Liver Function After Myocardial Infarction

Aber, CliveP.; Brunt, P.E.; Jones, E. Sherwood; Richards, Toby; Short, A. H.; Bernstein, Victoria

doi:10.1016/s0140-6736(66)90301-1

Cited by 17 publications

(7 citation statements)

References 5 publications

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“…Abnormalities of liver function have previously been reported in patients with severe heart failure (1) and also in patients with complicated acute myocardial infarction ( 2 ) . The following investigation was carried out in dogs with acute myocardial infarction to determine whether disturbances of liver function can be detected, and related to the relatively mild impairment of circulatory function which characterizes this experimental preparation.…”

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confidence: 88%

“…Previous clinical studies have suggested that cardiac impairment of rela-tively severe degree is required to produce abnormalities in the sensitive hepatic dyeexcretion tests (1,2). The mechanism for alteration in these tests is not known, but elevated right atrial filling pressures and hepatic venous congestion have been implicated (1).…”

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“…Since mine whether similar increases could be demonstrated in normal rats undergoing liver regeneration. Partial hepatectomy has been widely used as a device to investigate the synthesis of specific lipids or proteins by rapidly proliferating liver cells (2,3). However, no information is available on the synthesis of lipoproteins in rats following partial hepa tec tomy.…”

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Plasma Clearance of Indocyanine Green Following Experimental Myocardial Infarction in Dogs

Hood¹,

McCarthy²,

Letac³

et al. 1968

Experimental Biology and Medicine

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Abnormalities of liver function have previously been reported in patients with severe heart failure (1) and also in patients with complicated acute myocardial infarction ( 2 ) . The following investigation was carried out in dogs with acute myocardial infarction to determine whether disturbances of liver function can be detected, and related to the relatively mild impairment of circulatory function which characterizes this experimental preparation.Methods. Mongrel dogs weighing from 16-24 kg were anesthetized with 30 mg/kg of pentobarbital, and subjected to an openchested staged ligation of the left anterior descending coronary artery (3 ) . Twelve animals survived this procedure and the period of sustained ventricular arrhythmia which invariably occurred over the next 2 days. On the third or fourth day following ligation, a t a time when arrhythmias had ceased, the animals were premedicated with 1.5 mg/kg of morphine sulfate, then anesthetized with a mixture containing 200 rng of urethane, 30 mg of pentobarbital, and 50 mg of allobarbital per ml. The animals were ventilated with a Harvard respiratory pump. Animals were instrumented for hemodynamic measurements as described in detail elsewhere (4). A second group of 7 animals was subjected to a sham operation, and otherwise treated in an identical fashion; these served as controls. Arterial oxygen saturation exceeded 90% in every animal. Indocyanine green dye (12.5 mg) was injected as a bolus into the right atrium, and the arterial concentration was recorded continuously from a fiberoptic catheter placed * Supported by grants-in-aid from the National Institutes of Health (HE-07776-04, 5 TI-HE-5242 and PO-1-HE-11306-01) ; the John A. Hartford Foundation; and the Fund for Research and Teaching, Harvard School of Public Health, Department of Nutrition.in the arch of the aorta (5). Total blood volume was calculated by extrapolating the dye concentration curve to the time of injection. This was done from a replotted log dye concentration-time curve, utilizing only the exponential portion of the curve after mixing was completed. Plasma volume was calculated from duplicate microcrit determinations, without correction for trapped plasma. The halftime ( t 1 / 2 ) of disappearance of indocyanine green was also measured from the semilogarithmic plot of the fiberoptic tracing, and plasma clearance was calculated as described by Rowel1 et al. ( 6 ) , from the relationship: plasma clearance = (0.693/t1/2) (plasma volume).In an attempt to clarify the effect of acute changes in hemodynamics on removal of indocyanine green by the liver, an additional eight normal dogs were studied during selective alteration of aortic and hepatic venous pressure. This was accomplished by inflating a balloon catheter positioned fluoroscopically either in the thoracic aorta, above the celiac axis, or in the inferior vena cava, just above the level of the diaphragm. Pressures were measured from catheters positioned below the level of obstruction, in the abdominal aorta and inferior vena cava a t the...

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Plasma Clearance of Indocyanine Green Following Experimental Myocardial Infarction in Dogs

Hood¹,

McCarthy²,

Letac³

et al. 1968

Experimental Biology and Medicine

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“…Transient abnormalities of liver function tests have been reported after acute myocardial infarction even in the absence of severe haemodynamic changes (Aber et al, 1966;Das, Nussbaum and Leff, 1974). Observing raised bilirubin concentrations in the first few days after myocardial infarction, the authors investigated the frequency of this phenomenon by measuring total and conjugated bilirubin in consecutive cases of uncomplicated myocardial infarction during a 2-year period and studied its mechanism by measuring serum free fatty acid (FFA: nonesterified fatty acids) concentrations and by assessing liver blood flow, using indocyanine green (ICG) plasma clearance, in some patients.…”

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Plasma bilirubin and serum free fatty acids after myocardial infarction

Cowan¹,

Thompson²,

Kaye³

et al. 1981

Postgraduate Medical Journal

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SummaryFasting concentrations of plasma bilirubin were measured in 34 patients on admission to hospital and daily for 7 days after uncomplicated myocardial infarction. Mean concentrations increased significantly to reach maximum levels on the second day after admission, and fell during the following 5 days to reach the admission level by the 7th day. Unconjugated bilirubin accounted for most of this rise. Serum concentrations of free fatty acids (FFA), measured simultaneously in 12 patients, were highest within 12 hr of the onset of symptoms, when their level was significantly higher than at any time after the first day. It is suggested that the transient hyperbilirubinaemia after uncomplicated myocardial infarction is frequent and may result from interference by FFA with bilirubin metabolism.

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“…It has been shown that myocardial infarction may be followed by impairment of liver function (Aber et al, 1966) and even hepatic necrosis (Clarke, 1950).…”

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