Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the role of peripheral sympathetic nerves in the regulation of calcitonin release, rats subjected to superior cervical ganglionectomy (SCGx) 16-28 h earlier were used. The time periods selected allowed us to examine C cell response during the supraliminal release of sympathetic transmitter that accompanies anterograde degeneration of nerve varicosities as well as during the neural paralysis that ensues thereafter. At the time intervals examined, SCGx did not result in significant changes of basal serum calcitonin or Ca levels. The intraperitoneal administration of CaCl2 brought about an impending increase of serum Ca to the same extent in SCGx and sham-operated rats. A significant depression of calcitonin release was observed in rats killed around the time of nerve terminal degeneration (16-21 h post SCGx) but not about 10 h later. Additionally a delay to achieve a maximal calcitonin response was apparent during nerve degeneration. Injection of the alpha-adrenoceptor blocker phenoxybenzamine significantly increased basal calcitonin levels and restored the depressed calcitonin response to hypercalcemia seen in SCGx rats. Treatment with the beta-adrenoceptor-blocker propranolol counteracted phenoxybenzamine activity but was unable to modify per se calcitonin release in SCGx or sham-operated rats. Basal Ca levels and their increase after intraperitoneal CaCl2 were similar in all examined groups regardless of the drug injected. In an additional experiment phenoxybenzamine injected into SCGx rats in doses one-fifth those employed earlier still reversed both the depression in maximal calcitonin response as well as the delay to attain maximal release after CaCl2, but was unable to affect basal calcitonin levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in calcitonin release during sympathetic nerve degeneration after superior cervical ganglionectomy of rats. 374 8

Conduction disorders may be logically expected from the digoxin-verapamil association, since each of these drugs is known to increase conduction time (CT) and effective refractory period (ERP) in the atrioventricular (AV) node. When AV conduction is considerably depressed by verapamil (1.27 mg/kg over 90 min) in the absence of vagal tone, digoxin, infused at 1 microgram/kg/min rate over 40 min, elicits a progressive but incomplete regression of the verapamil effects, as does hypercalcaemia up to 5.5 mmol/l. Infused at the 2.5 microgram/kg/min rate over 20 min, its antagonistic effects, like those of hypercalcaemia exceeding 5.5 mmol/l, are less and less marked and even replaced by a certain synergism. When AV conduction is considerably depressed by digoxin (i.v. injection of 40 micrograms/kg) under high vagal tone, verapamil (twice 0.2 mg/kg) does not aggravate this depression and even attenuates it, this attenuation being however more significant on ERP than CT in the AV node. Consequently, as a rule, the interaction does not lead to block, since the maximum action of one drug is associated with the reduction in the action of the other or even the conversion of synergism into antagonism.
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PMID:Modification of atrioventricular conduction under the combined influence of a cardiac glycoside and a calcium antagonist in the dog. 379 71

The present report gives information both on the clinical features at presentation and the clinical course of 7 consecutive patients with nonsecretory multiple myeloma. It provides evidence that the nonsecretory variant was closely associated with high tumor cell mass, as determined by severe anemia and/or multiple areas of bone destruction. The marked depression of normal immunoglobulins and the absence of both renal failure and hypercalcemia differentiated nonsecretory from typical myelomatosis. Finally, the survival length of patients with nonsecretory myeloma appeared to be similar to that of comparably staged patients with secretory myeloma.
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PMID:Nonsecretory multiple myeloma. Presenting findings, clinical course and prognosis. 393 4

The combined effects of digoxin and hypercalcaemia were studied in the canine heart in situ on the sinoatrial (SA) and atrioventricular (AV) nodes. Measurements were made of heart rate, of conduction time in the AV node by the endocavitory recording of the His bundle potentials, and of the effective refractory period of this node by the extrastimulus method. In the presence of acetylcholine released by vagal endings or infused into the coronary blood, an increase in plasma calcium concentration from 2.50 to 4.60 mmol/l after a 80 micrograms/kg dose of digoxin considerably depressed conduction in the AV node and automatism in the SA node. In the absence of acetylcholine, no bradycardia occurred under the influence of digoxin alone or digoxin and hypercalcaemia, and hypercalcemia enhanced to a lesser extent digoxin-induced depression of conduction in the AV node. These results evidence a potentiation by acetylcholine of the combined effects of digoxin and hypercalcaemia on the SA and AV nodes.
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PMID:Vagal role in potentiation by Ca2+ ions of the action of cardiac glycosides on the atrial specialised tissue. 405 11

Amiodarone was administered to 80 patients with recurrent cardiac tachyarrhythmias previously resistant to drug treatment. Forty nine patients were treated for ventricular tachycardia or fibrillation and 31 for supra-ventricular arrhythmias. The mean (range six days to 51 months), permitting a total of 100 patient years of observation. Adverse reactions were observed in 69 patients. Severe side effects were encountered in 13: four patients developed interstitial pneumonitis, four patients developed incessant ventricular tachycardia, three patients taking amiodarone and digoxin sustained sinus node arrest with depression of escape foci, one patient developed hepatitis, and one patient developed hypercalcaemia with renal failure. Furthermore, a rise in the serum concentration of digoxin and potentiation of warfarin anticoagulation occurred in cases in which these agents were combined with amiodarone. Amiodarone was stopped in 14 patients because of side effects. Although amiodarone is effective in suppressing arrhythmias in most patients in whom extensive use of antiarrhythmic drugs has been unsuccessful, it is associated with diverse and serious toxicity. These observations suggest that at present the use of amiodarone should be reserved for patients with life threatening or seriously disabling arrhythmias in whom longer established drugs have been ineffective or are contraindicated.
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PMID:Adverse reactions during treatment with amiodarone hydrochloride. 640 40

According to the Subcommittee on Classification and Definition of Sarcoidosis, it is a multisystem granulomatous disorder of unknown etiology. It most commonly affects young adults and presents most frequently with bilateral hilar adenopathy, pulmonary infiltrates, and skin or eye lesions. The diagnosis is established when clinical findings and appropriate x-ray findings are supported by tissue biopsy specimens in which noncaseating epithelioid cell granulomas are found. Immunologic features of the disease include depression of delayed hypersensitivity reactions, suggestive of impaired cell mediated immunity, and increased or abnormal immunoglobulin levels. Hypercalciuria may occur, with or without hypercalcemia. The course and prognosis of the disease correlate with the mode of onset. An acute onset in the presence of erythema nodosum indicates a self-limited course with spontaneous resolution, whereas an insidious onset may be followed by a relentless course. Corticosteroids are useful when therapy is required, as well as to suppress inflammation and the occurrence of granulomatous changes.
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PMID:Sarcoidosis. 675 25

To study the response of function in the regionally ischaemic left ventricle to increased and decreased concentrations of plasma ionised calcium, twenty-two anaesthetised dogs were placed on right heart bypass with constant mean aortic pressure and heart rate. Regional (sonomicrometry) and global left ventricular function were assessed before coronary artery ligation. Then, following ligation, function after 45 min stable ionised hypercalcaemia [( Ca2+] = 1.68 +/- 0.01 mmol x litre-1) and hypocalcaemia [( Ca2+] = 0.73 +/- 0.02 mmol x litre-1) were each compared to function during an immediately preceding normocalcaemic period. Control of cardiac output enabled paired comparisons to be made at matched preloads: systolic shortening from common end-diastolic chord lengths (n = 10), and stroke work at common left ventricular end-diastolic pressures (n = 22). With hypercalcaemia, systolic shortening in the ischaemic region (2.11 +/- 0.39 mm preligation) increased from -0.62 +/- 0.17 to -0.04 +/- 0.20 mm (P less than 0.01), whereas in the control region systolic shortening increased from 1.47 +/- 0.12 to 2.00 +/- 0.15 mm (P less than 0.01) reaching its preligation value (1.67 +/- 0.13 mm). Stroke work at a left ventricular end-diastolic pressure of 1.37 kPa increased (0.248 +/- 0.019 to 0.299 +/- 0.021 joules x beat-1, P less than 0.001) but not to preligation levels (0.364 +/- 0.016 joules x beat-1). Hypercalcaemia also increased myocardial oxygen consumption (by 1.0 +/- 0.3 cm3 x min-1 x 100 g-1, P less than 0.005) but not coronary blood flow. With hypocalcaemia, systolic shortening decreased in ischaemic and control regions, global function curves were markedly depressed, and myocardial oxygen consumption did not change but coronary blood flow increased. Thus hypercalcaemia improved function in ischaemic and control regions but improvement in the ischaemic region was small compared with the depression associated with ischaemia itself. Hypercalcaemia also improved global function, but not to preischaemic levels, at an increased oxygen cost.
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PMID:Global and regional function in the regionally ischaemic left ventricle related to plasma ionised calcium. 688 17

Thirty-seven cases of canine hypoadrenocorticism were compared with 39 previously reported cases. The 2 series were compared because it was believed that a study of 37 consecutive cases diagnosed at 1 institution (Michigan State University) and compiled by 1 group of veterinarians would yield data that were more representative of the disease than multiple cases from various institutions. Age, sex, and breed data were similar in both series. The frequency of anorexia, vomiting, depression, and the mean values for the clinicopathologic data were similar for both series except for blood glucose concentration (P less than 0.025). The Michigan State University series was different in that it had a lower frequency of eunatremia, increased plasma total solids, and hypoglycemia but a higher frequency of lymphocytosis, lymphopenia, hyponatremia, hyperglycemia, and hypercalcemia. Further, 3 dogs in the Michigan State University series had azotemia plus near isosthenuric urine, suggesting renal disease, but they seemingly responded to therapy for hypoadrenocorticism. Only 1 such case was identified in the literature. Finally, we detected fewer instances of P waves not being evident in lead II of an electrocardiogram.
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PMID:Canine hypoadrenocorticism: report of 37 cases and review of 39 previously reported cases. 703 23

An unusual clinical presentation of moderate hypercalcemia as a result of primary hyperparathyroidism is described. The patient complained of fatigue, depression, thirst, polyuria, and focal neurologic symptoms including amaurosis fugax, anomia, right upper-extremity dysesthesias, and a left cerebral transient ischemic attack. No structural central nervous system abnormality could be documented. Signs and symptoms disappeared when serum calcium levels were reduced from 13.2 to 9.8 mg/100 ml. They have not recurred in 30 months of follow-up. The association of focal neurologic disease and hypercalcemia is uncommon. Although the precise pathophysiologic mechanism is unclear, this patient's symptoms suggest a vascular etiology.
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PMID:Focal neurologic symptoms in hypercalcemia. 718 1

The effect of plasma ionized calcium concentration on left ventricular function was studied in the canine heart on right heart bypass. Stroke volume, mean arterial pressure and heart rate were controlled. Plasma ionized calcium was lowered to 0.58 +/- 0.01 mM by citrate infusion and raised to 1.70 +/- 0.01 mM by calcium chloride infusion in random order in each dog. Left ventricular function at each of these ionized calcium levels was compared with that in an immediately preceding normocalcemic period. At a constant stroke work (16.9 +/- 0.2 g-m), sustained hypercalcemia was associated with a small decrease in left ventricular end-diastolic pressure (1.7 +/- 0.7 cm H2O, p less than 0.05) despite a marked increase in peak left ventricular dP/dt (first derivative of ventricular pressure) averaging 34 percent (p less than 0.001). Coronary blood flow, tension-time index and myocardial oxygen consumption were not significantly altered. Stroke work determined at a left ventricular end-diastolic pressure of 14 cm H2O, by interpolation in left ventricular function curves, was 11 +/- 4.4 percent above that at control normocalcemia (p less than 0.05). At a constant stroke work (16.9 +/- 0.2 g-m), sustained hypocalcemia was associated with a marked depression of left ventricular function as demonstrated by a substantial increase (from 4.9 +/- 0.3 to 12.7 +/- 1.1 cm H2O, p less than 0.0001) in left ventricular end-diastolic pressure (p less than 0.0001), decreased mean systolic ejection rate (p less than 0.01) and decreased peak left ventricular dP/dt (p less than 0.0001). Coronary blood flow increased (p less than 0.05) whereas myocardial oxygen consumption did not change significantly. A marked displacement of left ventricular function curves to the right (compared with curves obtained during normocalcemia) was observed, and stroke work determined at a left ventricular end-diastolic pressure of 14 cm H2O was 52 +/- 5.4 percent below control level (p less than 0.001). It appears that hypercalcemia, when initiated from a normal control level, provides only a small enhancement of ventricular pump performance (as indexed by the stroke work-left ventricular end-diastolic pressure relation) despite a marked increase in peak left ventricular dP/dt, whereas marked improvement of left ventricular performance may be expected when calcium infusion is initiated from an ionized calcium level that is below normal.
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PMID:Relation between ionized calcium concentration and ventricular pump performance in the dog under hemodynamically controlled conditions. 722 49


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