Plasma cyclic adenosine-3', 5'-monophosphate response to glucagon in patients with liver disease.

Davies, T F; Prudhoe, Kenneth; Douglas, A.G.

doi:10.1136/bmj.1.6015.931

Cited by 24 publications

(11 citation statements)

References 13 publications

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“…The plasma cAMP response is similar to previous studies in normal subjects in our laboratory [Davies et al, 1976]. Intrave nous cAMP and dibutyryl cAMP reduce ADP-induced platelet aggregation, both in vitro [Salzman and Levine, 1971] and in vivo [Zweifler and Sanbar, 1969] affecting both primary and secondary aggregation but only after doses which would produce great er plasma levels than our subjects achieved.…”

Section: Discussionsupporting

confidence: 75%

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Increased Platelet Aggregation Induced by Glucagon Administration

Proctor¹,

Davies²,

Oxley³

et al. 1980

Acta Haematol

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The effect of 1 mg of intravenous glucagon on platelet aggregation has been investigated in 12 normal subjects pre-treated with salicylate. All subjects demonstrated the expected inhibition of collagen-induced secondary aggregation but retained the normal adenosine diphosphate (ADP)-induced primary aggregation phase 18 h after the salicylate therapy (600–1,200 mg). Subsequent administration of glucagon caused a significant increase in the ADP-induced primary aggregation phase in the 12 subjects. This data indicates that glucagon increases the reactivity of platelets to ADP and may help to explain the common clinical association of raised plasma glucagon, increased platelet aggregation and vascular disease.

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Section: Discussionsupporting

confidence: 75%

“…Glucagon is a potent stimulator of plas ma cAMP, increasing basal levels thirty fold [Davies et al, 1976] and may therefore alter platelet function. In order to determine the influence of glucagon on the primary phase of aggregation we investigated its ef fect in normal subjects before and after pre treatment with aspirin.…”

Section: Introductionmentioning

confidence: 99%

Increased Platelet Aggregation Induced by Glucagon Administration

Proctor¹,

Davies²,

Oxley³

et al. 1980

Acta Haematol

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“…It has been known that hepatic reserve can be evaluated by the response of these parameters to glucagon [21 ]. In our study, a significant correlation was demonstrated between the liver glycogen con tent and the increase in the serum glucose after glucagon loading.…”

Section: Discussionsupporting

confidence: 62%

Significance of Donor Nutritional Status for Rewarming Injury of the Hepatic Graft in Rats

Wakiyama

Yanaga

Soejima³

et al. 1997

Eur Surg Res

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We studied the significance of donor nutritional status for hepatic rewarming injury and the usefulness of the glucagon loading test for the assessment of donor nutritional status in rats. In experiment 1 the animals were either free fed or fasted for 6, 24 or 48 h. The livers were preserved in chilled lactated Ringer’s solution for 4 h and were divided into eight groups according to the fasting and rewarming periods. The ammonia level in the graft effluent was increased in grafts preserved for 24 h or longer, which was augmented when rewarming time was increased from 15 to 30 min (p < 0.05). In experiment 2, the animals were divided into four groups (n = 3 each) according to the fasting period. The hepatic tissue glycogen content was measured after fasting, and the serum glucose was measured after the administration of 50 µg/kg of glucagon i.v. The hepatic tissue glycogen content correlated with the increase rate of serum glucose (p = 0.0001). We conclude that glycogen may protect the hepatic graft from rewarming injury by improving energy status, particularly in prolonged rewarming. The glucagon loading test seems to be useful for assessing the glycogen content of the hepatic graft.

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“…Nonetheless, insulin resistance is present in patients with cirrhosis, and this permits augmented gluconeogenesis, ketogenesis (2), and lipolysis during the postabsorptive period. Although there is no evidence for glucagon down-regulation (37)(38)(39), and the hyperglucagonemia accompanying cirrhosis may be needed to facilitate the mobilization of nutrients during fasting (40), it should be recognized that the elevated concentrations of immunoreactive glucagon observed in cirrhotic patients are due to three or four different molecular forms of glucagonlike materials (41). Therefore, it is difficult to be certain about the actual increase in circulating 3,500-D glucagon and the actual biological effects of hyperglucagonemia in cirrhotic patients.…”

Section: Discussionmentioning

confidence: 99%

Nature and quantity of fuels consumed in patients with alcoholic cirrhosis.

Owen¹,

Trapp²,

Reichard³

et al. 1983

J. Clin. Invest.

312

151

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A B S T R A C T Although alcoholism is a leading cause of morbidity and mortality of middle-aged Americans, there are no data available pertaining to the consequences of Laennec's cirrhosis on total body energy requirements or mechanisms for maintaining fuel homeostasis in this patient population. Therefore, we simultaneously used the techniques of indirect calorimetry and tracer analyses of ["4C]palmitate to measure the nature and quantity of fuels oxidized by patients with biopsy-proven alcoholic cirrhosis and compared the results with values obtained from healthy volunteers. Cirrhotic patients were studied after an overnight fast (10-12 h). Normal volunteers were studied after an overnight fast (12 h) or after a longer period of starvation (36-72 h).Total basal metabolic requirements were similar in overnight fasted cirrhotic patients (1.05±0.06 kcal/ min per 1.73 m2), overnight fasted normal subjects (1.00±0.05 kcal/min per 1.73 m2), and 36-72-h fasted normal volunteers (1.10±0.06 kcal/min per 1.73 m2).Indirect calorimetry revealed that in cirrhotic patients the percentages of total calories derived from fat (69±3%), carbohydrate (13±2%), and protein (17±4%) were comparable to those found in 36-72-h fasted subjects, but were clearly different from those of overnight fasted normal individuals who derived 40±6, 39±4, and 21±2% from fat, carbohydrate, and protein, respectively.These data are strikingly similar to data obtained through tracer analyses of ['4C]palmitate, which showed that in overnight fasted patients with alcoholic cir-

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Plasma cyclic adenosine-3', 5'-monophosphate response to glucagon in patients with liver disease.

Cited by 24 publications

References 13 publications

Increased Platelet Aggregation Induced by Glucagon Administration

Increased Platelet Aggregation Induced by Glucagon Administration

Significance of Donor Nutritional Status for Rewarming Injury of the Hepatic Graft in Rats

Nature and quantity of fuels consumed in patients with alcoholic cirrhosis.

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