Gene/Protein Disease Symptom Drug Enzyme Compound
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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of intravenously administered disopyramide phosphate were evaluated in seven patients with refractory ventricular tachycardia. All patients had organic heart disease, including acute infarction (three patients), chronic coronary artery disease (two patients) and cardiomyopathy (two patients). The severity of the heart disease was reflected in the advanced patient age (average 64 years) and the occurrence before disopyramide therapy of cardiac arrest in five patients and congestive heart failure in all seven patients. In five patients, disopyramide was given as a bolus injection, 2 mg/kg body weight, followed by an infusion of 20 to 40 mg/hour. The final two patients received 4 mg/kg divided as a bolus injection and an infusion over 1 hour followed by a 0.4 mg/kg infusion during the next hour. Intravenous administration of disopyramide resulted in more effective electrical stability in all patients and completely eliminated ventricular tachycardia in six. Recurrence of ventricular tachycardia was prevented in six patients with subsequent long-term oral administration of disopyramide. Possible dose-related cardiac pump depression occurred in two patients, but disopyramide was otherwise well tolerated. Therefore, these data document the therapeutic efficacy of disopyramide in the treatment of refractory life-threatening ventricular tachyarrhythmias.
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PMID:Efficacy of disopyramide phosphate in the treatment of refractory ventricular tachycardia. 32 16

A literature review of the effect of oral contraceptive (o.c.) use on various metabolic processes is presented. Several studies show an adverse effect of o.c. use on subclinical diabetes and on patients with manifest insulin-independent diabetes. Some researchers have found a beneficial effect of o.c. use on older diabetics. It has not been determined whether the estrogen or gestagen component of o.c.s is responsible for this decrease in glucose tolerance, nor has the mechanism for this effect been discovered. Changes in various plasma protein concentrations have been observed during o.c. use, which affect the blood coagulation and the blood pressure regulation systems. The estrogen component appears to be responsible for the increase in the serum triglyceride concentration during o.c. use; the mechanism is still unknown. Some studies indicate that o.c. use causes an increase in serum cholesterol levels, which could promote gall stone formation. An increase in Vitamin A concentration has been observed during o.c. use. Riboflavin, folic acid, vitamin B 12, and ascorbic acid levels have been shown to decrease during o.c. use. A decrease in pyridoxin levels during o.c. use indicates an increased metabolism of tryptophan to nicotinic acid robosyl-5-phosphate. This would cause a decrease in serotonin production, which could be a cause of the depression experienced by some o.c. users. An increase in the plasma copper and caeruloplasmin levels during o.c. use is apparently due to the estrogen component. An increase in transferrin and the serum iron levels have been observed during o.c. use. Contradictory findings are reported concerning the plasma concentration of zinc.
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PMID:[Metabolic studies under administration of oral contraceptives. A review]. 34 1

The effect of exogenous adenine or uracil upon the de novo pathway for synthesis of pyrimidine nucleotides in Escherichia coli K12 was investigated. Parameters studied were levels of the enzymes carbamoyl phosphate synthase (EC 2.7.2.9), aspartate carbamoyltransferase (EC 2.1.3.2) and orotate phosphoribosyltransferase (EC 2.4.2.10) and the intermediates carbamoyl phosphate, aspartate and orotate, together with the contributions of exogenous uracil and aspartate to intracellular pyrimidine nucleotide. Taken with earlier data [Bagnara, A.S. & Finch, L. R. (1974) Eur. J. Biochem- 41, 421--430] on contents of UTP, CTP and 5-phosphoribosyl 1-diphosphate in cultures of this strain after the addition of adenine or uracil, the results obtained provide new insights into the regulatory mechanisms operating on the pathway in vivo. These insights enable evaluation of the contributions of such factors as limitation for a substrate, feed-back allosteric control by end products and enzyme repression/depression mechanisms. The evidence presented indicates that depressed levels of orotate phosphoribosyltransferase in E. coli K12 result in the wasteful ultilization of asparatate for excess synthesis of pyrimidine nucleotide precursors during balanced growth of the strain in minimal medium. Exogenous adenine increases the excessive accumulation of these precursors by lowering the intracellular content of 5-phosphoribosyl 1-diphosphate (Bagnara and Finch, 1974). This causes a decrease in the conversion of orotate to orotidine 5'-monophosphate, thus lowering the utilization or orotate and its precursors for synthesis of pyrimidine nucleotides. Further, since the contents of these nucleotide end products are thereby decreased (Bagnara nad Finch, 1974), theri feed-back on the early steps in the pathway is diminished and the production of the precursors is increased. It is postulated that growth of E. coli K12 under these conditions is limited by a compound that is metabolically related to precursors to aspartate.
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PMID:Response of the pyrimidine pathway of Escherichia coli K 12 to exogenous adenine and uracil. 36 3

Thirty-four patients with cancer of the breast and 12 with cancer of the prostate were treated with testosterone and 32P-sodium phosphate for relief of pain from bony metastases. Thirty were treated with chemotherapy as well, and 34 were treated with external radiation to single ports for localized pain. Of the 46 patients treated, good results were achieved in 34, fair results in six, and no improvement in six. Subsequent marrow depression necessitated transfusion in 10 patients; no other side effect was observed.
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PMID:32P-sodium phosphate treatment of metastatic malignant disease. 42 5

Thirty-four patients with cancer of the breast and 12 with cancer of the prostate were treated with testosterone and 32P-sodium phosphate for relief of pain from bony metastases. Thirty received chemotherapy as well, and 34 received external radiation to single ports for localized pain. Of the 46 patients, 34 had good results, 6 fair, and 6 were failures. Ten patients needed transfusion for marrow depression; no other side effect was observed.
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PMID:32P-sodium phosphate treatment of metastatic malignant disease. 42 68

1 The antidysrhythmic, haemodynamic and metabolic effects of intravenously administered disopyramide phosphate (1 to 5 mg/kg) have been studied in greyhounds, anaesthetized with trichloroethylene. 2 In doses of 2.5 and 5.0 mg/kg, disopyramide significantly reduced the ventricular dysrhythmias that occur in the initial 30-min period following acute coronary artery ligation. None of the disopyramide-treated animals developed ventricular fibrillations. 3 The metabolic consequences of coronary artery ligation, assessed by local coronary venous sampling from the ischaemic area, were not modified by disopyramide except that K+ egress was prevented. 4 There was evidence for substantial disopyramide-induced myocardial depression (decreased cardiac output and left ventricular dP/drmax with elevated ventricular filling pressure and pulmonary oedema and shunting) and it is suggested that great care be taken when the drug is administered intravenously in conditions where cardiac function is already compromised. Disopyramide also reduced myocardial blood flow. 5 In chloralose-anaesthetized mongrel dogs, disopyramide (2.5 mg/kg) significantly reduced the ST-segment elevation (assessed from epicardial recordings) that resulted from short (3 min) coronary artery occlusions. This could indicate a reduction in the extent and severity of myocardial injury or simply reflect decreased K+ efflux (since locally administered K+ itself increased ST-segment elevation).
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PMID:The effects of disopyramide phosphate on early post-coronary artery ligation dysrhythmias and on epicardial ST-segment elevation in anaesthetized dogs. 46 77

Ten captive-reared African black-footed penguins (Spheniscus demersus) from a large outdoor colony were monitored for avian malaria, using several diagnostic tests. One treatment regimen was evaluated. Thin smear blood evaluation enabled detection of seven parasitemias involving Plasmodium relictum and Plasmodium elongatum in the penguins. Leukocytosis (relative lymphocytosis) was characteristic of infected birds. Parasitemia was detected as early as 21 days prior to onset of clinical signs (depression, anorexia, regurgitation, pale mucous membranes, and respiratory distress). The single bird that died had clinical signs only a few hours prior to its death. Treatment consisted of 0.03 mg of primaquine phosphate base/kg body weight, administered orally once daily for 3 days. Oral chloroquine phosphate therapy, given simultaneously, was administered in an initial loading dose of 10 mg of chloroquine phosphate base/kg body weight, followed by doses of 5 mg/kg at 6, 18 and 24 hours after the initial chloroquine dose. This treatment regimen prevented mortality and cleared parasites from the blood. Recurrences of malaria occurred in two birds that had received this treatment.
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PMID:Avian malaria in African black-footed penguins. 52 78

The effect of verapamil on Ca2+ and Mg2+ accumulation was investigated in isolated rat kidney cortex mitochondria. For the 50% inhibition of Ca2+ accumulation, 2 x 10(-4) M verapamil concentration was required in the presence of ATP (2 mM) and phosphate (5 mM). Omission of phosphate from the medium increased the inhibitory effect of verapamil on Ca2+ accumulation. Verapamil had no effect on Ca2+ accumulation in the presence of both ATP and succinate (7.8 mM), but further addition of phosphate resulted in a significant inhibition of Ca2+ accumulation by verapamil. Mg2+ accumulation of mitochondria was similarly depressed by verapamil. The same tendency was found as for the modification of verapamil effect by acetate in mitochondrial Ca2+ and Mg2+ accumulation. Succinate oxidation of mitochondria was not affected by verapamil in the absence of phosphate, but was inhibited by verapamil in the presence of phosphate. Therefore, it seemed reasonable to assume that the depression of Ca2+ and Mg2+ transport of mitochondria by verapamil is modulated by permeant anions.
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PMID:Effect of verapamil on the calcium and magnesium transports of rat kidney cortex mitochondria. 53 83

The effects of acute i.v. inorganic phosphate (Pi) loading were studied on nembutalized mongrel dogs previously subjected to unilateral splanchnicotomy ("renal denervation"). GFR (51Cr-EDTA) was not different on the intact and the denervated side, while urine output (V), sodium excretion (UNaV), and urinary excretion (UPiV) of inorganic phosphate of denervated kidneys were significantly increased at any plasma Pi level. Thus, tubular reabsorption of Pi in denervated kidneys was considerably depressed. Tubular transport rates of Na and Pi--as expressed in per cent of the filtered load--were positively correlated in both intact and denervated organs. Besides an impairment in tubular transport of Na a depression in the reabsorption of inorganic phosphate is brought about by renal denervation. A common mechanism of action for both Na and Pi can be supposed.
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PMID:Effect of splanchincotomy on the renal excretion of inorganic phosphate in the anaesthetized dog. 55 51

Exogenous ATP has been shown earlier to activate a permeability change in transformed 3T3 cultures leading to massive efflux of the acid-soluble pools. This leads to reduction of the basal rate of glycolysis to a very low level so that glycolysis becomes almost totally dependent on the addition to the medium of glucose, inorganic phosphate and ADP in order to restore the rate to that of untreated cells. No such depression of glycolysis is observed in untreated transformed cells or in ATP-treated normal 3T3 cells. In such permeabilized cultures, phosphorylated intermediates such as glucose-6-phosphate and fructose-1,6-diphosphate can serve as effective substrates for lactic acid formation. ATP treatment of cultured cells also allows molecules as big as NADP to enter the cells and participate in the pentose phosphate shunt pathway. This ability to temporarily and differentially render transformed cells permeable allows a review of several aspects of cellular metabolism and biosynthesis in the intact cell where the cellular organization is maintained. Furthermore, it deserves serious consideration as a means to achieve differential cytotoxicity of transformed cells by chemotherapeutic agents which, on their own, are indiscriminate in their action.
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PMID:Control of glycolysis and the pentose phosphate shunt in transformed 3T3 cultures rendered permeable by ATP. 56 77


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