Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: UMLS:C0085383 (hypocapnia)
1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study reports cerebral blood flow (CBF) measurements in 11 patients during attacks of classic migraine (CM)--migraine with aura. In 6 and 7 patients, respectively, cerebral vascular reactivity to increased blood pressure and to hypocapnia was also investigated during the CM attacks. The Xenon-133 intraarterial injection technique was used to measure CBF. In this study, based in part on previously published data, methodological limitations, in particular caused by scattered radiation (Compton scatter), are critically analysed. Based on this analysis and the results of the CBF studies it is concluded: During CM attacks CBF appears to decrease focally in the posterior part of the brain to a level around 20 ml/100 g/min which is consistent with a mild degree of ischemia. Changes of CBF in focal low flow areas are difficult to evaluate accurately with the Xe-133 technique. In most cases true CBF may change 50% or more in the low flow areas without giving rise to significantly measurable changes of CBF. This analysis suggests that the autoregulation response cannot be evaluated in the low flow areas with the technique used while the observations are compatible with the concept that a vasoconstrictive state, unresponsive to hypocapnia, prevails in the low flow areas during CM attacks. The gradual increase in size of the low flow area seen in several cases may be interpreted in two different ways. A spreading process may actually exist. However, due to Compton scatter, a gradual decrease of CBF in a territory that does not increase in size will also appear as a gradually spreading low flow area when studied with the Xe-133 intracarotid technique.
...
PMID:Blood flow and vascular reactivity during attacks of classic migraine--limitations of the Xe-133 intraarterial technique. 201 68

Since 1983, many papers tell of the usefulness of isoflurane for induced hypotension. It can induce and maintain stable arterial hypotension during neurosurgery, or any other surgical procedure requiring induced hypotension. Its use has proved to be simple. Although other hypotensive techniques are possible, especially if only moderate hypotension is required, the mechanism of action of isoflurane is very appealing: it reduces arterial pressure by reducing the peripheral resistances, without reducing the output, unlike halothane or trinitrin. Moreover, as it is anaesthetic, it reduces the overall oxygen consumption, such that if there were a fall in output one could assume that it was related to the level of oxygen consumption. When there is no severe hypocapnia, isoflurane, quite unlike sodium nitroprusside, lowers cerebral oxygen consumption without affecting cerebral blood flow rate. It does however increase intracranial pressure, like all the other hypotensive agents used. It does not increase filling pressures and has no effect on blood gas movements, unlike sodium nitroprusside and trinitrin which increase filling pressures and the intrapulmonary shunt. It is not toxic either, unlike sodium nitroprusside. The expensiveness of the drug is balanced by its many advantages, all the more so as this cost can be reduced by using a filter-system for some cases (e.g. middle ear surgery), or by using some drug combinations which need yet to be defined. However, there exist some disadvantages which may, in fact, be due to experimental conditions: failure of induced hypotension, coronary ischaemia, doubtful cerebral protection in case of focal areas of ischemia, different degrees of organ vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Can isoflurane be advised for controlled hypotension?]. 306 28

For many neurosurgical procedures, elective hypotension is used to reduce the risk of cerebral vessel rupture and hypocapnia is used to constrict cerebral vessels, thereby reducing cerebral blood volume. Although nitroglycerin (NTG) often is used to produce hypotension during neurological surgery, it is not known whether NTG-induced cerebral vasodilation interferes with the cerebral vasoconstrictor response to hypocapnia. This study examined cerebral vascular responses to hypocapnia during NTG-induced hypotension in eight dogs that were lightly anesthetized with halothane and had an open cranium. Cerebral vascular resistance (CVR) and cerebral blood flow (CBF) at PaCO2 = 40 mm Hg and at PaCO2 = 20 mm Hg were examined first at normal mean arterial pressure (MAP) and then at MAP = 50 mm Hg. CO2 responsiveness, as indicated by increased CVR and decreased CBF, was intact at normal MAP but absent during hypotension. These results suggest that the cerebral vasodilation that accompanies NTG-induced hypotension exerts a greater influence on cerebral vessels than the cerebral vasoconstricting influence of hypocapnia. It is concluded that, during NTG-induced hypotension and craniotomy, hypocapnia will not reduce cerebral blood volume or further decrease CBF to cause ischemia.
...
PMID:Cerebral vascular responses to hypocapnia during nitroglycerin-induced hypotension. 392 65

In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1-CBF) artificially ventilated rats, maintained on 70% N2O, were injected with insulin to provide either an EEG pattern of slow-wave polyspikes, or cessation of spontaneous EEG activity for 5, 15 or 30 min ("coma"). In other animals, glucose was injected at the end of a 30 min period of "coma" and 1-CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. In the slow-wave polyspike period 1-CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1-CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400--500% of control. The increase in 1-CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1-CBF were close to, or below, control values. During the subsequent recovery period 1-CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate-putamen) showing flow rates of only 20--35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypertension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long-lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred.
...
PMID:Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period following glucose injection. 744 74

Glutamate (GLU) is a neurotransmitter. Massive release of GLU and glycine (GLY) into the brain's extracellular space may be triggered by ischemia, and may result in acute neuronal lysis or delayed neuronal death. The aim of this study was to evaluate the possible relationship between hyperventilation and the level of GLU and GLY during brain ischemia. Rabbits were anesthetized with halothane and oxygen. Group 1 was allowed to hyperventilate (PaCO2 25-35 mmHg). PaCO2 was maintained throughout the study. Group 2 was a normal control group that maintained normocapnia. Two global cerebral ischemic episodes were produced. Microdialysate was collected during the periischemic and reperfusion periods from the dorsal hippocampus. GLU and GLY concentrations were determined using high-performance liquid chromatography. In the control group, GLU and GLY were significantly elevated during each episode of ischemia; these levels returned to baseline within 10 minutes after reperfusion. In contrast, in the hyperventilation group GLU and GLY concentrations increased during ischemia, but they were not statistically significant. Two way ANOVA for the periischemic periods (t = 15,80; p = 0.06) revealed lower GLU values for the hyperventilated animals. A similar analysis for periischemic GLY concentrations revealed significantly lower values in the hyperventilated group (t = 10,15,75,80: p = 0.03) as compared to normal controls. We were able to demonstrate that hypocapnia during periischemic period lowered extracellular GLU and GLY concentrations. These results can explain a part of the protective action of hypocapnia during cerebral ischemia.
...
PMID:Effect of hypocapnia on extracellular glutamate and glycine concentrations during the periischemic period in rabbit hippocampus. 748 47

The management of brain swelling that frequently occurs following severe traumatic brain injury (TBI) presents a difficult challenge for physicians treating these patients. A traditional cornerstone for the treatment of post-traumatic brain swelling has been prophylactic hyperventilation to reach PaCO2 levels of 25 to 28 torr. While there are anecdotal reports of improvement in intracranial pressure (ICP) and neurologic functioning following institution of this therapy, the only prospective, randomized trial of its use has found worse outcomes in those treated with prophylactic hyperventilation therapy for 5 days. That hyperventilation therapy might exacerbate secondary brain injury seems likely based on abnormalities in cerebral blood flow (CBF) and metabolism which result from TBI, and the potential for hyperventilation to worsen those abnormalities. Both global and regional CBF are critically reduced, and metabolism increased, during the first several hours and days after injury. As a result, focal ischemia is common following severe TBI. Hyperventilation causes a further decrease in CBF, often without a concomitant reduction in ICP. In some cases, TBI also causes an increase in cerebral vascular responsivity to hypocapnia, increasing the drop in regional CBF that occurs with hyperventilation. Thus, there is a well defined physiologic basis for expecting hyperventilation to cause worsened clinical outcomes following TBI. While this therapy clearly is indicated for the management of acute neurologic deterioration or intracranial hypertension refractory to all other forms of medical therapy, hyperventilation is no longer recommended as a first-line therapy for intracranial hypertension or as prophylactic therapy following severe TBI.
...
PMID:Hyperventilation therapy for severe traumatic brain injury. 749 52

Glutamate (GLU) is a neurotransmitter. Massive release of GLU and glycine (GLY) into the brain's extracellular space may be triggered by ischemia, and may result in acute neuronal lysis or delayed neuronal death. The aim of this study was to evaluate the possible relationship between hyperventilation and the level of GLU and GLY during brain ischemia. Rabbits were anesthetized with halothane and oxygen. Group 1 was allowed to hyperventilate (PaCO2 25-35 mmHg). PaCO2 was maintained throughout the study. Group 2 was a normal control group that maintained normocapnia. Two global cerebral ischemic episodes were produced. Microdialysate was collected during the peri-ischemic and reperfusion periods from the dorsal hippocampus. GLU and GLY concentrations were determined using high-performance liquid chromatography. In the control group, GLU and GLY were significantly elevated during each episode of ischemia; these levels returned to baseline within 10 minutes after reperfusion. In contrast, in the hyperventilation group GLU and GLY concentrations increased during ischemia, but they were not statistically significant. We were able to demonstrate that hypocapnia during periischemic period lowered extracellular GLU and GLY concentrations. These results can explain a part of the protective action of hypocapnia during cerebral ischemia.
...
PMID:Effect of hypocapnia on extracellular glutamate and glycine concentrations during peri-ischemic period in the rabbit hippocampus. 770 88

Currently, no ideal method exists for monitoring the injured brain. Recently, a single, compact, fiberoptic sensor has become available for measuring oxygen, CO2, pH and temperature in blood. We have adapted this instrument for continuous use in brain tissue to measure oxygen tension, carbon dioxide tension (pCO2), pH, and temperature. To evaluate this new technique, we produced hypercapnia, hypocapnia, intracranial pressure increase, and hypoxemia in seven normal cats. In an additional six animals, sensors were placed within a zone of focal brain ischemia induced by occluding the left middle cerebral artery. The sensor readings were compared with cerebral blood flow measurements, intracranial pressure, and brain histological findings. An in vitro experiment was also performed using human blood to test the accuracy of the sensor over a wide range of pCO2 and oxygen tension values. After careful precalibration and rigid cranium fixation, stable measurements could be obtained throughout the 6- to 8-hour experiments. In normal animals, brain oxygen was 42 +/- 9 mm Hg, brain CO2 was 59 +/- 14 mm Hg, brain pH was 7.0 +/- 0.2, and brain temperature was 36.7 +/- 0.7 degrees C. Hypocapnia and hypoxemia produced a significant decline in tissue oxygen (< or = 30 +/- 3 mm Hg; P < 0.001), whereas hypercapnia caused by hypoventilation and intracranial pressure increase produced a significant increase in tissue CO2 (> or = 74 +/- 4 mm Hg; P < 0.001). Focal ischemia produced a rapid 42% decline in brain oxygen (25 +/- 7 mm Hg) and a 25% increase in tissue pCO2 (71 +/- 23 mm Hg). Brain oxygen further decreased to 19 +/- 6 mm Hg toward the end of the experiment, 4 hours later. After middle cerebral artery occlusion, the regional cerebral blood flow decreased to 10 +/- 5 ml per 100 g per minute, within the 1st hour, from a baseline value of 65 +/- 15 ml per 100 g per minute. It then gradually increased to 15 +/- 5 ml per 100 g per minute by the end of the 4-hour experiment. Brain pH was closely and inversely related to brain CO2. The brain temperature in the focally ischemic tissue decreased from 36.7 +/- 0.7 to 35.5 +/- 1.6 degrees C by the end of the experiment. The in vitro experiment demonstrated good linear correlation between the sensor readings and the blood gas analysis. Continuous monitoring of oxygen, CO2, pH, and temperature in damaged or at-risk brain tissue using a single sensor is now feasible and will, thus, allow improved continuous monitoring of neurosurgical patients who are at risk of significant secondary brain damage.
...
PMID:Brain oxygen, CO2, pH, and temperature monitoring: evaluation in the feline brain. 858 58

The purpose of this study was to compare the effect of hyperventilation and indomethacin on cerebral circulation, metabolism and pressures in patients with acute severe head injury in order to see if indomethacin may act supplementary to hyperventilation. Fourteen severely head injured patients entered the study. Intracranial pressure (ICP), mean arterial blood pressure (MABP) and cerebral perfusion pressure (CPP) were monitored continuously. Within the first four days after the trauma the CO(2) and indomethacin vasoreactivities were studied by measurements of cerebral blood flow (CBF) (Cerebrograph 10a, intravenous (133)Xe technique) and arterio-venous difference of oxygen (AVdO(2)). Ischaemia was evaluated from changes in CBF, saturation of oxygen in the jugular bulb (SvjO(2)), lactate and lactate/oxygen index (LOI). Data are presented as medians and ranges, results are significant unless otherwise indicated. Before intervention ICP was well controlled ,(14.8 (9-24) mmHg) and basic CBF level was 39.1 (21.6-75.0) ml/100 g/min). The arterio-venous oxygen differences were generally decreased (AVdO(2) = 4.3 (1.8-8.1) ml/100 ml) indicating moderate luxury perfusion. Levels of CMRO(2) were decreased (1.54 (0.7-3.2) ml/100 g/min) as well. During hyperventilation (delta PaCO(2)=0.88 (0.62-1.55) kPa) CBF decreased with 11.8 (-33.4-29.7) %/kPa and ICP decreased with 3.8 (0-10) mmHg. AVdO(2) increased 34.0 (4.0-139.2) %/kPa, MABP was unchanged, CMRO(2) and CPP increased (delta CPP = 3.9 (-10-20) mmHg). AVD (lactate) and LOI were unchanged. No correlations between CBF responses to hypocapnia and outcomes were observed. An i.v. bolus dose of indomethacin (30 mg) decreased CBF 14.7 (-16.7-57.4)% and ICP decreased 4.3 (-1-17) mmHg. AVdO(2) increased 27.8 (-40.0-66.7)%, MABP (delta MABP = 4.9 (-2-21) mmHg) and CPP (delta CPP = 8.7 (3-29) mmHg) increased while CMRO2 was unchanged. No changes in AVd (lactate) and LOI indicating cerebral ischaemia were found. Compared to hyperventilation (changes per 1 kPa, at PaCO(2) level = 4.05 kPa) the changes in MABP, CPP and CBF were significantly greater after indomethacin, while the changes in AVdO(2), ICP, SvjO(2) and LOI were of the same order of magnitude. No correlation between relative reactivities to indomethacin and CO(2), evaluated from changes in CBF and AVdO(2), or between the decrease in ICP after the two procedures were found. Thus, some patients reacted to indomethacin but not to hyperventilation, and vice versa. These results suggest that indomethacin and hyperventilation might act independently, or in a complementary fashion in the treatment of patients with severe head injury.
...
PMID:CO(2) and indomethacin vasoreactivity in patients with head injury. 886 94

The present study tests the hypothesis that cerebral ischemia induced by severe hypocapnia modifies the N-methyl-D-aspartate (NMDA) receptor/ion channel complex in the cerebral cortical cell membranes of newborn piglets. Studies were performed in six newborn piglets subjected to ischemic hypoxia induced by hyperventilation (PaCO2, 9-11 mmHg) for 1 h. Comparisons were made to a normoxic group on room air (n = 6). Following hyperventilation, phosphocreatine decreased 80%, but ATP remained unchanged. NMDA receptor activation was determined by measuring [3H]MK-801 binding at concentrations varying from 2.5 to 50 nM. Following hyperventilation, Bmax decreased 52% to 0.50 +/- 0.04 pmol/mg protein (P = 0.001); however, the Kd value was unchanged at 7.45 +/- 0.79 nM. Spermine and magnesium dependent activation of the NMDA receptor was determined in the hyperventilated and control groups. With spermine concentrations increasing from 2.5 to 50 microM the maximal spermine dependent activation in the normoxic group was 13.7 +/- 7.93% which occurred at a concentration of 3.75 +/- 1.37 microM. In the hyperventilated group maximal activation was 32.4 +/- 23.5% (P = 0.095) at 4.58 +/- 2.46 microM (P = ns). With magnesium concentrations increasing from 2.5 to 100 microM the maximal magnesium dependent activation in the normoxic group was 17.0 +/- 13.6% which occurred at a concentration of 22.5 +/- 6.12 microM. In the hyperventilated group maximal activation was 26.3 +/- 14.9% (P = ns) at 4.58 +/- 2.92 microM (P < 0.0001). These data show that with less severe tissue hypoxia, as evidenced by conservation of ATP, there is less modification of the NMDA receptors. Ischemia induced by hyperventilation leads to an increase in spermine activation of the NMDA receptor, and the NMDA receptor is much more sensitive to magnesium as evidenced by the maximal activation occurring at a significantly lower magnesium concentration. Ischemia induced by hyperventilation modifies the spermine, magnesium, and MK-801 binding sites of the NMDA receptor and may result in increased NMDA receptor mediated neurotoxicity in the newborn brain.
...
PMID:Modification of the N-methyl-D-aspartate (NMDA) receptor in the brain of newborn piglets following hyperventilation induced ischemia. 893 73


<< Previous 1 2 3 4 Next >>

---