Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Co-enzyme Q10 (ubiquinone) is a naturally occurring substance which has properties potentially beneficial for preventing cellular damage during myocardial ischemia and reperfusion. It plays a role in oxidative phosphorylation and has membrane stabilizing activity. The substance has been used in oral form to treat various cardiovascular disorders including angina pectoris, hypertension, and congestive heart failure. Its clinical importance is now being established in clinical trails worldwide.
 ...
PMID:Co-enzyme Q10: a new drug for cardiovascular disease. 220 52

Seven (7) males with effort angina and listed for coronary by-pass surgery had muscle biopsies taken from their vastus lateralis muscle for determination of muscle fiber types (%ST), ubiquinone (vitamin Q, UQ), oxidative and fermentative enzyme activities. Graded cycle ergometer exercise to determine intensities corresponding to onset of blood lactate accumulation set to 2.0 mmol x l-1 (WOBLA) and symptom limited exercise ('maximal', WSL) were also undertaken. WOBLA was positively related to %ST (r = 0.92, p < 0.001). %ST was on the other hand inversely related to UQ (r = -0.82, p < 0.05), the heart specific LD subunit LD-H (r = -0.96, p < 0.001), the isozyme LD3 as the fraction of LD (%LD3) (r = -0.93, p < 0.01), and the CK isozyme CKMB as the fraction of CK (%CKMB) (r = -0.88, p < 0.05). It was suggested that muscle UQ depletion in the patients was related to molecular oxygen and free oxygen radical formation. The lack of antioxidants then caused a radical trauma specifically to the ST fiber and their mitochondria. This could be a cause and-effect explanation for the selective ST fiber downregulation in effort angina and heart failure in general.
 ...
PMID:Muscle ubiquinone in male effort angina patients. 909 75

Seventeen male patients with ischaemic heart disease (IHD) and effort angina performed OBLA exercise stress tests (set to 2.0 mmol x l-1). They had muscle biopsies from the vastus lateralis muscle the day before coronary by-pass grafting, and from the internal and external intercostal, diaphragm and gastrocnemius muscles during surgery. They had a low WOBLA (83 +/- 6 W, mean +/- 1 S.E.M), WOBLA corresponded to 79 +/- 4% (% WOBLA) of WSL (symptom limited or 'maximal' capacity = 111 +/- 11 W). Peak blood lactate concentration averaged 2.9 mmol x l-1. Muscle fibre composition disclosed a depressed percent slow twitch (ST or 'red') muscle fibres in the vastus lateralis and intercostal muscles (%ST). The diaphragm and gastrocnemius muscles had normal %ST. Intercostal muscles had elevated values for the fast twitch muscle fibre (FT) subgroup FTa indicative of endurance adaptation. The vastus lateralis, gastrocnemius and diaphragm muscles had normal muscle ubiquinone (UQ) contents, whereas the intercostals were depleted. Plasma contents of the antioxidants UQ and alpha-tocopherol were low as compared to healthy man.
 ...
PMID:Muscle fibers, ubiquinone and exercise capacity in effort angina. 909 76

Seven males with effort angina undertook graded ergometer tests and had muscle biopsies taken from their vastus lateralis muscle before, and three and six months after coronary bypass surgery. Muscle fibre composition (percentage of slow twitch fibres), ubiquinone (vitamin Q), and oxidative and fermentative enzyme activities were determined. After six months, muscle ubiquinone and oxidative enzymes were still depressed, indicating sustained muscle trauma. The only peripheral changes were that muscle lactate dehydrogenase and its skeletal muscle-specific subunits and isozymes were increased 35% to 40% (P < 0.001) three to six months postsurgery. Onset of blood lactate accumulation (2.0 mmol/L), symptom-limited ('maximal') exercise and peak blood lactate increased linearly over time (r = 0.52, P < 0.05; r = 0.63, P < 0.01; and r = 0.76, P < 0.001, respectively). It is suggested that the initial physical performance increase was due to improved circulatory capacity, oxygen delivery and lactate efflux, whereas the increased fermentative capacity ('anaerobic power') first contributed after a lag of three or more months. Whether the muscle histochemical changes reflected a healing process (recovery) is speculative.
 ...
PMID:Muscle characteristics in effort angina before and after CABG. 921 30

Coenzyme Q10 or ubiquinone normally present in many plant and animal cells is an antioxidant. Coenzyme Q10 deficiency has been observed in patients with congestive heart failure, angina pectoris, coronary artery disease, cardiomyopathy, hypertension, mitral valve prolapse and after coronary revascularization. Coenzyme Q10 is involved in the synthesis of ATP and hence is useful in preventing cellular damage during ischaemia-reperfusion injury. The clinical benefits are mainly due to its ability to improve energy production, antioxidant activity, and membrane stabilizing properties. Several studies showed that coenzyme Q could be useful in patients with congestive heart failure, angina pectoris, cardiomyopathy, coronary artery disease and in the preservation of myocardium. Coenzyme Q10 is normally present in the low density lipoprotein cholesterol fraction and inhibits its oxidation. It can also regenerate vitamin E. Coenzyme Q10 is known for producing minor gastrointestinal discomfort and elevation in SGOT and LDH when used.
 ...
PMID:Coenzyme Q in cardiovascular disease. 1127 51

Nitric monoxide (NO) exerts a great variety of physiological functions. L-Arginine supplies amino groups which are transformed to NO in various NO-synthase-active isoenzyme complexes. NO-synthesis is stimulated under various conditions increasing the tissue of stable NO-metabolites. The major oxidation product found is nitrite. Elevated nitrite levels were reported to exist in a variety of diseases including HIV, reperfusion injury and hypovolemic shock. Denitrifying bacteria such as Paracoccus denitrificans have a membrane bound set of cytochromes (cyt cd1, cyt bc) which were shown to be involved in nitrite reduction activities. Mammalian mitochondria have similar cytochromes which form part of the respiratory chain. Like in bacteria quinols are used as reductants of these types of cytochromes. The observation of one-e- divergence from this redox-couple to external dioxygen made us to study whether this site of the respiratory chain may also recycle nitrite back to its bioactive form NO. Thus, the aim of the present study was therefore to confirm the existence of a reductive pathway which reestablishes the existence of the bioregulator NO from its main metabolite NO2-. Our results show that respiring mitochondria readily reduce added nitrite to NO which was made visible by nitrosylation of deoxyhemoglobin. The adduct gives characteristic triplet-ESR-signals. Using inhibitors of the respiratory chain for chemical sequestration of respiratory segments we were able to identify the site where nitrite is reduced. The results confirm the ubiquinone/cyt be1 couple as the reductant site where nitrite is recycled. The high affinity of NO to the heme-iron of cytochrome oxidase will result in an impairment of mitochondrial energy-production. "Nitrite tolerance" of angina pectoris patients using NO-donors may be explained in that way.
 ...
PMID:Mitochondria recycle nitrite back to the bioregulator nitric monoxide. 1199 14