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

A case report of an 11-year-old Caucasian boy with the fragile X syndrome is presented. The fragile X syndrome is a form of X-linked mental retardation with a connective tissue component that involves mitral valve prolapse. Antibiotic prophylaxis, electrocardiographic abnormalities, and special anesthetic management considerations are elements of treating patients with fragile X syndrome. The patient received morphine sulfate and scopolamine as a preoperative premedication. Ketamine was also administered intramuscularly prior to induction to gaseous anesthetic. Pancuronium was used to facilitate nasotracheal intubation. A wandering atrial pacemaker and progressive hypocapnia, both of which were managed without complication, were the only problems encountered in the anesthetic procedure.
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PMID:General anesthesia and fragile X syndrome: report of a case. 293 7

The effects of halothane and isoflurane on regional cerebral blood flow (CBF) were studied in 18 New Zealand White rabbits anesthetized with nitrous oxide (N2O) and morphine sulfate (MS) at three different levels of PaCO2. CBF was measured using the hydrogen clearance technique. Monitored variables were intracranial pressure (ICP), central venous pressure, heart rate, mean arterial pressure, electroencephalogram, arterial blood gases, end-tidal (ET) volatile anesthetic, and ET CO2. Addition of 1 MAC halothane to the N2O/MS background anesthetic caused flow to increase significantly in all three regions studied (cortex, dorsal hippocampus, white matter) at all three levels of PaCO2 (low: 20-25 mmHg; normal: 35-40 mmHg; high: 50-55 mmHg). Addition of 1 MAC isoflurane to the background anesthetic caused CBF to decrease significantly in all regions during hypocapnia. During normocapnia, CBF was unchanged with the addition of 1 MAC isoflurane in all regions and during hypercapnia, CBF increased significantly only in the dorsal hippocampus following addition of 1 MAC isoflurane to the MS/N2O background anesthetic. Volatile anesthetic administration was associated with significant, although small, increases in ICP at all PaCO2 levels. We conclude that 1 MAC concentrations of halothane and isoflurane have opposite effects on CBF when added to a N2O/MS anesthetic during hypocapnia and that the effects of isoflurane on regional CBF are dependent on PaCO2 in rabbits under the anesthetic conditions of this experiment.
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PMID:Isoflurane, halothane, and regional cerebral blood flow at various levels of PaCO2 in rabbits. 308 28

Hypocapnia-induced constriction of peripheral airways may be important in regulating the distribution of ventilation in pathological conditions. We studied the response of the peripheral lung to hypocapnia in anesthetized, paralyzed, mechanically ventilated dogs using the wedged bronchoscope technique to measure resistance of the collateral system (Rcs). A 5-min hypocapnic challenge produced a 161 +/- 19% (mean +/- SE) increase in Rcs. The magnitude of this response was not diminished with repeated challenge or by atropine sulfate (1 mg base/kg iv), chlorpheniramine maleate (5 mg base/kg iv), or indomethacin (5 mg/kg iv). The response was reduced by 75% by isoproterenol (5 micrograms/kg iv) (P less than 0.01) and reduced by 80% by nifedipine (20 micrograms/kg iv) (P less than 0.05). During 30-min exposure to hypocapnia the maximum constrictor response occurred at 4-5 min, after which the response attenuated to approximately 50% of the maximum response (mean = 53%, range 34-69%). Further 30-min challenges with hypocapnia resulted in significantly decreased peak responses, the third response being 50% of the first (P less than 0.001). The inability of indomethacin or propranolol to affect the tachyphylaxis or attenuation of the response suggests that neither cyclooxygenase products nor beta-adrenergic activity was involved. Hence, hypocapnia caused a prompt and marked constrictor response in the peripheral lung not associated with cholinergic mechanisms or those involving histamine H1-receptors or prostaglandins. With prolonged exposure to hypocapnia there was gradual attentuation of the constrictor response with continued exposure and tachyphylaxis to repeated exposure both of which would tend to diminish any compensatory effect of hypocapnic airway constriction on the distribution of ventilation.
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PMID:Hypocapnia-induced constriction of the canine peripheral airways exhibits tachyphylaxis. 311 40

The intracranial pressure (ICP) responses to administration of either halothane or isoflurane were compared in New Zealand white rabbits following a standardized cryogenic brain injury. Animals were tracheally intubated and paralyzed, and background anesthesia was maintained with morphine sulfate and nitrous oxide. Following injury and attainment of an elevated and stable ICP, animals were divided into four groups. Animals in groups I and III were maintained normocapnic throughout the experiment and administered 1 MAC halothane or isoflurane, respectively. Group II and IV animals were made hypocapnic (PaCO2 = 20 mmHg) prior to the administration of either 1 MAC halothane or isoflurane, respectively. Monitored variables were mean arterial blood pressure, ICP (ventriculostomy), end-tidal (ET) CO2, ET volatile anesthetic, the electroencephalogram, temperature, and arterial blood gases. Prior to producing the lesion, ICP was approximately 5 mmHg in all animals with no differences among groups. Sixty to ninety minutes after injury, ICP increased significantly to approximately 20 mmHg in all animals. Introduction of either halothane or isoflurane was associated with significant increases in ICP in all groups to approximately 30 mmHg. These data suggest that further significant increases in ICP may occur following introduction of either halothane or isoflurane in the presence of acute brain injury and elevated ICP. Furthermore, these ICP increases may not be altered by the prior establishment of hypocapnia.
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PMID:The intracranial pressure effects of isoflurane and halothane administered following cryogenic brain injury in rabbits. 311 88

Xanthine oxidase and xanthine, a combination that produces hydrogen peroxide and superoxide anion radical, applied topically in anesthetized cats equipped with cranial windows caused arteriolar dilation during application, sustained dilation 1 h after washout, and reduced reactivity to the vasoconstrictive effects of arterial hypocapnia, discrete lesions of the endothelium, and morphological abnormalities of the vascular smooth muscle by electron microscopy. Similar effects were seen in small, but not in large, arterioles during topical application of hydrogen peroxide or hydrogen peroxide plus ferrous sulfate, a combination that produces free hydroxyl radical. The functional changes caused by xanthine oxidase plus xanthine were inhibited completely by superoxide dismutase plus catalase. Superoxide dismutase or catalase, each by itself, eliminated the residual effects seen after washout and reduced the dilation during application of xanthine oxidase. The results show that superoxide anion radical and hydrogen peroxide produce reversible arteriolar dilation and that consistent vascular damage is produced in the presence of both superoxide anion radical and hydrogen peroxide.
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PMID:Effects of oxygen radicals on cerebral arterioles. 391 62

The effects of topical application of agents which produce oxygen radicals on cerebral arterioles were studied in anesthetized cats. Xanthine oxidase plus xanthine, which produced superoxide anion radical, hydrogen peroxide, and hydrogen peroxide plus ferrous sulfate, which produced the free hydroxyl radical, induced sustained dilation, reduced responsiveness to the vasoconstrictor effect of hypocapnia, and destructive lesions of the endothelium and of the vascular smooth muscle. Similar effects were produced by arachidonate, 15-HPETE, and PGG2. The effect of arachidonate was inhibited by mannitol, a free hydroxyl radical scavenger, the effect of PGG2 was inhibited by SOD, the effect of 15-HPETE was inhibited by either catalase or SOD. These results suggest that these cerebral vascular abnormalities were produced by a single destructive free radical, probably the hydroxyl free radical, generated via interaction of superoxide and hydrogen peroxide. Cerebral vascular abnormalities similar to those produced by oxygen radicals were also seen after experimental concussive brain injury or after acute hypertension. After brain injury, activation of phospholipase C and increased brain prostaglandin concentration were demonstrated. The vascular effects of brain injury and acute hypertension were inhibited by free radical scavengers. The results suggest that, in these conditions, vascular damage is induced by oxygen radicals generated from arachidonate in association with increased prostaglandin synthesis.
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PMID:Oxygen radicals and vascular damage. 640 99

During acute respiratory alkalosis myocardial contractility first increases but then decreases towards control levels. The mechanism of this response was investigated in isovolumic perfused rabbit hearts. Developed pressure (DP) and its first derivative (dP/dt) were measured before, during and after hypocapnia induced by equilibrating the perfusate with 2% CO2 rather than the 5% used in control. pH of the perfusate (pHo) changed from 7.36 +/- .02 to 7.71 +/- .01. After about 20 s, an increase in DP of about 20% was detected. This increase in contractility is followed by a partial recovery towards control levels. After the partial recovery a new mechanical steady state is reached in about 2 min. Neither 5-[N-ethyl-N-isopropyl]amiloride (EIPA) 10(-6) M, a blocker of the Na+/H+ exchanger, nor 4,4'-diisothiocyanatostilbene-2-2'-disulfonic acid (SITS) 10(-4) M, or 5-[aminosulfonyl]-4-chloro-2-[(2-furanylmethyl)-amino] benzoic acid (furosemide) 10(-4) M, blockers of Cl-/HCO3- exchanger, abolished the recovery in contractility towards control levels. The recovery was not abolished by replacing 50% of extracellular Cl- concentration by either sulfate or gluconate. The lack of blockade of this mechanical recovery in spite of the intervention performed suggests a mechanism other than the exchangers as the cause of the biphasic changes.
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PMID:The effects of hypocapnic alkalosis on the myocardial contractility of isovolumic perfused rabbit hearts. 769 Dec 10