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

Mature newborns reveal the same pulmonal adaption to extrauterine conditions after forceps delivery in general anesthesia for the mother beginning with propanidid or hexobarbital as newborns after spontaneous delivery. Intervalls of apnoe, being physiological during neonatal adaption up to the fourth life-hour, occurred in all three tested groups in the same frequency. Genuine apnoe in combination with following bradycardia and cyanosis couldn't be observed. Moreover during the whole examination time all mean values of respiration frequency were physiological. Therefore we believe that there is no fundamental deterioration of newborns respiration, i.e. a depression in nerve-centre, caused by propanidid or by hexobarbital, despite of repeatedly contrary description.
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PMID:[Effects of various anesthesia procedures used in forceps delivery on the cardiopulmonary adaptation of the newborn infant. 2. Modification of pulmonary adaptation]. 401 51

A 2750-g female infant was born at 36 weeks' gestation to a 40-year-old woman treated with clonazepam throughout her pregnancy. The infant developed apnea, cyanosis, and hypotonia within a few hours of birth. The mother's serum clonazepam level at delivery was 32 ng/mL; the cord blood level was 19 ng/mL. The infant had no congenital malformations, evidence of infection, or seizures. Clinical episodes ceased by ten days of age. The woman elected to breastfeed; breast milk clonazepam levels were between 11 and 13 ng/mL. She was discharged with a cardiorespiratory monitor. The authors suggest that infants of mothers receiving this agent during pregnancy or while nursing have serum levels measured. Additionally, these infants should be monitored for central nervous system depression or apnea.
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PMID:Neonatal apnea associated with maternal clonazepam therapy: a case report. 402 13

To assess the etiology of depressed ventricular function in cyanotic congenital heart disease, an experimental model in immature puppies was devised in which the left atrial appendage is directly anastamosed to the distally banded pulmonary artery. The preparation results in significant cyanosis during a 3-month study period (PO2 = 91 +/- 4 vs 43 +/- 3, hematocrit = 33 +/- 3 vs 55 +/- 5). Compared to age- and weight-matched unoperated controls, cyanotic animals developed significant depression of biventricular ejection fraction (P less than 0.05), increased heart weight indexed for body weight (P less than 0.05), increased right ventricular weight (P less than 0.02), and increased right ventricular free wall thickness (P less than 0.05). There was no alteration in ventricular volumes. In addition, mean myocardial stores of high-energy phosphate compounds were unaltered. The model allows a reproducible level of hypoxemia to be produced in young animals, utilizes no prosthetic materials, and allows future experiments to be performed to ascertain the metabolic response of the cyanotic myocardium to exercise or surgically induced ischemia.
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PMID:A model of cyanotic heart disease: functional, pathological, and metabolic sequelae in the immature canine heart. 648 24

We report here on a case of primary alveolar hypoventilation in a 9 yr old child. From the age of 8 years, the patient has suffered from episodes of bronchopneumonia associated with severe respiratory insufficiency and lethargy. After recovery, cyanosis developed during the night and, later on, during the day. On two occasions, serious respiratory depression followed ketamine sedation for cardiac catheterization and total anaesthesia for cerebral angiography. Pulmonary function tests showed normal volumes and normal mechanics of breathing; blood gas analysis revealed a slight hypercapnic acidosis and hypoxia. The ventilatory response to CO2 was virtually absent, whereas voluntary hyperventilation normalized blood gas values. A polygraphic recording during sleep showed a marked worsening of hypoventilation, which occurred soon after falling asleep and continued throughout all sleep stages; sporadic central apnoeas, at times prolonged, were recorded only during light sleep. The patient, now 14 yr old, is maintained in satisfactory condition with low flow nocturnal oxygen administration combined with the use of a body respirator during sleep twice a week.
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PMID:A polygraphic study of one case of primary alveolar hypoventilation (Ondine's curse). 672 66

A newborn with massive tricuspid regurgitation, atrial flutter, congestive heart failure, and a high serum lithium level is described. This is the first patient to initially manifest tricuspid regurgitation and atrial flutter, and the 11th described patient with cardiac disease among infants exposed to lithium compounds in the first trimester of pregnancy. Sixty-three percent of these infants had tricuspid valve involvement. Lithium carbonate may be a factor in the increasing incidence of congenital heart disease when taken during early pregnancy. It also causes neurologic depression, cyanosis, and cardiac arrhythmia when consumed prior to delivery.
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PMID:Tricuspid valve regurgitation and lithium carbonate toxicity in a newborn infant. 679 56

This report presents our experience with producing a stable chronic hypoxemia preparation in the dog without the disadvantages of prosthetic graft insertion or sacrifice of pulmonary tissue. In 28 adult dogs, the intrapericardial inferior vena cava and the area of junction of the right and left inferior pulmonary veins were exposed through a right thoracotomy. The cava was clamped at the diaphragm and at the right atrium, divided at the atrial clamp, and quickly anastomosed to the inferior pulmonary veins. The mean arterial O2 tension (PaO2) decreased from 83.2 +/- 1.6 mmHg preoperatively in mechanically ventilated (room air) animals to 35.3 +/- 1.5 mmHg postoperatively in awake animals spontaneously breathing room air (P less than 0.001). There was persistent depression of the PaO2 (49.1 +/- 1.8 mmHg) and elevation of the hematocrit (64.8 +/- 2.0%) in six animals tested at 18.5 mo postoperatively. Shunt patency without significant stenosis was confirmed in each animal at autopsy. This method attains predictable and persistent hypoxemia and polycythemia and is simple to perform. It may be useful in studying various aspects of ventricular function and ventricular histological and biochemical changes with chronic cyanosis.
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PMID:A reproducible model of chronic hypoxemia. 684 63

Signs of acute hemolytic anemia developed in 4 adult horses from 2 Georgia farms 3 to 4 days after the ingestion of wilted leaves from cut red maple trees (Acer rubrum). Clinical findings included weakness, polypnea, tachycardia, depression, icterus, cyanosis, and brownish discoloration of the blood and urine. Blood changes included methemoglobinemia, free plasma hemoglobin, decreased pcv, and Heinz bodies in erythrocytes. These findings plus hemoglobinuria suggested intravascular hemolysis. Three of the 4 horses diet 5 to 7 days after ingestion of the leaves. Gross pathologic changes included generalized icterus, splenomegaly and swollen, black kidneys. Microscopic changes including tubular nephrosis with hemoglobin casts, vacuolization of centrilobular hepatocytes, and sequestration of erythrocytes in splenic sinusoids. A disease indistinguishable from the field cases was induced in a pony by the oral administration of dried, ground red maple leaves at a dosage of 1.5 g/kg. The findings of methemoglobinemia, hemolysis, and Heinz bodies suggested that the toxic principle of the red maple leaf was an oxidant.
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PMID:Hemolytic anemia in horses after the ingestion of red maple leaves. 705 81

Documented observations of a 5-week-old infant during a "near miss" for a Sudden Infant Death Syndrome (SIDS) episode by a physician were carried out during an in-hospital physiological recording of respiratory and cardiac activity. This "near miss" event occurred during quiet sleep and was characterized by a prolonged apneic attack with marked bradycardia, cyanosis and limpness which required immediate vigorous resuscitative efforts by a physician and trained nurse. Parental descriptions of similar events parallel these documented sudden unexpected changes in cardiorespiratory parameters. Objective polygraphic data were obtained immediately following the episode and at later ages during 24 and 48 hour continuous recordings of respiration, heart rate, sleep/wake and behavioral activity. The data show that numerous apneic episodes occurred following the "near miss" event, many accompanied by marked bradycardia. The moderately severe hypoxemia noted during these sleep-related apneas indicate that immediate intervention is required to prevent significant hypoxia and central depression in such infants.
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PMID:Respiratory and cardiac events observed and recorded during and following a "near miss" for Sudden Infant Death Syndrome episode. 716 85

Acute acetaminophen intoxication in the cat was studied to characterize the antidotal profile of acetylcysteine. Toxicosis was associated with cyanosis, hyperventilation, depression, and facial edema. Abnormal laboratory findings were methemoglobinemia and elevated serum glutamic-pyruvic transaminase activity. In one trial, each of ten cats was given a 325-mg tablet of acetaminophen, then another after 4 hours. Five of the cats were given antidotal treatment with acetylcysteine (140 mg/kg, per os) at the time of the second dosing with acetaminophen and at 8-hour intervals thereafter for a total of three treatments. All treated cats survived. Two of the untreated cats died. In another trial, doubling each dose of acetaminophen (650 mg) proved fatal in all of four untreated cats. When antidotal therapy was initiated at the time of the second dosing with acetaminophen and repeated at 8- or 4-hour intervals for three treatments, two of four cats in each treatment group survived. Although antidotal therapy was associated with a return of serum glutamic-pyruvic transaminase and methemoglobinemia values toward normal, only the methemoglobin value was a reliable prognostic indicator.
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PMID:Acetylcysteine for treatment of acetaminophen toxicosis in the cat. 740 22

The immature heart is more tolerant to ischemia than the adult heart, yet infants with cyanosis show myocardial damage after surgical correction of congenital cardiac defects causing hypoxemia. This study tested the hypothesis that the hypoxemic developing heart is susceptible to oxygen-mediated damage when it is reoxygenated during cardiopulmonary bypass and that this hypoxemic/reoxygenation injury is more severe than ischemic/reperfusion stress. Fifteen Duroc-Yorkshire piglets (2 to 3 weeks old, 3 to 5 kg) underwent 60 minutes of 37 degrees C cardiopulmonary bypass. Five piglets (control) were not made ischemic or hypoxemic. Five underwent 30 minutes of normothermic ischemia (aortic clamping) and 25 minutes of reperfusion before cardiopulmonary bypass was discontinued. Five others underwent 30 minutes of hypoxemia (bypass circuit primed with blood with oxygen tension 20 to 30 mm Hg) and 30 minutes of reoxygenation during cardiopulmonary bypass. Functional (left-ventricular contractility) and biochemical (levels of plasma and tissue conjugated dienes and antioxidant reserve capacity) measurements were made before ischemia/hypoxemia and after reperfusion/reoxygenation. Cardiopulmonary bypass (no ischemia or hypoxemia) caused no changes in left-ventricular function or coronary sinus levels of conjugated dienes. The tolerance to normothermic ischemia was confirmed, inasmuch as left-ventricular function returned to 108% of control values and coronary sinus levels of conjugated dienes did not rise after reperfusion. Conversely, reoxygenation raised plasma levels of conjugated dienes in coronary sinus blood in the hypoxic group 57% compared with end-hypoxic levels (p < 0.05 versus end-hypoxic levels and versus ischemia, by analysis of variance). Antioxidant reserve capacity showed the lowest levels (highest production of malondialdehyde) in the hypoxemic group (51% higher than control values; p < 0.05 by analysis of variance). These biochemical changes were associated with a 62% depression of left-ventricular function after bypass because end-systolic elastance recovered only 38% of control levels (p < 0.05 by analysis of variance). These data confirm the tolerance of the immature heart to ischemia and reperfusion and document a hypoxemic/reoxygenation injury that occurs in immature hearts reoxygenated during bypass. Hypoxemia seems to render the developing heart susceptible to reoxygenation damage that depresses postbypass function and is associated with lipid peroxidation. These findings suggest that starting bypass in cyanotic immature subjects causes an unintended reoxygenation injury that may potentially be counteracted by adding antioxidants to the prime of the extracorporeal circuit.
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PMID:Studies of hypoxemic/reoxygenation injury: without aortic clamping. III. Comparison of the magnitude of damage by hypoxemia/reoxygenation versus ischemia/reperfusion. 747 69


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