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PubMed1987

Cimetidine and neonatal small bowel adaptation: an experimental study.

Histamine2-blockers are being used more extensively in the pediatric short gut patient as an agent to accelerate small bowel adaptation. Reversal of lipid malabsorption and a direct trophic effect on the intestinal crypt cells have been postulated as the mechanism for the salutary influence of cimetidine. Weanling Sprague-Dawley rats underwent 85% small bowel resection. Controls had repair of a simple ileal transection. Rats received either a fat-defined rat chow only, or chow with high- or low-dose cimetidine, 2% cholestyramine, or cholestyramine/low-dose cimetidine. All animals were killed 2 weeks postresection, and ileal and jejunal sections were examined for changes in villous and crypt morphology. The animals receiving cimetidine showed earlier and more consistent weight gain than resected animals who received no adjunctive treatment. High- and low-dose regimens were equally efficacious. Cimetidine administered alone decreased fecal fat losses, but not when given with cholestyramine. The cimetidine/cholestyramine group showed increased weight gain when referenced to the resection controls despite continuing lipid malabsorption. Villous and crypt lengthening did not correlate with clinical evidence of adaptation. An augmented lymphocytic activity (plasma cell hyperplasia, enlargement Peyer's patches) was present in the hyperplastic ileal segments of the cimetidine-treated rats. Overall immunoreactivity was similar in all study groups. No significant differences in villous morphology or immunologic activity were seen in jejunal segments. The effects of H2-blockers on lipid absorption and intestinal hyperplasia are inadequate to explain the benefits of cimetidine in the short gut patient. Examination of the immunology of the short bowel complex merits further attention in elucidating cimetidine's action in this setting.

Adaptation, Physiological↗

PubMed1988

Management of lipids in primary and secondary prevention of cardiovascular diseases.

Although the frequency of cardiovascular disease is declining, it remains a major present and future threat to health in the United States. The deleterious effects of abnormal blood lipid concentrations have long been recognized, but the benefit of corrective intervention in this process has only recently been demonstrated. We review the major lipid abnormalities and the available clinical therapeutic interventions. In addition, we discuss data that address the premise that reducing low-density lipoprotein cholesterol or raising high-density lipoprotein cholesterol should decrease the progression of coronary atherosclerosis, and we summarize drug trials in which clofibrate, niacin, cholestyramine, and gemfibrozil decreased coronary heart disease events. Studies that used cholestyramine and the combination of colestipol and niacin resulted in decreased progression of coronary artery disease. On the basis of early experience with lovastatin, inhibitors of hydroxymethylglutaryl-coenzyme A reductase are likely to be effective in the treatment of hypercholesterolemia. The available information on the association of low cholesterol levels and cancer suggests that low total cholesterol is a consequence rather than a cause of carcinoma. Current data strongly support the concept of vigorous intervention directed at management of lipids, both with non-pharmacologic treatment and with drug therapy, for the primary and secondary prevention of coronary atherosclerosis.

Anticholesteremic Agents↗

PubMed1977

Aluminium hydroxide in bile-salt diarrhoea.

The treatment of choleraic diarrhoea remains a problem. Cholestyramine is effective but long-term treatment is often impracticable. In-vitro studies have shown that aluminium hydroxide has bile-acid-binding properties comparable with those of cholestyramine. The bile-acid-binding properties of aluminium hydroxide have now been investigated in vivo and applied to the treatment of patients with choleraic diarrhoea. Aluminium hydroxide increased the faecal bile-salt concentration of patients with a normal bowel habit whereas magnesium hydroxide had no effect. Eight patients with severe choleraic diarrhoea were treated with aluminium-hydroxide suspension: bowel motion became less frequent and daily faecal weight fell.

Adult↗

PubMed1977

Cerebrotendinous cholestanolosis in relation to other cerebral xanthomatoses.

A synopsis is given of 37 reported patients with cerebrotendinous xanthomatosis; divided in 11 possible, but not proven cases of C.T.Ch (cerebrotendinous cholestanolosis), and 26 proven cases. An increased content of cholestanol in serum or tissue, was used as the main criterion. The ophthalmological and neurological signs are tabulated. Attention is drawn to the fact that cholestanol is not mentioned in the extensive literature on related diseases with possible cerebrospinal xanthomas, such as eosinophilic granulomatosis and hyperlipoproteinemia. The importance of a possible role of cholestanol in these diseases is stressed. A hypothetical form of cerebrotendinous cholesterolosis is discussed. A family with a sibship of parents and twelve children, three of which showed C.T.Ch is described. The development of the clinical picture confirmed the variable expression of the autosomal recessive disease. Two patients showed disturbances of steroid metabolism. A first contribution to the search for linkage with the H.L.A. system is presented. Cholestanol over cholesterol ratio, appeared to be independent of the type of lipoprotein. In search for therapy we found in patients with hyperlipoproteinemia type II A, that cholestyramine alone gave dangerously high blood levels of cholestanol; in combined treatment of cholestyramine with clofibrate cholestanol, levels were comparable to those of the controls. The possibilities of therapy are discussed.

Adult↗

PubMed2002

Synthesis of cationic polysaccharide derivatives and their hypocholesterolaemic capacity.

High-capacity bile acid-sequestering biopolymers with cationic polysaccharide derivatives have been developed. Cholestyramine, the bile acid sequestrant most widely used for treating hypercholesterolaemia, has unpleasant side effects because of the hydrophobic nature of its backbone. Methylan, a high-viscosity polysaccharide produced by Methylobacterium organophilum, was selected as a model polysaccharide for derivatization. Methylan was aminated to add dialkylaminoalkyl and free amino groups at hydroxyl sites in the methylan backbone, and these derivatives were quaternized to produce pH-independent cationic polyelectrolytes. The in vitro bile acid-binding capacity of quaternized DEAE-methylan was approximately 50% higher than that of cholestyramine. The bile acid-binding capacity of methylan derivatives increased with the number of carbons in the alkyl groups, indicating that hydrophobic interaction is a secondary factor for the sequestration of bile acids.

Anticholesteremic Agents↗

PubMed1984

Independent regulation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase and chylomicron remnant receptor activities in rat liver.

Treatment of rats with pharmacological doses of oestrogen resulted in a 3-fold decrease in the activity of hepatic 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase) and a 4-fold increase in saturable binding of 125I-labelled chylomicron remnants to liver membranes in vitro. Intragastric administration of mevalonolactone to rats did not affect the capacity of the liver membranes to bind to labelled chylomicron remnants even though there was a substantial decrease in the activity of HMG-CoA reductase. Similar results were obtained after cholesterol feeding. Simultaneous treatment of rats with cholestyramine and compactin increased hepatic HMG-CoA reductase activity 6-fold. However, liver membranes derived from these animals showed no change in their capacity to bind to labelled chylomicron remnants in vitro. Administration of mevalonolactone to the cholestyramine/compactin-treated animals also failed to produce a change in remnant-binding capacity. Although administration of mevalonolactone alone produced a significant 3-fold decrease in the activity of hepatic HMG-CoA reductase it was unable to suppress significantly the increase in enzyme activity caused by treatment with cholestyramine and compactin.

Animals↗

PubMed1992

[The long-term therapy of familial hypercholesterolemia with heparin-induced extracorporeal LDL precipitation].

The long-term tolerance to and effectiveness of heparin-induced extracorporeal LDL precipitation (HELP) in combination with lipid reducing drugs and diet was tested in six patient (5 males, 1 female; mean age 48 +/- 4 years). Follow-up period was over 50 months, in one patient over 24 months, while one man had a sudden cardiac death 57 weeks after starting treatment. The study was divided into three phases. In phase I (24 months) treatment consisted of HELP and conventional lipid-reducing drugs; in phase II (12 months) of lovastatin (80 mg daily) and cholestyramine (12-24 g daily); and phase III (14 months) of HELP, lovastatin and cholestyramine. In phase I it was possible to lower the pre-treatment level of LDL-cholesterol from 306 +/- 18 mg/dl to 173 +/- 13 mg/dl (43.5%). A similar effect (from 307 +/- 21 mg/dl to 155 +/- 17 mg/dl [-49.5%]) was obtained in phase II. The resumption of HELP reduced the pre-treatment LDL concentration to 136 +/- 9 mg/dl (-55.7%). The various treatment regimens were well tolerated. Biochemical data remained unchanged except for iron loss requiring substitution. Thus combined HELP, lovastatin and ion exchange offer for the first time an effective and reliable means in familial hypercholesterolaemia of clearly reducing long-term the mean LDL cholesterol level below the atherosclerosis threshold of 120 mg/dl.

Anticholesteremic Agents↗

PubMed1990

Low density lipoprotein receptor-binding activity in human tissues: quantitative importance of hepatic receptors and evidence for regulation of their expression in vivo.

The heparin-sensitive binding of 125I-labeled low-density lipoprotein (LDL) to homogenates from 18 different normal human tissues and some solid tumors was determined. The binding to adrenal and liver homogenates fulfilled criteria established for the binding of LDL to its receptor--namely, (i) saturability, (ii) sensitivity to proteolytic destruction, (iii) inhibition by EDTA, and (iv) heat sensitivity. When the binding of 125I-labeled LDL was assayed at a constant concentration (50 micrograms/ml), the adrenal gland and the ovary had the highest binding of normal tissues. The highest binding per g of tissue overall was obtained in homogenates of a gastric carcinoma and a parotid adenoma. When the weights of the parenchymatous organs were considered, the major amount of LDL receptors was contained in the liver. To study the possible regulation of hepatic LDL-receptor expression, 11 patients were pretreated with cholestyramine (8 g twice a day for 3 weeks). Increased binding activity (+105%, P less than 0.001) was obtained in homogenates from liver biopsies from the cholestyramine-treated patients as compared with 12 untreated controls. It is concluded that the liver is the most important organ for LDL catabolism in humans and that the receptor activity in this organ can be regulated upon pharmacologic intervention. Further studies are needed to confirm the possibility that certain solid tumors can exhibit high numbers of LDL receptors.

Adrenal Cortex↗

PubMed1991

A fraction derived from brewer's yeast inhibits cholesterol synthesis by rat liver preparations in vitro.

Brewer's yeast was grown on a defined medium containing tracer 51Cr with or without added chromium. The two batches of yeast contained 10 microgram/g (high-Cr) or 80 ng/g (low-Cr). Extracts were prepared and fractionated. A third batch of yeast (third batch) was grown with added Cr, and fractionated. Rats were reared on either rat cubes (normal diet) or on a low-Cr diet (low-Cr), or on rat cubes with added cholestyramine (cholestyramine diet). Preparations of rat liver, both cell-free and intact hepatocytes, incorporated acetate-carbon into fatty acids and cholesterol. These processes were inhibited by a yeast fraction containing small, neutral, water-soluble compounds. The degree of inhibition was the same whether the liver came from normal rats or rats fed on the low-Cr diet. Similarly the inhibitory effect was found with identical amounts of extracts from low- or high-Cr yeasts. Therefore, Cr compounds do not appear to account for the inhibitory effects of brewer's yeast. Use of other substrates indicated that the site of inhibition of sterol synthesis was apparently between acetyl-CoA and mevalonate. One inhibitory substance was isolated from yeast and was found to be nicotinamide riboside. This may have been produced from NAD(P) during the preparation of yeast extracts, and it may be produced from dietary yeast supplements during digestion in vivo. Nicotinamide riboside may be partly responsible for the reported effects of yeast supplements on plasma lipids in humans.

Animals↗

PubMed2004

No difference between two doses of diclofenac in prophylaxis of heterotopic ossifications after total hip arthroplasty.

BACKGROUND: In a monocentric, randomized, placebo-controlled double-blind study, we investigated the efficacy of two doses of diclofenac-cholestyramine for the prevention of heterotopic ossification (HO). PATIENTS: The study comprised 245 patients undergoing total hip arthroplasty (THA). RESULTS: With 150 mg cholestyramine-bound diclofenac (2 x 1 capsule Voltaren resinate) daily during a postoperative period of 14 days, 19% of patients showed slight HO (Brooker grade 1), and no patient had more severe ossifications (grades 2-4). In the group receiving 75 mg daily (1 x 1 capsule), 17% of patients showed grade 1 HO and 4% grade 2 HO. No patient had grades 3-4 HO. No differences in clinical results were seen between the two groups 6 months after THA. INTERPRETATION: Since the rate of adverse gastrointestinal events was lower (23% versus 38%, p = 0.02) in the group receiving the lower dose, we recommend it.

Aged↗

PubMed1987

Dietary fiber supplementation and fecal bile acids, neutral steroids and divalent cations in rats.

Young adult rats were fed ad libitum for 4 wk on defined diets containing either no fiber, 10% levels of insoluble fiber sources [cellulose, wheat bran, alfalfa, mixed fibers (Fibyrax)], 5% levels of soluble fiber sources [pectin, guar gum, psyllium (Metamucil)] or 2% cholestyramine (Questran), a bile acid sequestrant. Fecal samples were obtained from paired rats over a 3-d period, were analyzed for neutral and acidic steroid levels and compositions and, together with the food, were assayed for divalent cations (Ca2+, Mg2+, Fe2+ and Zn2+). Animals in all groups were in balance for divalent cations, and there appeared to be no relationship between the extent of cation balance and the type of fiber fed. All insoluble fiber diets and the guar gum and psyllium diets resulted in significantly higher daily fecal mass and, in general, resulted in significant dilution of total fecal steroids. With the insoluble fibers, there was a general dilution of fecal neutral steroids, which was not apparent with the soluble fibers or cholestyramine. In addition, except for the pectin- and mixed fiber-containing diets, there was reduced bacterial conversion of the primary bile acids to secondary bile acids or metabolites.

Animals↗

PubMed1983

The metabolism of chenodeoxycholic acid to beta-muricholic acid in rat liver.

1. The synthesis of conjugated chenodeoxycholic acid and tauro-beta-muricholic acid in isolated rat hepatocytes was measured by radioimmunoassay. Production of tauro-beta-muricholic acid was linear over 4 h of incubation at 37 degrees C. The net synthesis of conjugated chenodeoxycholic acid was very much lower than that of tauro-beta-muricholic acid. 2. When hepatocytes were prepared from rats in which the enterohepatic circulation had been broken, either by feeding the bile salt sequestrant, cholestyramine or by total biliary drainage for 48 h, synthesis of tauro-beta-muricholic acid was increased compared to that in cells from control rats. Conjugated chenodeoxycholic acid accumulation during incubation of the hepatocytes was increased by cholestyramine feeding but not by total biliary drainage. These results suggest that there is a metabolic difference between the two methods of breaking the enterohepatic circulation with regard to chenodeoxycholic acid synthesis. 3. Hepatocytes prepared from rats given 1% cholesterol in the diet for at least 2 weeks synthesised significantly more tauro-beta-muricholic acid than those from control rats. The total amount of conjugated cholic, chenodeoxycholic and tauro-beta-muricholic acids synthesised by cells from cholesterol fed animals, however was not significantly different from that produced by hepatocytes from normal rats. 4. Exogenous taurochenodeoxycholic acid was metabolised to tauromuricholic acid by isolated hepatocytes. Production of tauro-beta-muricholic acid reached a maximum at a concentration of 20 microM taurochenodeoxycholic acid. The total metabolism of taurochenodeoxycholic acid, however, increased linearly up to the highest concentration measured, 50 microM. 5. The biliary content of tauro-beta-muricholic acid during total biliary drainage fell rapidly in the first 10 h and thereafter continued to decline, reaching a minimum after about 24 h. No significant rise was observed during the remainder of the experimental period. 6. It is concluded that a large proportion of the conjugated chenodeoxycholic acid synthesised by isolated hepatocytes in vitro is metabolised to tauro-beta-muricholic acid, and therefore it is necessary to take this into account when using this system to study bile salt synthesis.

Animals↗

PubMed1983

The effect of dibutyryladenosine 3',5'-monophosphate on the synthesis of bile salts in isolated hepatocytes from rat.

The effect of dibutyryladenosine 3',5'-monophosphate (Bt2cAMP) on the synthesis of conjugated cholic, chenodeoxycholic and beta-muricholic acids has been investigated. Hepatocytes were incubated with 1 mM Bt2cAMP for 3 h at 37 degrees C. In cells from rats with a basal rate of bile salt synthesis (soft-diet-fed rats) production of conjugated cholic acid was increased about two fold, synthesis of conjugated chenodeoxycholic acid was increased 10-20-fold but formation of its metabolite, conjugated beta-muricholic acid, was decreased by 30-50% in the presence of the cyclic nucleotide. The sum of the amounts of the three bile salts produced (total bile salt synthesis) was increased 30-50% by Bt2cAMP. When hepatocytes were prepared from rats in which bile salt synthesis had been stimulated by feeding the bile salt sequestrant, cholestyramine, Bt2cAMP had no effect on conjugated cholic acid synthesis, increased conjugated chenodeoxycholic acid production 3-5-fold and decreased conjugated beta-muricholic acid synthesis by about 50%. Total bile salt synthesis was unchanged. The ratio of the amount of conjugated cholic acid to conjugated chenodeoxycholic acid + conjugated beta-muricholic acid produced, an indication of the activity of 7 alpha-hydroxycholest-4-en-3-one 12 alpha-hydroxylase, was raised by Bt2cAMP in hepatocytes from soft-diet-fed but not in those from cholestyramine-fed rats. The effects of the cyclic nucleotide on the synthesis of the three bile salts in hepatocytes from soft-diet-fed rats were found to be saturable at a concentration of about 2 mM. Responses were half-maximal at concentrations of Bt2cAMP varying between 0.5 and 1.5 mM. These results suggest that in hepatocytes from rats with a basal rate of bile salt synthesis Bt2cAMP has effects at three different stages in the pathway, at the level of cholesterol 7 alpha-hydroxylase, 7 alpha-hydroxycholest-4-en-3-one 12 alpha-hydroxylase and chenodeoxycholine acid 6 beta-hydroxylase. In cells from rats in which bile salt synthesis has been stimulated only the effect at the chenodeoxycholic acid 6 beta-hydroxylase level is apparent. Bt2cGMP and Bt2cCMP had no effect on the synthesis of any of the bile salts measure, showing that the effects are specific for Bt2cAMP. The ratio of the amounts of the three bile salts found inside the cells to those found in the medium was decreased by about 90% when Bt2cAMP was present in the hepatocyte incubations. This effect was mimicked by Bt2cGMP and to a lesser extent by Bt2cCMP.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1993

Cholesterol 7 alpha-hydroxylase is up-regulated by the competitive inhibitor 7-oxocholesterol in rat liver.

Rats of the Sprague-Dawley strain were infused intravenously with a fat emulsion (Intralipid, trademark of Kabi Pharmacia, Uppsala, Sweden) containing 7-oxocholesterol. This resulted in an increased cholesterol 7 alpha-hydroxylase activity in liver microsomes as compared to controls and was accompanied by increased levels of cholesterol 7 alpha-hydroxylase mRNA and microsomal cholesterol 7 alpha-hydroxylase protein. Rats were also fed a cholestyramine-supplemented diet and infused with 7-oxocholesterol. These animals excreted about half as much bile acids in faeces as cholestyramine-fed controls. Addition of 7-oxocholesterol to liver microsomes from normal rats in amounts corresponding to those present in microsomes from 7-oxocholesterol-treated rats inhibited the cholesterol 7 alpha-hydroxylase activity by about 75%. Cholesterol induced a type-I binding spectrum when added to a purified bacterial-expressed cholesterol 7 alpha-hydroxylase (P-450c7 delta 2-24). 7-Oxocholesterol competitively inhibited the cholesterol binding spectrum, while 7 beta-hydroxycholesterol did not interfere with binding of cholesterol to the enzyme. It is concluded that treatment with the competitive inhibitor 7-oxocholesterol leads to a reduced bile acid biosynthesis and, as a consequence of reduced bile acid inhibition, a compensatory increase in cholesterol 7 alpha-hydroxylase synthesis. The high enzyme activity measured in microsomal preparations from 7-oxocholesterol-treated rats may be due to a continuous conversion of 7-oxocholesterol into less inhibitory metabolites, e.g. 7 beta-hydroxycholesterol. The latter compound was found in high concentrations in liver microsomes from rats treated with 7-oxocholesterol. The physiological importance of these results is discussed in relation to the previous findings that 7-oxocholesterol is accumulated in liver after cholesterol feeding and that 7-oxocholesterol is formed from cholesterol during lipid peroxidation.

Animals↗

PubMedDate not supplied

Pruritus and cholestasis: therapeutic options.

The pathogenesis of pruritus of cholestasis remains unclear. Bile salts do not appear to be the sole prurogens in cholestasis. Histaminergic pathways may be involved, and central opiate receptor processes seem much more important than has previously been recognized. The therapeutic options for relief of cholestatic pruritus are summarized in Table 2. Resins such as cholestyramine are the first line of therapy. In cases where cholestyramine has failed, rifampicin and antihistamines may be beneficial. Opiate antagonists hold great potential if opioid withdrawal-like syndromes can be avoided. Ursodeoxycholic acid and methotrexate have an advantage in not only relieving pruritus but also potentially retarding disease progression in PBC and PSC, respectively, although this remains to be proved. Other agents such as EPO and SAMe remain experimental and require further study to clarify their effectiveness before they can be recommended.

Cholestasis↗

PubMed2006

Pneumonitis associated with leflunomide: a profile of New Zealand and Australian reports.

BACKGROUND: Pneumonitis has very rarely been observed in patients taking leflunomide in clinical trials. Evidence is emerging that it is more frequent in clinical practice. AIM: The aim of this study was to investigate voluntary reports of suspected respiratory reactions to leflunomide held by the New Zealand Pharmacovigilance Centre (NZPhvC) and the Australian Adverse Drug Reactions Unit (ADRU) to ascertain if they fulfilled the criteria for pneumonitis and to define characteristics of this reaction. METHOD: Reports of respiratory adverse reactions attributed to leflunomide and received by the NZPhvC and the ADRU were analysed to identify those that were likely to be pneumonitis based on the criteria of Searles and McKendry. Features of these reports were examined to provide further information about this adverse reaction. RESULTS: The NZPhvC and the ADRU received 14 reports considered to be pneumonitis occurring in patients taking leflunomide. Two case reports fulfilled the Searles and McKendry criteria for definite or probable hypersensitivity pneumonitis. The patients in the remaining reports had radiological evidence of pulmonary infiltrates, an acute respiratory illness and no evidence of precipitating infection. In two cases the patients were taking leflunomide alone; one improved when it was withdrawn. In the other 12 cases, patients were taking leflunomide in combination with methotrexate. In nine of these 12 patients pneumonitis occurred after leflunomide was added to methotrexate, usually within 12-20 weeks. One of the two patients who died had possible previous methotrexate pneumonitis. Leflunomide washout with cholestyramine was used to treat three patients, one with life-threatening illness, with good results. CONCLUSION: This case series supports observations that leflunomide can cause pneumonitis either as monotherapy or in combination with methotrexate. The case histories indicate that prompt recognition is important to avoid life-threatening disease and support the use of cholestyramine to remove leflunomide.

Adult↗

PubMed1996

Endothelium-dependent coronary vasomotion relates to the susceptibility of LDL to oxidation in humans.

BACKGROUND: Oxidatively modified LDL has been shown to markedly impair endothelium-dependent dilation in experimental studies. The aim of the present study was to determine the relationship between the coronary vasomotor response to the endothelium-dependent agonist acetylcholine and the in vitro susceptibility of LDL to oxidation in patients. METHODS AND RESULTS: Endothelium-dependent coronary vasomotion in response to acetylcholine (10(-8) to 10(-6) mol/L) was assessed in 23 patients with hypercholesterolemia (mean age, 56 +/- 9 years) after 1 year of therapy with either an American Heart Association Step 1 diet (seven patients), lovastatin and cholestyramine (seven patients), or lovastatin and probucol (nine patients). The susceptibility of LDL to oxidation was determined by measuring the lag phase of conjugated diene formation induced by Cu2+. Patients treated with lovastatin and probucol had prolongation of the lag phase (263 +/- 64 minutes) compared with diet- (91 +/- 22 minutes) or lovastatin and cholestyramine-(118 +/- 57 minutes) treated patients (P<.0001). By univariate analysis, the coronary vasomotor response to acetylcholine was significantly related to the lag phase of conjugated diene formation (P=.002), cholesterol-lowering therapy (P=.002), and serum cholesterol (P=.02). By multivariate analysis, the lag phase remained a significant predictor of the acetylcholine vasomotor response, independent of the effect of cholesterol-lowering treatment. CONCLUSIONS: In patients treated with lipid-lowering agents, the vasodilator response to acetylcholine is related to the susceptibility of LDL to oxidation. These findings suggest that oxidative stress is an important determinant of the coronary endothelial dysfunction observed in patients with atherosclerosis and hypercholesterolemia.

Acetylcholine↗

PubMed1990

Drug adsorption to charcoals and anionic binding resins.

1. The in-vitro binding of four drugs with differing physiochemical properties to two commercial charcoal preparations and two anionic binding resins was studied at 37 degrees C and pH 7.4. 2. The two charcoal preparations (Carbomix and Medicoal) behaved similarly and adsorbed metoclopramide and antipyrine to a greater degree than warfarin or paracetamol. 3. Cholestyramine had a significantly greater maximum adsorption capacity (K2) for warfarin and significantly lower adsorption capacity for paracetamol and metoclopramide than did the charcoals. 4. Colestipol behaved similarly but also bound metoclopramide to a significantly greater extent than did either cholestyramine or charcoal and antipyrine to a significantly lesser extent than did Carbomix. 5. There appeared to be no consistent relationship between the maximum adsorption capacity of the adsorbents for the drugs tested and the physicochemical properties of those drugs (e.g. basic or acidic structure, pKa or molecular weight).

Adsorption↗