Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-seven cases of sinusoidal fetal heart rate were studied. This group had a mean scalp pH of 7.288, significantly lower (p less than 0.005) than that of the control group. The mean one-minute Apgar score was 7.148, significantly lower (p less than 0.001) than the control group's mean score. Almost half (48,15%) of the fetuses had a one-minute Apgar score of 7 or less. Every fetus was viable. Amplitude of the pattern was found to correlate with neonatal depression, the larger the amplitude, the more profound the depression. Over 96% of the fetuses had cord-related deceleration patterns, and nearly 63% had obvious cord complications. It is postulated that sinusoidal patterns are an umbilical cord-related phenomenon, resulting from an alternating hypovolemia and hypervolemia. Clinicians are urged to scrutinize carefully any cases of this pattern, and perform an immediate fetal scalp blood pH determination. If the pH determination obtained is less than 7.25, the authors suggest intervention and operative delivery.
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PMID:The significance of sinusoidal fetal heart rate pattern during labor and its relation to fetal status and neonatal outcome. 3 1

Blood volume and clinical data are reported on 8 premature and 3 full-term infants who presented with symptoms apparently due to polycythemia or hypervolemia. These cases termed 'symptomatic neonatal plethora' were caused by large placental transfusions associated with delayed clamping of the umbilical cord. Tachypnea, mild cyanosis, plethoric skin color, and neurological depression persisted on average for 30 h after birth. Chest X-rays showed mild cardiomegaly, pulmonary congestion and edema, and pleural effusions. Although the course was in general benign, phlebotomy was considered to be indicated in three infants to treat progressive clinical deterioration. The symptomatology and blood volume on these infants were compared with infants in an ongoing study with controlled time of cord clamping. Neonatal plethora must be considered as one cause of 'transient tachypnea of the newborn'.
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PMID:Symptomatic neonatal plethora. 90 82

Functional reserves of the cardiovascular system during sharp depression of the cardiac output in the postreanimation period after 15-minute cardiac arrest were studied in experiments on dogs (by loading with different fluid volumes). Acute hypervolemia did not produce any circulatory decompensation. Reinforcement of venous return and changes in the peripheral circulation due to polyglucine loading augmented the CVP temporarily, and produced a stable increase of the AP, of the cardiac output, systolic volume, the work of the left cardiac ventricle and of the total oxygen consumption by the organism. Meanwhile there was a decrease of the peripheral vascular resistance. In model experiments on dogs, which sustained 20-minute isolated compression ischemia the syndrome of low cardiac output developed too. This indicated the relation of this phenomenon to the disorders in the neuro-humoral regulation of blood circulation.
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PMID:[Pathogenesis of the low cardiac output syndrome in postreanimation states]. 95 32

We used differential solute clearances and a theoretical analysis of glomerular ultrafiltration and dextran sieving to characterize the hemodynamic response of nine healthy humans to infusion of isoncotic, 5% albumin in saline or saline vehicle alone. During albumin infusion (10.2 +/- 0.2 ml.kg-1.30 min-1) plasma volume increased by 18%, but oncotic pressure rose by only 0.8 mmHg. Despite the hypervolemia, renal blood flow (RBF) declined by 140 ml/min and glomerular filtration rate (GFR) declined by 16 ml/min during the infusion. RBF increased progressively postinfusion, exceeding baseline by 135 ml/min after 4 h; GFR was restored to baseline. Although oncotic pressure declined by 2 mmHg, a similar transient decline in GFR (-13 ml/min) was associated also with infusion of saline vehicle alone (9.4 +/- 0.3 ml.kg-1.30 min-1), which increased plasma volume by 9%. Sieving coefficients of dextrans (radius 32-42 A) were lowered during and after either infusion, a phenomenon that we compute to reflect a reduction in glomerular pore size. Assuming that the transcapillary hydraulic pressure difference was not lowered, we calculate that there was a simultaneous depression of the ultrafiltration coefficient (Kf) during volume expansion with saline and possibly also to a lesser extent with albumin. The hypofiltration during either infusion delayed the onset of a natriuretic response until the filtered sodium load was restored to baseline in the postinfusion period. We propose that the net effect of changes in intracapillary pressures and Kf during volume expanding infusions is to transiently lower GFR, thereby preventing the human kidney from mounting an immediate natriuretic response to acute hypervolemia.
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PMID:Filtration dynamics and natriuretic response to volume expansion in humans. 138 Jul 73

Blood volume and whole kidney and single nephron function were evaluated 2 and 10 days after nephrotoxic serum nephritis (NSN) induction in Wistar rats. Progressive proteinuria, hypervolemia and edema were observed in NSN rats. Sodium retention was associated with a progressive depression of single nephron glomerular filtration rate and elevated fractional tubular reabsorption rates. Since hypervolemia rather than hypovolemia was observed in this study, edema formation must have been a consequence of intrarenal rather than extrarenal phenomena.
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PMID:Progressive hypervolemia despite hypoproteinemia and massive edema formation in rats with nephrotoxic serum nephritis. 169 61

Outpatient arthroscopic knee surgery carries with it certain risk factors similar to those accompanying other major knee procedures. These risks may be related to the complexity of the procedure, exposure to anesthesia, or risk factors from previous medical history. Two cases of acute pulmonary edema following arthroscopic knee surgery in otherwise healthy teenage athletes are presented. Both patients developed acute respiratory distress in the recovery room after uneventful arthroscopic knee surgery. The patients in both cases recovered and were able to return to sporting activity with no sequelae. The similarities in both cases prompted a retrospective investigation of the events from the induction of general anesthesia to the admission of the patients to the intensive care unit. Several possible causes of acute post-operative pulmonary edema include fluid overload, cardiac arrhythmia, respiratory depression, systemic drug reaction and sickle cell trait or disease. Outpatient arthroscopy still remains the procedure of choice for meniscal pathology of the knee, but the surgeon and the anesthesia personnel must be aware of and prepared for pulmonary complications that may arise in the immediate post-operative period.
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PMID:Post-arthroscopic pulmonary edema in two healthy teenage athletes. 202 15

The influence of a 6-week treatment of female Wistar rats with one-kidney, one clip (1-K, 1 C) renal hypertension, with the calcium antagonist nifedipine on plasma volume, red cell Na+ handling and plasma atrial natriuretic peptide immunoreactivity (ANP-IR) was studied. Measurements were performed at 2 and 6 weeks after surgery. In 1-K, 1 C rats plasma volume was increased and red cell Na+ pump activity was reduced only after 2 weeks. Blood pressure, heart weights and plasma ANP were massively increased after both 2 and 6 weeks. 1-K, 1 C-rats treated with nifedipine had normal plasma volume, plasma ANP, and red cell Na+ pump activity in comparison with sham-operated rats. Increases in blood pressure and heart weights were attenuated. It is concluded that 1-K, 1 C hypertension in the rat is associated with cardiomegaly, rise in plasma ANP, initial hypervolemia and depression of the membrane Na+ pump. Nifedipine prevents the occurrence of hypervolemia and secondary phenomena such as rises in plasma ANP and cardiomegaly. This may play an important contributory role in the prevention of pathological sequelae.
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PMID:Modulation by chronic nifedipine of plasma atrial natriuretic peptide, cell Na+ transport and plasma volume in rats with renal hypertension. 284 89

We recently showed that patients with compensated cirrhosis can dispose of their fluid overload while reclining. In contrast, patients with ascites fail to develop supine-induced natriuresis. To assess the effect of reclining on renal sodium handling in patients with advanced cirrhosis and the mechanisms blunting natriuresis in this situation, renal function and plasma concentrations of atrial natriuretic factor, aldosterone and norepinephrine were evaluated in 10 nonazotemic patients with cirrhosis and ascites and 10 healthy controls standing for 2 h and reclining for 2 h. While standing, all patients showed marked sodium retention and significantly elevated plasma atrial natriuretic factor levels, aldosterone and norepinephrine. Glomerular filtration rate did not differ from healthy controls. The reclining increased renal sodium excretion in both groups, but this change was far less marked in patients; natriuresis only rose to the control range in two of them. An increase in atrial natriuretic factor and a depression of plasma aldosterone and norepinephrine was seen in both controls and patients. In the latter, despite the greater change in atrial natriuretic factor and aldosterone, the aldosterone to atrial natriuretic factor ratio, which was inversely correlated with natriuresis during both standing and reclining remained significantly elevated. In the two patients who achieved normal natriuresis during reclining, reclining was associated with both the normalization of the aldosterone/atrial natriuretic factor ratio, and with an increase in glomerular filtration rate. The supine-induced increase in atrial natriuretic factor was not only preserved but was even enhanced in cirrhosis with ascites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal sodium handling in cirrhosis with ascites: mechanisms of impaired natriuretic response to reclining. 769 37

A 39-year-old man was diagnosed as having acute myeloid leukemia and received 6 courses of chemotherapy. The bone marrow revealed complete remission. He had no prior history of cardiac or pulmonary disease. HLA-matched unrelated bone marrow transplantation (BMT) was performed in September 1995. Pre-transplant studies including chest X-ray, electrocardiogram and pulmonary function test were normal. The procedure of BMT was smooth and serial bone marrow examination showed successful engraftment. Serial chest X-rays done every week after BMT were normal. There were no evidence of fluid overload but severe mucositis was noted. On the 38th day after BMT, intravenous injection of 10 mg morphine was prescribed to relief severe oral pain. Respiratory depression developed right after, and naloxone 0.4 mg was given by an intravenous route. One hour later, severe shortness of breath was noted and the emergent chest X-ray revealed acute pulmonary edema. He became unconscious 2 hours later and expired 24 hours after naloxone injection in spite of intensive medical treatment. Naloxone-induced acute pulmonary edema is an extremely rare but lethal complication. Only a few cases have been reported in English literature. We report a case of acute myeloid leukemia receiving unrelated BMT to develop acute pulmonary edema rapidly after intravenous injection of naloxone. The clinical features and pathogenesis are discussed.
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PMID:Lethal acute pulmonary edema following intravenous naloxone in a patient received unrelated bone marrow transplantation. 943 52

Normal physiological changes in the cardiovascular system in pregnancy such as increase in cardiac output, vasodilatation and hypervolemia are of clinical relevance as they are able to aggravate, mask or even imitate cardiovascular diseases. There is an increase of cardiac size and volume during pregnancy; furthermore hormonal changes lead to diaphragmatic elevation and barrel-shaped thorax followed by a rotation of the cardiac axis to the left (15 degrees-30 degrees). Cardiac topography and size, changes in cardiac functioning and physiology as well as hemodynamic changes lead to auscultatory and ECG changes (i.e. S1-Q3-type, ST-depression, T wave flattening). In addition there is a high incidence of functional systolic and diastolic sounds during pregnancy, which are also able to imitate cardiovascular diseases. The physiological changes in pregnancy are similar to those under heavy exercise. This results in continuous cardiac stress during the whole pregnancy. This stress is specifically high from the 28th to the 34th week of pregnancy and in the post-partum period; the maximum of cardiac stress is reached during labor. Important for the specific cardiac risk during pregnancy is not the type of heart disease but cardiac functioning and the severity of complaints before pregnancy. Principally it has to be expected that preexisting heart diseases will experience an aggravation of one grade according to NYHA during pregnancy. In cases of heart diseases with shunt defects, with shunt defect and injured myocardium, with continuous arrhythmia or atrial fibrillation, patients are at extremely high risk of cardiac death. A termination of pregnancy should be considered in all patients with heart diseases grade III or IV according to NYHA, severe pulmonary hypertension, Eisenmenger's syndrome, severe aortic or pulmonary stenosis, Marfan's syndrome, and severe continuous cardiac insufficiency. The drug therapy of cardiac diseases during pregnancy depends on the specific type of heart disease. Prescription of most drugs is principally possible during pregnancy and breast feeding. However, for most drugs there is only very limited therapeutic experience during this period. Definitively contraindicated during pregnancy and breast feeding are ACE inhibitors, angiotensin I and II blocking agents, vasopeptidase inhibitors and molsidomin, a NO-prodrug. In life-threatening conditions, however, sometimes it will be necessary to administer drugs with only poor experiences in pregnancy.
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PMID:[Risks of pharmacotherapy in heart diseases in pregnancy]. 1137 45


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