THE INFLUENCE OF NITROUS OXIDE AND BARBITURATE ANAESTHESIA UPON THE ENERGY AND THE ACID-BASE METABOLISM OF THE BRAIN IN NORMOXIA AND HYPOXIA

1970 ◽  
Vol 14 ◽  
pp. 143-144
Author(s):  
L. Nilsson and B. K. Siesjö
Keyword(s):  
Nitrous Oxide ◽  
Acid Base ◽  
The Brain

Changes in the tone of cerebral vessels in patients with bronchial asthma after glomectomy

1982 ◽  
Vol 63 (1) ◽  
pp. 56-56
Author(s):  
E. S. Karashurov ◽  
S. E. Karashurov
Keyword(s):  
Blood Flow ◽  
Bronchial Asthma ◽  
Cerebral Vessels ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
The Brain

Frequent complications of glomectomy are headaches and a mild, less-like state for several days or weeks after surgery, and sometimes hemi- and monoparesis. The reasons for these complications have not yet been revealed. In search of their explanation, we decided to study the volumetric blood flow of the brain and the acid-base state (ACS). Volumetric blood flow was studied by rheoencephalography (REG) in 43 patients, and acid base balance - in 100 patients (age from 22 to 67 years). The course of bronchial asthma before the operation in the examined patients was moderate and severe.

Studies on the Pathophysiology of Encephalopathy in Reye's Syndrome: Hyperammonemia in Reye's Syndrome

PEDIATRICS ◽  
1975 ◽  
Vol 56 (6) ◽  
pp. 999-1004
Author(s):  
Daniel C. Shannon ◽  
Robert De Long ◽  
Barry Bercu ◽  
Thomas Glick ◽  
John T. Herrin ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Venous Drainage ◽  
Respiratory Alkalosis ◽  
Ammonia Concentration ◽  
Reye's Syndrome ◽  
Acid Base ◽  
Arterial Blood ◽  
Cerebral Venous Drainage ◽  
Acid Base Status ◽  
The Brain

The initial acid-base status of eight survivors of Reye's syndrome was characterized by acute respiratory alkalosis (Pco2=32 mm Hg; Hco3-= 22.0 mEq/liter) while that of eight children who died was associated with metabolic acidosis as well (HCO3-=10.0 mEq/liter). Arterialinternal jugular venous ammonia concentration differences on day 1 (299 mg/100 ml) and day 2 (90 mg/ 100 ml) reflected cerebral uptake of ammonia while those on days 3 and 4 (-43 and -55 mg/100 ml) demonstrated cerebral release. Arterial blood hyperammonemia can be detoxified safely in the brain as long as the levels do not exceed approximately 300µg/100 ml. Beyond that level lactic acidosis is observed, particularly in cerebral venous drainage. Arterial blood hyperammonemia was also related to the extent of alveolar hyperventilation. These findings are very similar to those seen in experimental hyperammonemia and support the concept that neurotoxicity in children with Reye's syndrome is at least partly due to impaired oxidative metabolism secondary to hyperammonemia.

COMBUSTION PERFORMANCE OF JATROPHA BIODIESEL IN AN OIL BURNER SYSTEM

2015 ◽  
Vol 77 (8) ◽  
Author(s):  
Arizal, M. A. A ◽  
Azman, A. H. ◽  
Jaafar, M. N. M. ◽  
Wan Omar, W. Z.
Keyword(s):  
Nitrous Oxide ◽  
Alternative Energy ◽  
Temperature Profiles ◽  
Gaseous Emissions ◽  
Jatropha Oil ◽  
Acid Base ◽  
Edible Plant ◽  
Combustion Performance ◽  
Combustion Properties ◽  
Conventional Diesel Fuel

Jatropha Curcas is a non-edible plant that can be used for renewable or alternative energy. The seeds of Jatropha contain up to 60 percent oil. The oil can be converted into biodiesel by well-known two-step using acid-base catalytic transesterification. This paper shows the combustion performance of biodiesel derived from Jatropha oil in an oil burner designed for conventional diesel. Biodiesel used in this study is a blend of diesel with Jatropha Methyl Ester (JME) and combustion performance was measured and compared with that of conventional diesel fuel (CDF). The combustion performance of Jatropha biodiesel is based on wall temperature profiles and the amount of gaseous emissions emitted such as nitrous oxide (NOx), sulphur dioxide (SO2) and carbon monoxide (CO). It was demonstrated that biodiesel derived from Jatropha is comparable to the combustion properties of CDF and has high potential to be used as alternative fuel for diesel machines.

Changes in brain surface pH during acute isocapnic metabolic acidosis and alkalosis

1981 ◽  
Vol 51 (2) ◽  
pp. 276-281 ◽  
Author(s):  
S. Javaheri ◽  
A. Clendening ◽  
N. Papadakis ◽  
J. S. Brody
Keyword(s):  
Cerebrospinal Fluid ◽  
Metabolic Acidosis ◽  
Interstitial Fluid ◽  
Acid Base ◽  
Surface Ph ◽  
Brain Surface ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
The Mean ◽  
The Brain

It has been thought that the blood-brain barrier is relatively impermeable to changes in arterial blood H+ and OH- concentrations. We have measured the brain surface pH during 30 min of isocapnic metabolic acidosis or alkalosis induced by intravenous infusion of 0.2 N HCl or NaOH in anesthetized dogs. The mean brain surface pH fell significantly by 0.06 and rose by 0.04 pH units during HCl or NaOH infusion, respectively. Respective changes were also observed in the calculated cerebral interstitial fluid [HCO-3]. There were no significant changes in cisternal cerebrospinal fluid acid-base variables. It is concluded that changes in arterial blood H+ and OH- concentrations are reflected in brain surface pH relatively quickly. Such changes may contribute to acute respiratory adaptations in metabolic acidosis and alkalosis.

scholarly journals Tissue S-adenosylmethionine levels in fruit bats (Rousettus aegyptiacus) with nitrous oxide-induced neuropathy

1983 ◽  
Vol 50 (2) ◽  
pp. 325-330 ◽  
Author(s):  
J. van der Westhuyzen ◽  
J. Metz
Keyword(s):  
Nervous System ◽  
Nitrous Oxide ◽  
Fruit Bats ◽  
Fruit Bat ◽  
The Mean ◽  
The Brain ◽  
Mean Concentration

1. The effect of cobalamin inactivation by the anaesthetic gas nitrous oxide on the concentration of S-adenosylmethionine (Ado Met) in brain and liver of fruit bats (Rousettus aegyptiacus) was examined.2. Test animals exposed to N2O–oxygen (50:50, v/v) developed ataxia and paralysis leading to death after an average of 9·8 weeks (n 6). Animals receiving pteroylmonoglutamic acid supplements in the diet became ataxic earlier (mean 8·8 weeks) while those receiving methionine supplements survived for significantly longer periods (12·5 weeks, P < 0·01).3. Plasma cobalamin levels indicated severe depletion of cobalamin stores in N2O-exposed animals.4. The mean concentration of Ado Met in the brain of N2O-treated bats was nearly 50% higher than that of untreated controls. Ado Met levels in treated bats receiving pteroylmonoglutamic acid or methionine supplements were respectively 18 and 25% higher than in controls. In contrast, the concentration of Ado Met in the liver of all the N2O-treated groups was slightly lower than in controls.5. These results suggest that the N2O-induced neuropathy in the fruit bat is not related to a depletion of Ado Met in the nervous system.

CSF bicarbonate regulation in respiratory acidosis and alkalosis

1975 ◽  
Vol 38 (3) ◽  
pp. 504-511 ◽  
Author(s):  
J. Wichser ◽  
H. Kazemi
Keyword(s):  
Carbonic Anhydrase ◽  
Lactic Acidosis ◽  
Glial Cells ◽  
Respiratory Acidosis ◽  
Dissociation Curve ◽  
Cerebral Ventricles ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Csf Lactate ◽  
The Brain

CSF bicarbonate regulation was studied in respiratory acidosis and alkalosis of 4h duration in antsthetized dogs. PCO2, pH, HCO3, ammonia, and lactate in CSF and arterial and safittal sinus bloof were measured when equal volumes of saline or acetazolamide (8 mg) were injected into lateral cerebral ventricles. The brain CO2 dissociation curve was determined at the end of all experiments. CSF and arterial bicarbonate increased 11.8 and 5.9 meg/l, respectively, in acidosis. Acetazolamide limited the rise in CSF bicarbonate to 4.2 meg/l, and prevented the CSF bicarbonate increase associated with hyperammonemia. During alkalosis CSF bicarbonate fell 6.5 meg/l and CSF lactate increased almost 2 meg/l while arterial bicarbonate fell 5.7 meg/l and lactate remained unchanged. Thus plasma bicarbonate changes account for some of the CSF unchanged. Thus plasma bicarbonate changes account for some of the CSF bicarbonate alterations in respiratory acid-base-disturbances. In acidosis additional CSF bicarbonate is formed by the choroid plexus and glial cells on the inner and outer surfaces of the brain--a reaction catalyzed by the locally present carbonic anhydrase. In alkalosis the greater fall in CSF bicarbonate than blood is due to selective brain and CSF lactic acidosis.

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