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)

Endothelium-derived relaxing factor [EDRF, nitric oxide (NO) or a NO-containing compound] influences basal tone of cerebral blood vessels and mediates vasodilation in response to several stimuli. It is not known whether EDRF also modulates responses to cerebral vasoconstrictor stimuli in vivo. Our goal was to determine whether formation of EDRF inhibits constrictor responses of large cerebral arteries to serotonin. We measured cerebral blood flow (microspheres) and pial microvascular pressure (servo null) in anesthetized rabbits and calculated resistance of large cerebral arteries. Responses to an inhibitor of NO formation, NG-nitro-L-arginine (L-NNA, 3 mg/kg i.v.), were examined. L-NNA produced an increase in resistance of large arteries and total cerebral vascular resistance of approximately 15% (p less than 0.05 for both variables) and a small decrease in cerebral blood flow (35 +/- 9 vs. 32 +/- 7 ml min-1 100 g-1, mean +/- SD, p less than 0.05). Under control conditions, infusion of serotonin (10 micrograms kg-1 min-1, into the left atrium) produced an increase in resistance of large arteries. Following treatment with L-NNA, the change in resistance of large arteries in response to serotonin was increased more than twofold (0.20 +/- 0.17 vs. 0.43 +/- 0.21 mm Hg ml-1 min 100 g, p less than 0.05). In contrast, L-NNA did not alter the increase in resistance of large arteries during hypocapnia. L-arginine inhibited the effects of L-NNA on baseline cerebral vascular resistance and on responses of large arteries to serotonin.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cereb Blood Flow Metab 1992 May
PMID:Endothelium-derived relaxing factor inhibits constrictor responses of large cerebral arteries to serotonin. 156 43

To evaluate the role of different vasomotor stimuli for the measurement of cerebrovascular vasomotor reactivity (VMR), 47 patients (i.e., 93 hemispheres) with various degrees of internal carotid artery (ICA) occlusive disease were studied. Patients were divided into clinical [asymptomatic, transient ischemic attack (TIA) or completed stroke] as well as angiological subgroups. Low-grade or high-grade unilateral ICA lesions were compared to bilateral ICA occlusive disease. Relative flow velocity changes within the middle cerebral artery were measured by means of transcranial Doppler during hyper- and hypocapnia (VMRTOT), during hypercapnia alone (VMRCO2), and after injection of 1 g acetazolamide (VMRACE). VMR was expressed as the percentage change in flow velocity after stimulus application as compared with flow velocity at rest. There was a close and statistically highly significant correlation of CO2-induced with acetazolamide-induced VMR (r = 0.69 in VMRTOT versus VMRACE and 0.79 in VMRCO2 versus VMRACE; P less than 0.0001; linear regression), indicating a strong similarity of the vasodilatative effects of CO2 and acetazolamide on cerebral arteries. Both stimulation techniques highly significantly differentiated between asymptomatic patients and those with TIA or completed stroke. Angiological subgroups were separated best by the acetazolamide test. Reclassification of patients into angiological subgroups by linear discriminant analysis was equally good with all three methods. We conclude that both acetazolamide- and CO2-induced stimulation of the cerebral vasomotors are valid techniques to measure reduction in perfusion reserve due to extracranial cerebrovascular occlusive disease.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cereb Blood Flow Metab 1992 Jan
PMID:Evaluation of cerebral vasomotor reactivity by various vasodilating stimuli: comparison of CO2 to acetazolamide. 172 37

Neuronal cultures from chick embryo cerebral hemispheres were protected against a hypocapnic injury by adding to their growth medium 10(-6)M CDP-choline before or after the injury. The protection obtained with CDP-choline was analyzed by a morphometric analysis and showed that pretreatment of neuronal cultures with CDP-choline maintained the number of cell aggregates and of primary neuronal processes at control values after hypocapnic shock. Various experiments showed that the intact molecule was responsible for the protective action, since pretreatment with different concentrations of various nucleosides and nucleotides (up to 10(-5) M), choline, and phosphorylcholine was without protective effect. The addition of CDP-choline after the hypocapnic injury resulted in a protection of the cultures as shown by morphological observation. Incubation of neurons with radioactive choline showed that hypocapnia increased the incorporation of the label into phospholipids whereas the presence of CDP-choline reduced it. The de novo synthesis of choline was affected by neither hypocapnia nor CDP-choline treatment. The results indicate that CDP-choline may have the capacity to protect neurons under conditions of basic pH and that cellular proliferation may be stimulated by the compound.
 ...
PMID:Effect of CDP-choline on hypocapnic neurons in culture. 308 4

The study examined the role of cerebral blood volume (CBV), cerebrospinal fluid (CSF) volume, and brain tissue water and electrolytes on CSF pressure during 4 h of hypocapnia in dogs. Group I (n = 6) was examined during hypocapnia (PaCO2 20 mm Hg), with no intracranial mass being present. Group II (n = 6) was examined with an intracranial mass present (epidural balloon, CSF pressure 35 cm H2O), but no hypocapnia. In group III (n = 6), an intracranial mass was present, and hypocapnia was used to lower CSF pressure. In group I, hypocapnia initially reduced CBV from 3.4 to 2.4 ml. With continued hypocapnia, CBV reexpanded to 3.4 ml by 4 h. CSF volume changed reciprocally, so that intracranial CSF pressure remained constant. In group II, CBV remained steady (2.7 ml), and CSF volume fell only slightly, so that CSF pressure remained elevated. In group III, hypocapnia initially reduced CBV from 2.8 to 2.2 ml, and CSF pressure fell from 35 to 19 cm H2O. With continued hypocapnia, CBV rose to 2.8 ml by 4 h, but CSF volume fell from 6.1 to 5.0 ml, so that CSF pressure remained low. Net intracranial absorption of CSF did not exceed net intracranial CSF production, suggesting that CSF volume fell because hypocapnia improved access of intracranial CSF to spinal sites of CSF reabsorption. Brain tissue composition was not different among groups. The results indicate that hypocapnia lowers elevated CSF pressure initially by lowering CBV. This CSF pressure-lowering effect is sustained (despite reexpansion of CBV) by a further reduction of CSF volume.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cereb Blood Flow Metab 1987 Aug
PMID:Reduction of cerebrospinal fluid pressure by hypocapnia: changes in cerebral blood volume, cerebrospinal fluid volume, and brain tissue water and electrolytes. 311 69

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.
J Cereb Blood Flow Metab 1988 Oct
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

Hypocarbia results in an increase in brain adenosine concentrations, presumably because of brain hypoxia associated with hypocarbic vasoconstriction. It was hypothesized that adenosine limits the degree of hypocarbic vasoconstriction. To test this hypothesis, the effects of dipyridamole and theophylline on CO2 reactivity during hypocarbia were investigated in anesthetized rats. Dipyridamole should reduce the vasoconstriction by potentiating adenosine action, whereas theophylline should increase the vasoconstriction by blocking adenosine receptors. Cortical pial arterioles of mechanically ventilated and anesthetized rats were displayed on a video monitor system through a closed cranial window. Arterial blood pressure and oxygen tension were stable. CO2 reactivity, formulated as 100 X [delta diameter (micron)/resting diameter (micron)]/delta PaCO2 (mmHg), in the hypocarbic phase was calculated before and after topical superfusion of dipyridamole (10(-6) M; n = 7) and theophylline (5 X 10(-5) M; n = 6). CO2 reactivity was significantly decreased after superfusion of dipyridamole (0.57 +/- 0.08; mean +/- SEM) as compared with mock cerebrospinal fluid (CSF) (0.97 +/- 0.17, p less than 0.05, n = 7). On the other hand, CO2 reactivity after superfusion of theophylline was increased (1.63 +/- 0.28) as compared with mock CSF (1.00 +/- 0.20, p less than 0.05, n = 6), indicating that adenosine is involved in hypocarbic vasoconstriction.
J Cereb Blood Flow Metab 1988 Dec
PMID:The effects of dipyridamole and theophylline on rat pial vessels during hypocarbia. 314 92

The effects of the interaction between sympathetic nerves and prostaglandins in the cerebral circulation were examined. The hypothesis tested was that inhibition of prostaglandin synthesis by indomethacin would potentiate decreases in CBF caused by sympathetic nerve stimulation. In anesthetized rabbits, following administration of either indomethacin (10 mg/kg) or vehicle, CBF was measured with 15-micron microspheres prior to stimulation and following 3-5 min of electrical stimulation (4, 8, 16 Hz) of both superior cervical ganglia. In the vehicle group, CBF was 33-42 ml/min/100 g prior to stimulation. Bilateral sympathetic stimulation reduced blood flow to the cerebrum by 12 +/- 6% (mean +/- SEM) (p less than 0.05) at 4 Hz (n = 8), by 20 +/- 4% (p less than 0.05) at 8 Hz (n = 12), and 21 +/- 6% (p less than 0.05) at 16 Hz (n = 11). In the indomethacin group, CBF was 37-48 ml/min/100 g prior to stimulation. Bilateral stimulation decreased blood flow to the cerebrum by 7 +/- 5% (NS) at 4 Hz (n = 8), by 25 +/- 3% (p less than 0.05) at 8 Hz (n = 6), and by 20 +/- 6% (NS) at 16 Hz (n = 6). Decreases in CBF during nerve stimulation were blocked by prazosin, an alpha-adrenergic antagonist. In additional experiments, cerebral vascular constrictor responses to hypocapnia were found to be similar in the vehicle and indomethacin groups. This study provides evidence that sympathetic nerves can decrease CBF substantially even at low stimulation frequencies. Further, results of this study indicate that prostaglandins do not attenuate the effects of sympathetic stimulation on the cerebral circulation.
J Cereb Blood Flow Metab 1985 Mar
PMID:Role of prostaglandins in modulating sympathetic vasoconstriction in the cerebral circulation in anesthetized rabbits. 397 19

Concern has often been expressed that hypocapnia produced by controlled hyperventilation might further reduce cerebral perfusion during drug-induced hypotension. In the present studies, hypotension was induced in cats with either practolol/trimetaphan (five experiments) or practolol/nitroprusside (five experiments) together with controlled haemorrhage. Arterial PCO2 was altered between 17 and 51 mm Hg by varying inspired CO2 during constant-volume ventilation, first during control conditions of light halothane/nitrous oxide anaesthesia and then during hypotension to mean blood pressure of 36-37 mm Hg. Cerebral cortical perfusion was measured by the krypton clearance technique and pial artery diameter by the image-splitting method. Cerebral cortical blood flow did not alter with PaCO2 changes during trimetaphan hypotension, but some responsiveness to CO2 persisted during nitroprusside hypotension, though at less than half control levels. No changes in pial artery diameter were seen with CO2 during hypotension under either technique. It is postulated that CO2 responsiveness persisted with nitroprusside because cerebral blood flow (CBF) values were higher when hypotension was produced with this drug, as compared with trimetaphan. It would appear that hypocapnia does not further reduce CBF during trimetaphan hypotension but does do so with nitroprusside. However, the combination of hypocapnia and nitroprusside hypotension did not in any instance lower CBF below the values found during trimetaphan hypotension.
J Cereb Blood Flow Metab 1981
PMID:CO2 responses of the cerebral circulation during drug-induced hypotension in the cat. 679 28

The arterial supply and venous drainage of the rabbit's brain were characterized by intravascular injection of casting material and intra-arterial administration of markers (crystal violet or dissolved hydrogen gas). The internal carotid artery supplies the homolateral cerebral cortex and subcortical structures except for the thalamus and the posterior portion of the nucleus caudatus; it also supplies the homolateral retina and optic nerve. No noncerebral structures are supplied by this artery. The dorsal sagittal sinus drains the dorsal and lateral parts of the frontal and parietal areas of the cerebral cortex, with no detectable extracerebral contamination. Electromagnetic measurement of flow in the internal carotid artery (ICBF), volumetric or H2-clearance measurement of flow in the dorsal sagittal sinus (SSBF), and H2-clearance determination in cerebral cortex yield comparable results on the cerebrovascular response to hyper- and hypocapnia. ICBF and SSBF are reliable and valid estimates of average blood flow through the homolateral cerebral hemisphere and the cerebral cortex, respectively.
J Cereb Blood Flow Metab 1982
PMID:Cerebrovascular anatomy and blood flow measurements in the rabbit. 706 3

To investigate the effect of the level of baseline cerebral blood flow (CBF) on local CBF augmentation by activation, we have used positron emission tomography to measure regional CBF (rCBF) in 12 normal volunteers with and without photic stimulation during hypocapnia, normocapnia, and hypercapnia. The increase in rCBF in the primary visual cortex by photic stimulation was 10.8 +/- 3.1, 18.6 +/- 9.3, and 19.5 +/- 6.1 ml 100 ml-1 min-1 in hypo-, normo-, and hypercapnia, respectively. The increase was significantly smaller in hypocapnia than in normocapnia (p < 0.005). The fractional CBF increase caused by the photic stimulation was the same in all breathing conditions. This result indicates that the magnitude of the CBF increase induced by neuronal activity correlates proportionally with the level of baseline CBF.
J Cereb Blood Flow Metab 1995 Jan
PMID:Photic stimulation study of changing the arterial partial pressure level of carbon dioxide. 779 27


1 2 3 4 Next >>