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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The induction of alkalosis has been proposed as provocative test of coronary spasm in patients affected by vasospastic angina. We submitted to the test 43 patients, affected by angina with a previous documentation of spontaneous ischemia (19 patients with ST elevation and 24 patients with ST depression at the EKG registered during pain). Twelve patients had normal coronary arteries; in 14 patients a significant stenosis of a single vessel was present; in 15 patients 2 vessels were involved and in 2 a 3-vessel disease was demonstrated. The test induced ischemia in 17 patients (39.6%). The positivity of the test was strictly dependent on the period of time elapsed between the last documented crisis of angina and the provocative test: it induced ischemia in 75% of the patients who underwent the test in the acute phase: on the other hand it was constantly negative in patients who had not complained of anginal pain for more than 6 months. In the screening of patients with chest pain at rest, the test of alkalosis does not seem, therefore, useful as a diagnostic tool.
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PMID:[The alkalinization test in the diagnosis of spontaneous angina]. 673 5

Alkalosis was used for stress testing for coronary artery spasm in 70 patients (average age: 56 years) with resting angina. A rapid intravenous infusion of an alkaline buffer (THAM) immediately followed by 5 minutes' maximal ventilation increased the arterial pH to 7.67 +/- 0.5. Anginal pain and ECG changes were observed in 24 Patients, with ST elevation in 10 cases and ST depression in 14 cases. The ischaemic changes occurred during hyperventilation in 16 cases and in the 3 minutes following the test in 8 cases. The heart rate increased from 66 +/- II to 71 +/- 14 bpm (p less than 0,01) but systolic blood pressure fell from 139 +/- 12 to 130 +/- 12 mm Hg during hyperventilation; there was no significant change in the rate-pressure product (1130 +/- 1750 to 8990 +/- 2690). In all cases, the angina and ischaemic changes regressed after intravenous Trinitrin. Coronary angiography was performed in 56 patients: in the 24 patients with positive responses (Group I) and in 30 of the 46 patients with negative responses (Group II). Significant coronary artery narrowing (greater than 70%) was observed in 21 patients of Group I: in the 3 patients without coronary lesions an intravenous injection of 0.4 mg methylergometrine provoked coronary spasm. In Group II, significant narrowing was demonstrated in 18 patients: in the 12 other patients, coronary spasm could not be induced by methylergometrine. Therefore, in the absence of organic coronary lesions, an excellent correlation has been shown between the alkalosis and methylergometrine tests. This stress test was repeated in 16 of the 24 patients in Group I one hour after administration of 20 mg of Nifedepine: the test was negative in all cases. We conclude that the alkalosis test could be useful in the coronary care unit as a stress test for coronary spasm to determine the antianginal treatment of choice and to evaluate its efficacity.
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PMID:[Clinical application of the alkalosis induction test for coronary artery spasm]. 680 Mar 22

Succinylated Acinetobacter glutaminase-asparaginase (SAGA) has broader antitumor activity than Escherichia coli L-asparaginase in experimental systems; moreover, drug resistance does not develop in tumor cell lines initially sensitive to this enzyme. We have investigated the pharmacology and toxicology of SAGA after both single-dose and serial daily dose injections in 20 adult patients. Glutaminase activity in plasma after i.v. injection of single doses did not follow simple first-order kinetics (half-life during the initial 24 hr was 21 +/- 9 hr. A linear relation was observed between increasing doses of SAGA and resultant levels of plasma enzyme activity and blood glutamate. Assay of whole blood which had been deproteinized immediately following phlebotomy showed that single doses of SAGA lowered glutamine only transiently to nondetectable levels; serial daily doses were required to achieve and maintain continuous glutamine depletion. Reversible depression of the central nervous system, ranging from encephalopathy to coma, occurred in a dose-related manner and was dose limiting. Other prominent reactions included respiratory alkalosis, hyperglycemia, nausea, and vomiting. Transient antitumor effects were noted in two patients with solid tumors and in two patients with leukemia. SAGA causes considerable neurotoxicity in adults which requires close patient monitoring. Phase II studies in leukemic patients are in progress.
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PMID:Phase I evaluation of succinylated Acinetobacter glutaminase-asparaginase in adults. 743 89

Changes in circulatory, ventilatory and acid-base variables were studied in Siberian sturgeon (Acipenser baeri) exposed to acute and severe hypoxia (PWO2 = 10 torr), followed by a rapid return to normoxia. This treatment caused a significant stress, revealed by the high levels of plasma catecholamines and cortisol. The moderate circulatory changes firstly observed would represent the effects of increased plasma catecholamine levels together with an increased adrenergic nervous tone on the cardiovascular system. Then, these effects were masked by a possible vagal reflex resulting in bradycardia. Deep hypoxia induced a ventilatory alkalosis combined with a moderate metabolic acidosis. The latter amplified concomitantly with a massive flush of lactate into the blood stream. The initial hyperventilation was followed by a deep ventilatory depression. During return to normoxia, hyperventilation resumed consistent with the repayment of an oxygen debt. Thus, the sturgeon, although considered as an archaic fish, developed the same adaptative responses as teleosts submitted to comparable hypoxic conditions.
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PMID:Circulatory and respiratory effects of an hypoxic stress in the Siberian sturgeon. 748 Nov 9

Unless renal function is impaired or rhabdomyolysis is severe, hyperkalemia is a relatively uncommon metabolic complication of poisoning. In contrast, marked hypokalemia is a more common problem and may have serious sequelae. Most potassium disturbances in acute poisoning are due to disruption of extra-renal control mechanisms, notably the activity of Na+/K+ ATPase and K+ channels. Hypokalemia occurs because of increased Na+/K+ ATPase activity (e.g. beta 2 agonist, theophylline or insulin poisoning), competitive blockade of K+ channels (e.g. barium or chloroquine poisoning), gastrointestinal losses and/or alkalosis. Hyperkalemia follows inhibition of Na+/K+ ATPase activity (e.g. by digoxin), increased uptake of potassium salts, disruption of intermediary metabolism (e.g. cyanide poisoning), activation of K+ channels (e.g. fluoride poisoning), and the presence of acidosis and rhabdomyolysis, particularly if the latter is complicated by renal failure. Hypokalemia results in generalized muscle weakness, paralytic ileus, ECG changes (flat or inverted T waves, prominent U waves, ST segment depression) and cardiac arrhythmias (atrial tachycardia +/- block, AV dissociation, VT, VF). Hyperkalemia is associated with abdominal pain, diarrhea, muscle pain and weakness, ECG changes (tall peaked T waves, ST segment depression, prolonged PR interval, QRS prolongation) and cardiac arrhythmias (VT, VF). Significant disturbances of potassium homeostasis are often unrecognized and may cause considerable morbidity and mortality. Prompt recognition and appropriate treatment of these disturbances could be life-saving.
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PMID:Disturbances of potassium homeostasis in poisoning. 762 96

Our patient's acid-base disturbance may be among the highest recorded in nonfatal cases of metabolic alkalosis. This case also shows that life-threatening alkalemia can be safely and effectively treated by defining and removing the causes of alkalosis and applying aggressive supportive therapy with fluid repletion and potassium and electrolyte replacement. The need for potentially dangerous therapy such as exogenous acid administration, dialysis, or forced mechanical depression of respiration should not routinely be used on the basis of blood pH alone, and it should never replace thoughtful, organized supportive care.
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PMID:Severe metabolic alkalosis. 797 15

A total of 34 children with normal renal function underwent either gastrocystoplasty or continent urinary reservoirs with stomach at our institutions. Severe hypochloremic hypokalemic metabolic alkalosis developed in 2 patients, manifested by intractable seizure disorder in 1 and altered mental status with respiratory depression in 1. Symptoms developed at 4 and 6 months, respectively. Despite severe alkalosis, urinary pH was less than 5.0 and fractional excretion of chloride remained high in both patients. Resuscitation with sodium chloride, arginine hydrochloride and potassium chloride restored electrolyte balance in less than 48 hours in both patients. Serum gastrin was slightly elevated in 1 patient (137 pg./ml., normal 0 to 125) who responded to long-term histamine-blocker therapy. The other patient had significant hypergastrinemia (624 pg./ml.) with secondary hyperaldosteronism. Maximum doses of histamine blockers, oral replacement of sodium chloride and potassium chloride, and the proton pump inhibitor omeprazole failed to control recurrent bouts of severe hypochloremic metabolic alkalosis. This patient ultimately underwent removal of three-quarters of the gastric augmentation and replacement with ileum. Postoperatively, serum gastrin levels and electrolytes reverted to normal. The pathophysiology of this potentially lethal complication is further discussed.
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PMID:Metabolic complications of the use of stomach for urinary reconstruction. 832 30

Changes in body fluid homeostasis during acute hypoxaemia suggest a crucial role of renal function in acclimatization processes. Hypoxaemia stimulates sympathetic nervous activity, and also the cardiovascular system is affected with increases in heart rate and cardiac output. In most subjects, a hypoxic ventilatory response produces hypocapnia and respiratory alkalosis. Acute hypoxaemia depresses aldosterone secretion secondary to a direct effect on adrenal cells. Also plasma renin is decreased in resting hypoxaemic conditions, but the mechanism remains unknown. These hormonal changes may have the advantage of opposing excessive sodium and water retention, which characterizes acute mountain sickness. Short-term isocapnic or hypocapnic hypoxaemia in spontaneously breathing humans causes moderate if any increases in renal blood flow and only minor changes in GFR. In contrast, renal blood flow and GFR decreases during hypercapnic hypoxaemia. Renal clearance studies in humans after 24-48 hours in altitude hypoxia (4,350 m) demonstrate that glomerular and tubular function is only slightly changed in spite of marked depression of the renin-aldosterone system and increased plasma levels of norepinephrine. However, renal vascular tone may increase most probably secondary to the increased adrenosympathetic activity. In the first hours, acute hypoxaemia may induce an increased excretion of sodium and water. Previous studies suggest that the natriuretic response is caused by decreased reabsorption of sodium and bicarbonate in the proximal tubules secondary to the associated hyperventilation and hypocapnia. After 6 hours, sodium and water excretion is normalized or even depressed, dependent on the severity of acute mountain sickness. In view of the prompt increase in sodium and water excretion found during short-term hypoxaemia, the absence of such a response to more prolonged hypoxaemia suggests an adaptive time-dependent course of renal functional changes in hypoxaemia. Taken together, previous studies suggest that effects of acute hypoxaemia on renal haemodynamics are minor compared with effects on cerebral and coronary circulation. This might be the result of an appropriate resetting of autoregulatory mechanisms that would maintain the role of the kidney as a major sense organ to hypoxaemia and, subsequently, as a mediator of plasma volume regulation and erythropoietin synthesis.
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PMID:Effect of hypoxaemia on water and sodium homeostatic hormones and renal function. 859 71

Systemic toxicity of local anesthetics causes cardiac and central nervous system (CNS) depression that could be enhanced in the presence of respiratory acidosis. We examined a potential suppression of baroreflex function with bupivacaine and ropivacaine during hypercapnic acidosis or hypocapnic alkalosis. Baroreflex sensitivity (BRS) was randomly tested in rats with one of 13 conditions during intravenous administration of saline (control), bupivacaine 1, 2, or 3 mg/kg, or ropivacaine 2, 4, or 6 mg/kg. The effects of bupivacaine (3 mg/kg) or ropivacaine (6 mg/kg) on BRS were also examined during hypercapnic acidosis or hypocapnic alkalosis. The BRS was assessed using a value of delta heart rate/ delta mean arterial pressure after infusion of phenylephrine (3 micrograms/kg). Both bupivacaine and ropivacaine (at the largest dose) significantly suppressed BRS. Acute respiratory acidosis (pHa 7.24 +/- 0.04, Paco2 63 +/- 4 mm Hg) enhanced BRS. The BRS enhanced during acidosis was also suppressed with bupivacaine and ropivacaine, but less so than in the absence of acidosis. The presence of hypocapnic alkalosis (pHa 7.55 +/- 0.03, Paco2 25 +/- 2 mm Hg) did not affect BRS and reversed BRS suppression caused by both drugs. Thus, bupivacaine and ropivacaine affect neuronal control mechanisms for maintaining cardiovascular stability, and acute changes of respiration could significantly modify such suppression.
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PMID:The effects of bupivacaine and ropivacaine on baroreflex sensitivity with or without respiratory acidosis and alkalosis in rats. 902 37

In cattle with hepatic lipidosis, hepatic abscessation, leptospirosis, biliary calculi or fasciolosis, the progression of the disease was studied by serial measurements of serum total bile acid concentrations, plasma glutamate dehydrogenase, gamma-glutamyltransferase, 5'-nucleotidase and leucine aminopeptidase activities Terminalia avicennioides and by liver biopsy. Regardless of the cause of the hepatic disease, weight loss, anorexia, dullness and depression were consistent features. Signs of hepatic encephalopathy, such as blindness, head pressing, excitability, ataxia and weakness were less common and, together with pyrexia and jaundice, were grave prognostic signs. Plasma ammonia concentrations were significantly elevated compared to clinically normal cattle, but such changes were not always accompanied by a decline in plasma urea concentrations. In normal, healthy cattle, the plasma ammonia:urea concentration ratio is 9:1 and the plasma ammonia:glucose concentration is 11:1. In hepatic disease, a plasma ammonia:glucose ratio > 40:1 or plasma ammonia:urea ratio > 30:1, particularly with a rising total ketone body concentration and a declining glucose concentration, carried a guarded prognosis. The study suggested that other factors, such as hypokalaemia, alkalosis, short-chain volatile fatty acids, and false and true neuro-transmitters, may be important in the pathogenesis of hepatic coma in cattle.
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PMID:Clinical and pathological studies in cattle with hepatic disease. 909 45


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