase was comprised chiefly of CSF. When isoflurane, fentanyl, or thiopental were used for anesthesia, the CSF pressure-lowering effect of hypocapnia was sustained. Ra did not increase and the sum of CBV and CSF volume remained reduced.
 ...
PMID:Reduction of cerebrospinal fluid pressure by hypocapnia: changes in cerebral blood volume, cerebrospinal fluid volume and brain tissue water and electrolytes. II. Effects of anesthetics. 313 52

The relationship between striated muscle tissue oxygenation during hyper- and hypocapnia, and lactate levels and venous pO2 (pvO2) was studied in a rabbit model. Seven rabbits were ventilated with constant volume during ether anesthesia, and arterial pCO2 (paCO2) was varied by addition of CO2. Muscle tissue oxygenation was measured with a multichannel electrode on the striated muscle surface, the results presented as oxygen pressure distributions (OPD:s). The principal result during hypercapnia (paCO2 9.9 kPa) was a tendency toward increased mean oxygen pressure (ptxO2) of the OPD; OPD shape was normal in 5/7 runs. Arterial lactates (aLa) decreased. During duplicate hypocapnia to paCO2 2.9 and 2.8 kPa ptxO2 decreased, but only in 4/14 runs were tissue oxygen pressures (ptO2) below 0.6 kPa found. OPD shape was scattered in 6/14 runs indicating disturbance in regulation of tissue oxygenation (but without signs of hypoxia). An increase in aLa was found, as well as a decrease in arterio-venous lactate difference (avDLa). Lacking direct blood flow measurements, these two results could not be interpreted as increased lactate efflux per se. Muscle lactates (mLa) were high but, on average, not higher than a control group. A decrease in pvO2 was seen during hypocapnia. Subgrouping OPD:s according to shape and presence of low ptO2 values did, however, suggest that lactate was released in cases with low ptO2 values: a covariation was seen in runs with low oxygen pressures between high arterial and muscle lactates, decreased avDLa and pvO2; runs with scattered OPD:s had only intermediately high lactates and low avDLa and pvO2 when compared to normally shaped OPD:s. In this study, hypercapnia influenced striated muscle tissue oxygenation only to a minor degree while hypocapnia influenced it more but not as much as expected. Only when low oxygen pressures were present in the OPD:s were there indications of peripheral lactate release.
 ...
PMID:Striated muscle tissue oxygenation and lactate levels during normo-, hyper- and hypocapnia. A study in the rabbit. 313 18

The effect of isoflurane on intraventricular pressure (IVP) was examined during nitrous oxide with fentanyl anaesthesia in patients undergoing craniotomy during normocapnia or hypocapnia. Hypocapnic patients (n = 30, PaCO2 3.3 (0.1) kPa) were allocated to three groups (A, B, C; n = 10 each) according to the inspired concentration of isoflurane (1%, 1.5%, 2%). Normocapnic patients (n = 10, PaCO2 4.7 (0.1) kPa) received an inspired concentration of 1% isoflurane (group D). In patients in groups C and D, IVP increased significantly in response to isoflurane (P less than 0.01). In groups A and B, IVP did not change significantly (P greater than 0.05). Mean arterial pressure and cerebral perfusion pressure decreased significantly (P less than 0.001) in all groups in response to isoflurane.
 ...
PMID:Effects of isoflurane on intraventricular pressure in neurosurgical patients. 314 Aug 63

The use of room air alone to ventilate patients who were anaesthetized with total intravenous anaesthesia, including morphine 2 mg.kg-1, was studied in ten patients. The were scheduled for gastrectomy for peptic ulcer or stomach carcinoma. The patient's minute-ventilation was measured the day previous to surgery; this, together with a frequency of 14 c.min-1, was used to preset the ventilator. Alveolar ventilation, end-expiratory CO2, arterial blood gases and acid-base balance were monitored throughout the procedure. The blood oxygen level was found to remain similar to the reference value; there was a moderate hypocapnia, a low end-expiratory CO2 and minimal changes in acid-base balance. No pulmonary complication was encountered in the postoperative course. These results showed that room air could be used in unusual circumstances for healthy patients for whom a total intravenous anaesthetic technique has been chosen.
 ...
PMID:Room air ventilation for total intravenous general anaesthesia. 314 35

The study pertains to a series of investigations on the effects of CO2 inhalation as used for pre-slaughter anaesthesia in swine. Acid/base parameters, blood oxygen tension, plasma Na, K, Ca and stress hormone concentrations were monitored in Yorkshire swine before, during, and for 10 min after the animals were descended for 1 min into 80% CO2 in air. Severe respiratory acidosis (PaCO2 approximately 50 kPa, arterial pH approximately 6.6) and hypoxia (PaO2 approximately 4kPa) had developed after 45 s of the CO2 inhalation. The corresponding changes in venous blood were less drastic (PvCO2 approximately 17 kPa, pH 7.1, PvO2 approximately 4 kPa). Readjustment to PaCO2 approximately II kPa, arterial pH 7.2, and PaO2 approximately 13 kPa had occurred at 1 min post CO2. Four minutes later the respiratory acidosis had become converted into metabolic acidosis subjected to partial respiratory compensation (arterial pH 7.3 in the presence of moderate hypocapnia and hyperoxaemia). The cause of this metabolic acidosis (present also at 10 min post CO2) was apparently hypoxia-induced anaerobic metabolism (= lactic acid production). Apparently due to hydrogen ion transport into the cells in exchange for other cations, hyperkalaemia (K approximately 6.6 mmol l-1), and a 7 mmol l-1 increase in plasma Na had developed at 1.5 min later. The CO2 inhalation did not change the total plasma Ca significantly. The transport of the swine from the stable to the immediate pre-experimental situation induced a 3-fold increase in plasma cortisol concentration (PC, to approximately 130 mmol l-1). No further increase in PC occurred in response to the CO2 inhalation. It indicates that no additional emotional strain was imposed upon the animals during the CO2 exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Acidosis, hypoxia and stress hormone release in response to one-minute inhalation of 80% CO2 in swine. 314 71

Spinal cord blood flow (SCBF) and its response to alterations in blood gases and to systemic hypotension, haemodilution and barbiturate anaesthesia were measured in 47 rats at the level of Th 7-8 by quantitative autoradiography with [14C]iodoantipyrine ([14C]IAP) as tracer. During normocapnia and normoxia the mean SCBF values in the grey and white matter were 94 +/- 21 and 17 +/- 3 ml min-1 100 g-1, respectively. SCBF was highly dependent on PaCO2. Thus in hypercapnic animals (PaCO2 greater than 9 kPa) SCBF was increased in grey and white matter to 228 +/- 22 and 54 +/- 7 ml min-1 100 g-1, while during hypocapnia (PaCO2 less than 3.9 kPa) it was decreased to 64 +/- 14 and 11 +/- 2 ml min-1 100 g-1, respectively. Mean arterial blood pressure (MABP) was reduced by withdrawal of blood to 80 +/- 8 mmHg in a light hypotension group and to 53 +/- 11 mmHg in a severe hypotension group, compared with 126 +/- 13 mmHg in a control group. There was no significant difference in SCBF between the control group and the hypotension groups, suggesting that autoregulation is maintained down to an MABP of at least 50 mmHg. Normovolaemic haemodilution, with a reduction of the haematocrit from 50 +/- 2 to 33 +/- 3, increased SCBF to 113 +/- 9 ml min-1 100 g-1 in grey matter and to 21 +/- 12 ml min-1 100 g-1 in white matter.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Regulation of spinal cord blood flow in the rat as measured by quantitative autoradiography. 322 34

This paper reviews the literature on the EEG effects of hyperventilation, with particular emphasis on the literature concerning the mechanism of EEG slowing with hyperventilation. We suggest that there is no definite evidence to support the theory that the EEG slowing and "activation" are caused by hypoxia secondary to cerebral vasoconstriction induced by hypocapnia during voluntary hyperventilation. Since it is known that hypocapnia produces decreased activity in the mesencephalic reticular formation and that lesions of the thalamus abolish the hyperventilation response, we propose a strong, albeit speculative, analogy between awake-sleep transitory states and the mechanism of EEG "activation" by hyperventilation. Furthermore, it is proposed that both the EEG changes and the associated clinical symptomatology (as well as changes in level of anesthesia, which vary with arterial PCO2) may be explained by altered arousal, and that the vasoconstriction observed during hyperventilation is a central neurogenic response to hypocapnia at a brainstem level.
 ...
PMID:How hyperventilation alters the electroencephalogram: a review of controversial viewpoints emphasizing neurophysiological mechanisms. 330 71

Ten patients with intracerebral tumours (TC) and 13 patients with subarachnoid haemorrhage (SAH) from a ruptured cerebral arterial aneurysm were studied before intracranial surgery, and during a 3-h postoperative period. Cerebrospinal fluid pressure (CSFP) determined by an intraventricular (TC group) or intraspinal (SAH group) catheter, and mean arterial blood pressure (MABP) were recorded under neurolept anaesthesia (control) followed by isoflurane inhalation. These two measurements were performed during normocapnia. A third measurement was made during hypocapnia, with unchanged isoflurane concentration. After the experimental period, isoflurane remained the main anaesthetic agent throughout the surgical procedure. After recovery from anaesthesia, the patients were monitored with CSFP and blood pressure during the first postoperative hours, and the quality of breathing was assessed by hourly blood-gas analyses. The results show that isoflurane causes a 10-14% reduction of MABP with no further changes during hyperventilation. Mean CSFP increased 27% in the TC group, and 12% in the SAH group after isoflurane induction and decreased from these levels by 29% during hyperventilation in both groups. Consequently, the impact on cerebral perfusion pressure (CPP) by isoflurane was a 19% and 21% mean decrease in the TC and SAH group, respectively. Controlled hyperventilation reduced this effect by partially restoring control CPP values, with 8% and 14% increase, respectively. In the postoperative follow-up, all patients had normal breathing and blood pressure with low values of CSFP. It is concluded that isoflurane can be used in intracranial surgery with adequate safety if combined with controlled hyperventilation.
 ...
PMID:The effect of isoflurane on cerebrospinal fluid pressure in patients undergoing neurosurgery. 334 70

A 31-year old primigravida was admitted at 31 week gestation for subarachnoid haemorrhage. Cerebral angiography revealed an aneurysm on the left middle cerebral artery. Eleven days later, the aneurysm was clipped off. General anaesthesia was induced with thiopentone, pancuronium and fentanyl, and maintained with fentanyl (40 micrograms.kg-1) and isoflurane in air/O2 with a non-rebreathing circuit. The patient was mechanically ventilated to maintain mild hypocapnia. Arterial hypotension was induced by increasing the inspired isoflurane concentration from 1 to 3 vol%. The response was immediate and a mean arterial pressure of 60 mmHg was maintained for 80 min with an inspired isoflurane concentration of 2.5 vol%. Foetal heart rate was monitored before, during and after general anaesthesia. Loss of beat to beat variation was observed after induction, and foetal heart rate slowly decreased from 150 to 115 b.min-1 at the end of the operation. Postoperative state was good, except for transitory aphasia. At 35 week gestation, the patient went into premature labour, with hypothermia of 39.5 degrees C; an emergency caesarean section was performed. The 2,340 g female infant had a 10 min Apgar score of 8. One month later, clinical examination of the mother and daughter was quite normal. The precautions and anaesthetic management of patients suffering from ruptured cerebral aneurysm during the end of pregnancy are reviewed. Hypotensive agents are discussed.
 ...
PMID:[Hypotension induced by isoflurane for the treatment of intracranial aneurysm in late pregnancy]. 343 89

Effects of mechanical ventilation of the lungs of fetal lambs in utero are described. Feasibility studies were performed acutely on four fetuses at 140-142 days gestational age. Five fetuses were prepared for chronic experiments at 122-128 days gestation. Mechanical ventilation was used to produce changes in fetal blood gases for periods of up to 24 h in acute preparations or for repeated periods of 3-9 h on consecutive days in chronic preparations. This technique permits the study of fetal lambs in utero under conditions which normally occur after birth without producing maternal changes or using anesthesia and whilst the umbilical circulation remains open. Four situations were examined using ventilation in these chronic preparations: (1) expansion of the lungs whilst maintaining fetal normoxia and normocapnia; (2) fetal normoxia and hypocapnia; (3) hyperoxia and normocapnia; (4) hyperoxia and hypocapnia. None of these situations produced continuous fetal breathing, either during ventilation or after switching off the ventilator. We conclude that they do not provide appropriate stimuli to mimic those which normally produce continuous breathing after birth.
 ...
PMID:Breathing activity in fetal sheep during mechanical ventilation of the lungs in utero. 366 75


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