Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental damage of the aortal heart valve in rabbits caused taurine accumulation in the heart. Taurine content in the heart increased for two months 2.7 times in the left ventricle and 1.8 times in the right one. Taurine concentration in the blood began rising 5-10 days after the operation, reached the maximal value of about 150% as compared with its initial level and then decreased to the level near the initial one. Animals with insignificant taurine accumulation in the heart died for the first two months after the operation. Results are discussed from consideration on the protective role of taurine for the myocardium under the heart failure.
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PMID:[Taurine level in the blood and myocardium of rabbits with experimental heart failure]. 208 83

The present study was designed to investigate in chick heart whether oral pretreatment with taurine or taurine added directly to the perfusate has any effect upon calcium paradox-induced heart failure. In both protocols, taurine significantly reduced the mechanical dysfunction resulting from the calcium paradox. Taurine pretreatment partially inhibited the excess accumulation of calcium in the myocardium that occurs upon calcium repletion, and microscopy revealed almost normal structure. This protective effect of taurine was accompanied by (a) reduction of the gain of sodium content that occurs during calcium depletion, and (b) reduction of the late gain in calcium that occurs during calcium repletion. It is proposed that taurine plays a role in the regulation of calcium homeostasis and membrane stabilization.
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PMID:Taurine prevention of calcium paradox-related damage in cardiac muscle. Its regulatory action on intracellular cation contents. 339 Feb 25

To examine the effect of daily treatment with taurine on improving the status of congestive heart failure (CHF), we used rabbits with artificially induced aortic regurgitation. Ten rabbits were treated daily with taurine (100 mg/kg by mouth) and eight with guanidinoethyl sulfonate (GES) (100 mg/kg by mouth) immediately after induction of aortic regurgitation. The cumulative mortality rate at 8 weeks in the taurine-treated CHF group was 10% (1 of 10) compared with 53% (16 of 30) in the nontreated CHF group and 75% (6 of 8) in the GES-treated CHF group (p less than 0.05). Although cardiac function (max dP/dt) in CHF rabbits was significantly decreased (p less than 0.001), taurine-treated CHF rabbits maintained the same values as control rabbits. Taurine content of the left ventricular tissue of the CHF rabbits was significantly increased (p less than 0.01). Administration of taurine and GES to control rabbits for 8 weeks affected neither the hemodynamics nor the taurine content of the heart. It was concluded that taurine slowed the rapid progression of heart failure and consequently prolonged life expectancy.
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PMID:Beneficial effect of taurine in rabbits with chronic congestive heart failure. 378 75

The loss of mechanical function in rat hearts subjected to either the calcium-paradox or global ischemia heart failure models was found to correlate with decreases in myocardial taurine levels. Therefore, the effect of taurine treatment was assessed in the two failure procedures. The presence of taurine protected against loss of mechanical function resulting from the calcium paradox and prevented both the large decline in sarcolemmal ATPase activities and the increase in sarcolemmal calcium binding normally associated with this model. Parallel studies on reperfused, taurine-untreated ischemic hearts showed only minor changes in these sarcolemmal functions. Taurine treatment normalized the slight increase in calcium binding associated with ischemia, but had no observable effect on recovery of mechanical function. Although taurine returns selected parameters of the sarcolemma toward normal in both models, it only improves mechanical function in the paradox model. This suggests that calcium paradox-induced heart failure is more closely associated with sarcolemmal dysfunction than ischemic heart failure.
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PMID:Effect of taurine on calcium paradox and ischemic heart failure. 645 Nov 84

Taurine (2-aminoethanesulfonic acid) is known to have a cardiotonic action. The present study was designed to see whether oral treatment with taurine could improve the status of congestive heart failure induced by aortic regurgitation. Nine rabbits were treated daily with taurine (100 mg/kg) after producing aortic regurgitation. Cumulative mortality at 8 weeks in the non-treated group was 52% compared with 11% in the taurine-treated group (p less than 0.05). Cardiac function (max dP/dt) was significantly decreased in rabbits with aortic regurgitation, whereas in taurine-treated rabbits, cardiac function was maintained the same as control. The present data suggest that taurine prevented the rapid progress of heart failure, and consequently prolonged the life expectancy.
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PMID:Beneficial effect of taurine on congestive heart failure induced by chronic aortic regurgitation in rabbits. 648 12

1. Taurine has recently been known to protect against ischemia and heart failure. Taurine possesses plenty of actions on the ion channels and transports, but is very non-specific. 2. Taurine may directly and indirectly help to regulate the [Ca]i level by modulating the activity of the voltage-dependent Ca2+ channels (also dependent on [Ca]i/[Ca]o), by regulation of Na+ channels, and secondly via Na-Ca exchange and Na(+)-taurine cotransport. 3. Taurine can prevent the Ca2+ ([Ca]o or [Ca]i)-induced cardiac functions. 4. Therefore, it seems possible that taurine could exert the potent cardioprotective actions even under the condition of low [Ca]i levels as well as under the Ca2+ overload condition. 5. The electrophysiological actions of taurine on cardiomyocytes, smooth muscle cells, and neurons from recent studies are summarized.
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PMID:Review of some actions of taurine on ion channels of cardiac muscle cells and others. 952 60

During ischemia, hypoxia and cardiac failure, the heart undergoes several adverse changes, including a reduction in taurine (2-aminoethanesulfonic acid). Oral administration of taurine under these disease conditions would be expected to act like a mild cardiac glycoside. Taurine would exert improvement in the accumulation of [Na]i and the loss of alpha-amino acids. Nonetheless, when intracellular taurine content is raised, there would be the benefit of increased Ca2+ release from the sarcoplasmic reticulum and increased Ca2+ sensitivity of the contractile proteins, as well as possible changes in the action potential associated with the actions of taurine on ion channels. In fact, intracellular application of taurine produces the opposite actions to extracellularly administration of the amino acid. From our previous experiments, the electrophysiological actions of taurine on cardiac muscle cells include the following. (a) Prolongation of action potential duration (APD) at high [Ca]i and shortening of APD at low [Ca]i. In multicellular preparations, however, taurine did not always prevent [Ca]o-induced effects. (b) Stimulation of spontaneous activity at low intracellular and extracellular Ca2+ concentrations ([Ca]i and [Ca]o), and vice versa. (c) Inhibition of the L-type Ca2+ current (ICa(L)) at high [Ca]i, and vice versa. (d) Enhancement of the T-type Ca2+ current (ICa(T)). (e) Inhibition of fast Na+ current (INa). (f) Enhancement of TTX-insensitive slow Na+ current. (g) Inhibition of delayed rectifier K+ current (IKrec) at high [Ca]i, and vice versa. (h) Enhancement of the transient outward current (Ito). (i) Inhibition of the ATP-sensitive K+ current (IK(ATP)). Since taurine acts on so many ion channels and transporters, it is clearly non-specific. Although it is very difficult to understand the diversity of taurine's actions, it is possible that taurine can exert its potent cardioprotective actions under the conditions of low [Ca]i, as well as Ca2+ overload. Thus, although taurine-induced modulation of ion channels located on the cardiac cell membrane is complex, the multiple effects may combine to yield useful therapeutic results.
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PMID:Cardiac actions of taurine as a modulator of the ion channels. 963 23

Taurine is not only present in foods, tonics and nutrient drinks but is also used as a medicinal agent mainly for treatment of chronic heart failure and liver disease. However, little is known about its influence on drug-metabolizing enzymes, especially cytochrome P450 (CYP), in human. We examined whether taurine could affect the expression of CYP3A4 mRNA in the presence or absence of rifampicin (RFP), which is a potent inducer of CYPs, with HepG2 cells. Taurine enhanced twice the induction of CYP3A4 mRNA by RFP, but did not affect the expression by itself. This effect was both concentration- and time-dependent. On the other hand, taurine did not affect the induction by phenobarbital. Taurine did not increase intracellular uptake of RFP. Therefore, we conclude that taurine is an enhancer for the induction of CYP3A4 by RFP.
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PMID:Taurine modulates induction of cytochrome P450 3A4 mRNA by rifampicin in the HepG2 cell line. 1243 88

Taurine, an amino acid that exhibits anti-angiotensin II and osmoregulatory activity, is found in very high concentration in the heart. When the intracellular content of taurine is dramatically reduced, the heart develops contractile defects and undergoes an eccentric form of hypertrophy. The development of myocyte hypertrophy has been largely attributed to angiotensin II, whose growth properties are antagonized by taurine. Overt heart failure is usually associated with myocyte death, including death due to angiotensin II-induced apoptosis. However, the effect of taurine deficiency on angiotensin II-induced apoptosis has not been examined. To investigate this effect, taurine-deficient cells, produced by incubating rat neonatal cardiomyocytes with medium containing the taurine transport inhibitor, beta-alanine, were exposed to angiotensin II. The peptide increased terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL) staining and caspase 9 activation more in the taurine-deficient than the normal cell. Angiotensin II also promoted the translocation of protein kinase C (PKC)epsilon and PKCdelta, the expression of Bax, and the activation of c-Jun N-terminal kinase (JNK), effects that were greater in the taurine-deficient cell. However, the data ruled out a role for extracellular signal-related kinase (ERK), Bad, and p38 mitogen-activated protein kinase in the beta-alanine-angiotensin II interaction. Because PKC and JNK affect the expression and phosphorylation state of certain Bcl-2 family members, they appear to contribute to the potentiation of angiotensin II-induced apoptosis by taurine deficiency.
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PMID:Possible cause of taurine-deficient cardiomyopathy: potentiation of angiotensin II action. 1271 6

Conditionally essential nutrients (CENs) are organic compounds that are ordinarily produced by the body in amounts sufficient to meet its physiological requirements. However, in disorders, such as cardiovascular disease (CVD), and in other physiologically stressful conditions, their biosynthesis may be inadequate. Under these circumstances, CENs become essential nutrients, comparable to vitamins. The CENs of primary importance in CVD, based on the quantity and quality of human clinical studies, are l-arginine, l-carnitine, propionyl-l-carnitine, and coenzyme Q10. Controlled studies of these CENs are reviewed in depth. Taurine is a CEN of secondary importance caused by a limited human database. Other putative CENs include alpha-lipoic acid, betaine, chondroitin sulfate, glutamine, and d-ribose, each of which is mentioned in passing. Collectively, CENs have demonstrated favorable clinical effects in CVDs, including chronic heart failure, myocardial infarction, angina pectoris, and in CVD risk factors, such as hypertension, hyperlipidemia, and lipoprotein(a). Limited research has pointed to possible benefits in CVD therapy accruing from supplementation with several CENs in combination. Additional controlled clinical studies of CENs in CVD are urgently needed. In view of the efficacy and safety of appropriate supplementation with CENs, it is strongly suggested that healthcare professionals become knowledgeable of these potentially important additions to the CVD therapeutic armamentarium.
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PMID:Supplemental conditionally essential nutrients in cardiovascular disease therapy. 1640 31


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