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)

In 4 dogs injected intravenously (i.v.) with 125I labeled fibrinogen, 51Cr labeled platelets and 99mTc labeled albumin, and subjected to successively increasing amounts of i.v. infused monomethylmethacrylate, doses corresponding to the amounts released into the blood stream following implantation of acrylic cement during total hip replacements did not affect the clotting mechanism, did not cause trapping of platelets and fibrin in the lungs, did not generate fat emboli, and did not cause depression of the arterial oxygen tension or blood pressure. Monomethylmethacrylate in whole blood was associated with both blood cells and plasma.
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PMID:Effects of graded infusions of monomethylmethacrylate on coagulation, blood lipids, respiration and circulation. An experimental study in dogs. 0 Jan 68

In healthy, closed-chest dogs, dose-dependent depression of ventricular function was produced by the anesthetics halothane, methoxyflurane, and fluroxene, as evidence by decreases in left venticular stroke volume, stroke work, dP/dt, and an increased enddiastolic pressure. Myocardial blood flow and oxygen consumption decreased concomitantly and were correlated with aortic blood pressure decreases. There was no change in myocardial lactate extraction with halothane and methoxyflurane, suggesting that myocardial oxygenation was adequate in spite of the decrease in blood flow. However, even with marked increases in arterial lactate concentration during fluroxene anesthesia, extraction did not chance and, in fact, tended to decrease. The hemodynamic effects of halothane and methoxyflurane are similar to those previously reported in man, but those of fluroxene are different. Consequently, clinical speculation from these results is not justified at this time.
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PMID:Effects of inhalation anesthetics on cardiac function and metabolism in the intact dog. 0 33

Fifty healthy mothers, with normal placental function, were anaesthetised with ketamine for Caesarean section. Anaesthesia was maintained with nitrous oxide, oxygen, muscle relaxants and controlled ventilation. Surgery was conducted in the lateral tilt position. Arterial blood samples were drawn from the mothers, and from the vessels of a double clamped section of umbilical cord, for blood-gas analysis. Results obtained were compared with those of a previous series anaesthetised with thiopentone, nitrous oxide, oxygen and muscle relaxants. Eight infants were clinically depressed, judged on the basis of their modified Apgar score 2 minutes after delivery. The average time to sustained respiration (TSR) was 58.1 seconds. The mean maternal pH and base excess values in the ketamine group were significantly greather than those reported after thiopentone anaesthesia. Mean Uv and Ua pH levels were also significantly higher after ketamine; in contrast, the average fetal base excess values did not differ from those obtained previously with thiopentone. The mean (Ma-Uv) and (Ma-Ua), pH gradients were 0.019 and 0.025 pH units greater respectively in the ketamine group compared to the thiopentone (P less than 0.005). The average (Uv-Ua) PO2 gradient was 3.4 mmHg less after ketamine anaesthesia (P less than 0.005). A significant inverse correlation was observed relating the I-D interval to the Ma and Ua pH values. Maternal arterial base deficit values appeared to increase with delay in delivering the fetus. Prolongation of the uterine incision to delivery (U-D) interval was associated with a decrease in Ua pH and base excess values. (Ma-Ua) pH and base excess gradients increased with lengthening of the U-D interval. No convincing evidence of awareness during anaesthesia was found during the study. Five patients, appeared to be hallucinated in the immediate post-anaesthetic period. Unpleasant dreams were reported in 5 instances. In this study ketamine appeared to be unassociated with significant biochemical asphyxia, but may have been responsible for some element of drug induced neonatal depression. In view of our own experience and that of other workers, it is suggested that ketamine induction for Caesarean section should be re-evaluated using a lower dose of the drug.
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PMID:Anaesthesia for Caesarean section with ketamine. 0 39

Their frequency is estimated with difficulty, although on autopsy pulmonary edema is found almost routinely. It is a major complication of overdoses (48 p. 100 of severe intoxications). Their formation can be suspected, when after the first phase of respiratory depressions, with coma, myosis, and a variable latent period, a second attack of respiratory insufficiency occurs with tachypnea, and cyanosis. The chest X-ray shows diffuse alveolar infiltration, sparing the apices. The heart being generally of normal size. Rapid disappearance of this infiltrate (24 to 48 hours) enables the elimination of two diagnoses: pneumonia due to inhalation of gastric fluid, an infectious pneumonia. Their pathogenesis remains very debatable: - in the majority of cases abrupt L.V.F. can be eliminated: -on the other hand it could be an allergic accident of the anaphylactic type, or local liberation of histamine, or a local toxic action on the pulmonary capillaries; - hypoxia, secondary to respiratory depression, could lead to pulmonary edema, by the same mechanism as at altitude; - finally, owing to the central neurological disorders a neurogenic theory can be put forward. Their treatment is essentially a combination of Nalorphine with oxygen therapy (by mask, or if necessary by assisted, controlled ventilation) with prevention of inhalation of gastric fluid (gastric emptying) or curative treatment of possible aspiration by antibiotics, and cortico-steroids. Diuretics can be useful, as well as cardiotonics.
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PMID:[Pulmonary edemas due to acute heroin poisoning]. 0 75

Controlled, dosed, uninterrupted and continuous oxygen treatment was applied in 63 patients with global respiratory insufficiency, through a nasopharyngeal catheter in concentrations to 30 per cent. PaO2, is elevated with and average of 12 mm mercury column after 30 minutes 25% oxygen breathing and PaCO2--at an average of 8 mm mercury column. PaO2 level was kept after 24 hours whereas PaCO2 decreased at an average of 4 mm mercury column. Besides, respiration and pulse rate are decelerated, secondary polyglobulia decreases, cardiac and renal function is improved. Those changes are interpreted as patients' adaptation to oxygen breathing. The adaptation to oxygen breathing decreases the danger of critical intensification of the respiratory depression in the course of the treatment and conditions for a successful application of O2 treatment at home are created.
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PMID:[Adaptation to oxygen breathing]. 1 37

This study tests the hypothesis that postischemic myocardial depression can be reduced by providing an initial reperfusate pH which is appropriate for myocardial temperature (i.e., metabolic systems function optimally when pH is kept slightly alkaline to the neutral point, which changes with temperature in concordance with the pK of water). Ten dogs underwent 1 hour of ischemic arrest with topical hypothermia (intramyocardial temperature 16+/-2 degrees C). The initial reperfusate (500 cc of blood from the extracorporeal circuit) was infused (100 cc/minute) into the proximal aorta just before removing the cross-clamp. Reperfusate pH was kept at 7.4 in five dogs (control) and raised to 7.8 with THAM [tris (hydroxymethyl) aminomethane] in five dogs. Measurements 30 minutes after reperfusion showed that raising reperfusate pH to 7.8 resulted in (1) higher subendocardial blood flows (109+/-20 vs 61 cc+/-8 cc/100 gm/minute), (2) redistribution of postischemic blood flow toward the subendocardium (endocardial/epicardial flow 1.25+/-0.1 vs 1.0+/-0.03), (3) higher left ventricular oxygen uptakes (0.046 vs 0.033 cc/100 gm/beat), (4) better postischemic left ventricular compliance (56+/-3% more compliant), and (5) improved left ventricular performance (88+/-7% recovery vs only 57+/-3% recovery at pH 7.4). Postischemic edema (2% water gain) was unchanged by pH modification. We conclude that initial reperfusion with the appropriate pH provides an optimal milieu for restoration of cellular metabolism, counteracts the acidosis of ischemia, and improves postischemic left ventricular blood flow, distribution, oxygen uptake, compliance, and performance.
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PMID:Studies on myocardial reperfusion injury. I. Favorable modification by adjusting reperfusate pH. 1 28

Halothane, methoxyflurane, and enflurane produce dose-dependent depression in ventricular function in the dog. Myocardial blood flow and oxygen consumption are decreased accordingly without evidence of myocardial tissue hypoxia. Low-dose fluoxene does not depress the heart, while there is less depression with high-dose fluroxene than with the other anesthetics. In spite of this depression, myocardial blood flow was unchanged, and the decreased oxygen consumption during high-dose fluroxene was a result of decreased oxygen extraction by the heart. Sympathetic nervous system stimulation produced by fluroxene anesthesia is probably responsible for these effects, but further work is necessary for confirmation of this hypothesis.
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PMID:Dose-dependent depression of cardiac function and metabolism by inhalation anesthetics in chronically instrumented dogs. 2 4

Model systems of respiratory infection in mice were established with Streptococcus pneumoniae, influenza virus, and Mycoplasma pulmonis. The LT50 for S. pneumoniae was 2 1/2 days, for lethal influenza 6 days, and for M. pulmonis 5 days. Morbidity in sublethal influenza infections reached a peak during days 5 to 10, with recovery indicated by the third week. The course of each pulmonary infection was followed by use of the animal's maximal ability to consume oxygen (VO2max by determining the weight, compliance, and stability of the excised lung, and in some cases by following O2 consumption of minced tissue. Depression of VO2max began early in each infection; reductions ranged from 9% at the peak of sublethal influenza infection to 50% 12 to 48 hr before the LT50 of fatal infections. The depressions were not relieved by 100% O2. The noninvasive VO2max test, evoked by cold air, was simple, rapid, and reproducible and appeared to serve as a quantitative measure of over-all function during infection. Each type of infection caused an increase in lung weight, with the largest noted during fatal Mycoplasma illness and lethal influenza. The effects on lungs by influenza and M. pulmonis infections were similar but could be differentiated from those with S. pneumoniae. With sublethal influenza, CL was reduced 30% between days 5 to 10, with recovery by the third week. Ctis was not affected. M. pulmonis infections and lethal influenza caused depressions in CL of over 60% by day 4 but only a 30% decrease in Ctis. The data suggest that the decreased compliance in influenza and M. pulmonis infections was due primarily to increased surface tension. In contrast, S. pneumoniae did not affect compliance.
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PMID:Oxygen uptake and lung function in mice infected with Streptococcus pneumoniae, influenza virus, or Mycoplasma pulmonis. 2 1

Complete global ischemia was produced in 39 dogs by temporary ligation of the aorta. Prior to the ischemic episode, pentobarbital (30 to 45 mg per kilogram of body weight) was administered to 19 of these dogs. The neurological effects of cerebral ischemia episodes lasting 8, 9, or 10 minutes were compared in dogs treated with pentobarbital and those not treated. At 48 hours following the ischemic episode most of the dogs made ischemic for 8 minutes were normal, whereas most animals made ischemic for 10 minutes were dead or comatose. The 9-minute ischemic period resulted in a relatively even distribution of normal and damaged dogs. There were no differences between treated and untreated dogs. Cerebral blood flow, cerebral metabolic rate for oxygen, and various cerebral metabolites were measured in dogs surviving 48 hours. Again, there were no differences between treated and undertreated dogs. We conclude that barbiturates provide no protection in this model of complete global ischemia. This conclusion supports the hypothesis that the likely mechanism of barbiturate protection in models of incomplete ischemia or hypoxia is based on cerebral metabolic depression; such a mechanism would not be expected to be effective in complete global ischemia.
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PMID:No barbiturate protection in a dog model of complete cerebral ischemia. 3 25

Vectarion has a powerful respiratory stimulant effect in animals and in man which is manifested by a significant and lasting increase in ventilation, as shown by a marked lowering of arterial P. CO2 and an increase in blood pH. This activity is maintained in dogs with experimental alkalosis or acidosis as well as during morphine or oxygen-induced respiratory depression. This respiratory stimulating action originates at the level of the aortic and carotid chemo-receptors: this explains why Vectarion is devoid of any epileptogenic risk. The aim of the present study was to demonstrate the peak of activity and duration of action of an intravenous perfusion of Vectarion, in such a way as to be able to plan administration all through the day and night.
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PMID:[Kinetics of action of Vectarion. Ventilatory chemo-stimulant (author's transl)]. 3 8


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