Effect of Induced Metabolic Alkalosis in Hepatic Encephalopathy

James, Ian; Sampson, D; Nashat, Shaimaa M; Williams, Helen L.; Garassini, M

doi:10.1016/s0140-6736(69)90706-5

Cited by 36 publications

(20 citation statements)

References 9 publications

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“…001) lSI values found in our cirrhotics agree with previous results (James et al, 1969;Morgan et al, 1980;Rodriguez et al, 1983) but not with those from Bories et al (1985), who reported normal CBF values in cir- rhotics, although the rCBF methodology they em ployed was different from our one.…”

Section: Discussionsupporting

confidence: 66%

Reduction of Cerebral Blood Flow in Subclinical Hepatic Encephalopathy and its Correlation with Plasma-Free Tryptophan

Rodriguez¹,

Testa

Celle

et al. 1987

J Cereb Blood Flow Metab

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Summary: Cerebral blood flow (CBF), measured by the noninvasive xenon-133 inhalation method, EEG, and plasma levels of ammonia (NH3) and free tryptophan were determined in 18 hospitalized cirrhotic patients af fected with subclinical hepatic encephalopathy, as diag nosed by the Kurtz test. CBF results were significantly lower (p < 0.001) in the patients' group as compared with a sex-and age-matched normal control popUlation, al though seven patients had values in the normal range. NH3 was increased only in six, while free tryptophan was Brain dysfunction has been ascribed to several metabolic alterations commonly found during cir-

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Section: Discussionsupporting

confidence: 66%

Reduction of Cerebral Blood Flow in Subclinical Hepatic Encephalopathy and its Correlation with Plasma-Free Tryptophan

Rodriguez¹,

Testa

Celle

et al. 1987

J Cereb Blood Flow Metab

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“…Cellular respiration may also be impaired in liver failure, since components of the cellular oxidoreductive system are shifted to a more reduced state in some tissues (Henley & Laughrey, 1970). In addition the proportion of glucose metabolized with oxygen by the brain is reduced in patients with hepatic coma (James et al, 1969b), which suggests a greater reliance on anaerobic metabolism to maintain cerebral oxygen requirements even in the normoxic state. Alternatively the hypoxic depression of CMRoz at relatively high Pcv,oz values may reflect increased cerebral arteriovenous shunting, or variation in capillary density, so that the Poz in cerebral venous blood is much higher than in the cerebral capillaries.…”

Section: Cerebral Circulatory Response To Hypoxiamentioning

confidence: 99%

“…In patients with liver cirrhosis there is a reduction in CBF'') and CMRo2, which is related to the severity of hepatic encephalopathy (Fazekas, Ticktin, Ehrentraut & Alman, 1956;Posner & Plum, 1960;James, Nashat, Sampson, Williams & Garassini, 1969b). The response of CBF to an increase in arterial C 0 2 tension is also depressed in liver failure, and a further reduction in CMRo2 occurs during hypercapnia (Stanley, Salisbury, McHenry & Cherniack, 1975).…”

Section: Introductionmentioning

confidence: 99%

Effect of Liver Failure on the Cerebral Circulatory and Metabolic Responses to Hypoxia in the Goat

Stanley

Cherniack

1976

Clinical Science

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1. Six unanaesthetized goats were used to evaluate the effect of liver failure on the hypoxic responsiveness of cerebral blood flow. The animals breathed air and several different hypoxic gas mixtures enriched with sufficient CO2 to maintain an isocapnic state. The cerebral metabolic rate for O2 (CMRo2) was also measured in four of these goats. 2. In baseline studies there was a linear relationship between cerebral blood flow and arterial O2 saturation (Sa,o2) measured at different levels of isocapnic hypoxia. The slopes of the cerebral blood flow/Sa,o2 response lines were used to quantify the response of cerebral blood flow to hypoxia. In the healthy goat, CMRo2 was not depressed by hypoxia until the O2 tension (Po2) in arterial and cerebral venous blood had fallen below critical threshold values of approximately 3-2 and 2-2 kPa (24 and 16 mmHg) respectively. 3. Liver failure was accompanied by a fall in cerebral blood flow and CMRo2. There was also a depression in the response of cerebral blood flow to hypoxia and a disproportionate reduction of cerebral O2 delivery in hypoxia. CMRo2 was further reduced at arterial and cerebral venous Po2 values, which were much higher than the critical threshold values for producing hypoxic CMRo2 depression in health. 4. It is concluded that the brain becomes more vulnerable to the adverse effects of hypoxia during liver failure. This may be of practical importance in the management of patients with arterial hypoxaemia or other complications (e.g. anaemia or shock), which may reduce cerebral oxygen delivery.

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“…Hyperventilation, respiratory alkalosis (Vanamee, Poppell, Glicksman, Randall & Roberts, 1956;Tyor & Sieker, 1959;Reinicke, Friis & Mullertz, 1963) and reduced cerebral blood flow (Fazekas, Ticktin, Ehrentraut & Alman, 1956;Posner & Plum, 1960;James, Nashat, Sampson, Williams & Garassini, 1969) are common features in acute and chronic liver failure. They are possibly interrelated since hypocapnia reduces cerebral blood flow (Kety & Schmidt, 1946) and diminished cerebral perfusion may stimulate ventilation by increasing the brain extracellular Pco, (Comroe, 1965).…”

Section: Introductionmentioning

confidence: 99%

Effect of Liver Failure on the Response of Ventilation and Cerebral Circulation to Carbon Dioxide in Man and in the Goat

et al. 1975

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1. The acid-base state of arterial blood and cerebrospinal fluid, and the ventilatory response to CO2, were measured in twelve patients with liver disease. The CO2 response was also measured in eight goats before and after the experimental production of liver failure. Arterial PCO2 and pH, cerebral blood flow and the cerebral metabolic rate for oxygen were also measured in four of the goats while they breathed air and various CO2-enriched gas mixtures. 2. Liver failure was accompanied by a respiratory alkalosis in both the patients and in the goats. Decreased PCO2 and increased pH occurred in the cerebrospinal fluid and in the arterial blood of the patients. 3. The slope of the ventilatory response to CO2 was reduced when liver failure was severe, in patients and goats alike. In addition there was a reduction in the extrapolated PCO2 at zero ventilation, even when liver failure was mild. 4. Cerebral blood flow and metabolic rate were consistently reduced in the goats during liver failure. There was also less cerebral vasodilatation and a greater reduction in cerebral metabolism during experimental hypercapnia when these animals were in liver failure. 5. The decreases in the ventilatory and cerebral circulatory responsiveness to CO2 indicate that the brain is less well defended against hypercapnia in liver failure, and these changes are especially unfavourable as cerebral function deteriorates when the PCO2 is increased.

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Effect of Induced Metabolic Alkalosis in Hepatic Encephalopathy

Cited by 36 publications

References 9 publications

Reduction of Cerebral Blood Flow in Subclinical Hepatic Encephalopathy and its Correlation with Plasma-Free Tryptophan

Reduction of Cerebral Blood Flow in Subclinical Hepatic Encephalopathy and its Correlation with Plasma-Free Tryptophan

Effect of Liver Failure on the Cerebral Circulatory and Metabolic Responses to Hypoxia in the Goat

Effect of Liver Failure on the Response of Ventilation and Cerebral Circulation to Carbon Dioxide in Man and in the Goat

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