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)

To clarify the mechanisms involved in the ventilatory response to the inhalation of low concentrations of CO (0.18-0.22% in air), the roles of the arterial chemoreceptors and the forebrain structures have been investigated in unanesthetized adult cats. The ventilatory response was observed in conscious animals intact, after carotid denervation (CD), and after midcollicular decerebration. The results show that the initial small ventilatory depression was unaffected by CD but that the subsequent characteristic tachypnea was blunted after CD even after more prolonged exposure to CO. The CO tachypnea was not observed after decerebration, but a residual hyperventilation was noted with the higher concentration used. It may be concluded that carotid chemoreceptors do not mediate the CO tachypnea, which may then originate in suprapontine structures as shown by comparison of intact and decerebrate animals. The blunting of the tachypnea after CD may be caused by the relative hypercapnia observed in CD animals. The residual hyperventilation observed in decerebrate animals may be caused by central acidosis and/or some peripheral potentiation of chemoreceptor activity resulting from the decrease in arterial blood pressure that accompanied CO inhalation in decerebrate animals.
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PMID:Effects of carotid denervation and decerebration on ventilatory response to CO. 226 65

Effects of opioid kappa agonist ethylketazocine (EKC), sigma agonist (+-)-N-allylnormetazocine (NANM), and naloxone alone and in combination on mean blood pressure (MBP), heart rate (HR), respiratory rate (RR) and minute volume (MV) were studied in acutely decerebrated dogs. EKC (0.5 mg/kg) decreased HR, MBP, RR and MV. Post-EKC NLX increased RR and MV and reversed the bradycardia and hypotension produced by EKC. NANM (1 mg/kg) produced respiratory depression and tachycardia without changing MBP. Post-NANM NLX antagonized tachycardia, increased MBP, however did not significantly change RR and MV. When decerebrate dogs were spinalized at the C-1 level, EKC decreased MBP and HR. These effects were antagonized by NLX. NANM did not change HR but raised MBP in spinalized decerebrate dogs. Since EKC- and NANM-induced cardiovascular and respiratory depression were not observed in conscious intact or chronic spinal dog, it is suggested that: 1) kappaergic system rostral to mesencephalon may play a role in counteracting these depressant effects of EKC; 2) sigma receptor-mediated tachypnea and tachycardia are dissociable; the tachypneic effect may be mediated through higher center while the medulla oblongata is involved in producing tachycardia. These results also suggest that (+-)-NANM probably has several mechanisms of action at several brain sites in producing its effects on respiration and cardiovascular function.
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PMID:Cardiovascular and respiratory effects of an opioid kappa agonist ethylketazocine and sigma agonist N-allylnormetazocine in acutely decerebrated dogs. 269 44

Qualitative and quantitative evaluations of the cellular components of bronchoalveolar washings of calves with experimental parainfluenza-3 virus pneumonitis and control calves were made. Calves were exposed to 10(9) TCID50 of PI-3 by intranasal aerosol exposure and bronchoalveolar cells obtained 7 days after infection by volume-controlled bronchopulmonary lavage. Transient tachypnea and pyrexia occurred in all infected calves, and virus was recoverable at 7 days from nasal swabs and lung tissue. Pulmonary lesions were typical of viral pneumonitis, characterized by patchy alveolitis and bronchiolitis with accumulations of cells and inflammatory debris. The mean total lavage cell yield was elevated in the virus-infected calves, and the percentage of neutrophils was elevated (P less than 0.05). Increased numbers of pulmonary alveolar macrophages (PAM) were also recovered but the difference was not significant. Linear regression equations showed that a decreased proportion of PAM from virus-infected animals were phagocytic. The mean initial phagocytic rates of macrophages from calves with viral pneumonitis were significantly decreased (P less than 0.05) over controls. This difference was concentration dependent and required a phagocytic stimulus in excess of 12.5 X 10(6) beads/ml. Studies of phagocytic kinetics showed that PAM from calves with viral pneumonitis had a lower Vmax than PAM from control calves, but that Km values were comparable. No differences in PAM beta-glucuronidase and acid phosphatase activity were observed. These results indicate depressed phagocytic function in PI-3 virus-inflamed lungs relative to controls. In concert with virus-induced airway lesions, such in vivo depression of PAM phagocytic functions would be expected to depress pulmonary particulate clearance and lung defense mechanisms.
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PMID:Alveolar macrophage phagocytic kinetics following pulmonary parainfluenza-3 virus infection. 303 12

The mycotoxin citreoviridin (CIT) isolated from Penicillium citreoviride was studied to elucidate the mechanism of its toxic actions. In CF#1 mice, near lethal doses of CIT decreased motor activities, body temperature and had cataleptic effects. Male mice appeared to be more susceptible to CIT and had lower subcutaneous (sc) LD50 values and longer CIT-induced hypothermia and hypokinesia. In CIT-treated mice the weights and histology of liver, kidneys and adrenals were normal one week after sc treatment, except for the increased adrenal weights in female mice. Single doses of CIT (sc), given on either day 4 or 5 of pregnancy (perinidation period), had no adverse effect on the rates of pregnancy, implantation of ova and embryonal resorptions in those mice examined on day 12 of pregnancy. CIT (40 mg/kg ip) produced a brief electro-encephalographic (EEG) activation, cardiac sinus arrhythmias and tachypnea in the rabbit. Intravenous (iv) lethal doses of CIT (greater than or equal to 5 mg/kg) caused an EEG activation followed by high voltage delta waves, increased the T wave in the electrocardiogram (ECG) and depressed the respiratory amplitude. The death caused by iv CIT started with the respiratory arrest, followed by isoelectric EEG and ECG was the last to stop. In urethane-anesthetized rabbits CIT decreased the blood pressure, and in succession it lowered, flattened and inverted the T wave of ECG suggesting heart ischemia. These observations indicated that the toxic effects of CIT resulted from respiratory and cardiovascular failures (apnea, delta EEG waves, sinus arrhythmia, hypotension) leading to central nervous system depression due to systemic hypoxia.
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PMID:Toxicity of citreoviridin. 325 34

Ketamine was the normal anaesthetic drug for carrying out the baths of severely burnt patients. It was compared with propofol in a study of 50 patients (greater than 50 UBS) randomly assigned to two groups: 2.5 mg . kg-1 propofol and 2 mg . kg-1 ketamine. The speed of induction was the same for both groups, surgery beginning within the same time intervals. In the propofol group, however, apnoea was seen more often and lasted longer (p less than 0.05) than in the ketamine group. The times between repeat injections were short (about 5 min) and constant with propofol, whereas they were larger and irregular with ketamine; this was due to the shorter distribution half-life and lack of accumulation of propofol. During anaesthesia with propofol, haemodynamic parameters remained steady after an initial period of cardiovascular depression. Respiratory rate increased, because of the lack of analgesia. Recovery was very quick, complete and with no bothersome adverse effects in the propofol group. These hypercatabolic patients could therefore be fed early postoperatively; also, there was no deleterious psychological interference in these deeply disturbed patients.
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PMID:[Comparative trial of propofol and ketamine in anesthesia for the baths of severely burnt patients]. 330 50

The pathophysiology, clinical features, and management of cyanide toxicity are reviewed and sources of cyanide are listed. Cyanide is a deadly poison that is found in many foods and household and industrial products, including some that are readily available. Cyanide binds with cytochrome oxidase, the enzyme responsible for oxidative phosphorylation, and paralyzes cellular respiration. Because the tissues cannot use oxygen that is delivered, aerobic metabolism ceases. The signs and symptoms of cyanide poisoning reflect the extent of cellular hypoxia. Manifestations may include respiratory abnormalities (progressing from tachypnea and dyspnea to respiratory depression and apnea), hemodynamic instability, metabolic acidosis, and, possibly, local irritant effects after oral ingestion of cyanide. The mainstays of therapy are 100% oxygen and specific antidotes to cyanide. Sequential treatment with amyl nitrite by inhalation, intravenous sodium nitrite 3%, and intravenous sodium thiosulfate 25% is directed toward decreasing the amount of cyanide available for cellular binding. Nitrites convert hemoglobin to methemoglobin, which reacts with cyanide to form cyanomethemoglobin. Sodium thiosulfate serves as a source of sulfur groups, which are needed for conversion of cyanide to thiocyanate, a compound that is relatively less toxic and is excreted renally. Supportive care also is important. Cobalt EDTA, hydroxocobalamin, and aminophenols have also been used but are not considered standard treatments. Cyanide poisoning is a medical emergency that requires prompt recognition and immediate and aggressive treatment.
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PMID:Clinical features and management of cyanide poisoning. 353 Jun 15

We compared the ability of tolazoline and yohimbine to antagonize xylazine-induced central nervous system depression, bradycardia, and tachypnea in 9 ewes and 5 rams. Once a week for 3 weeks, each sheep received one IV treatment of 0.4 mg xylazine/kg, 0.4 mg xylazine/kg followed in 10 minutes by 2 mg tolazoline/kg, or 0.4 mg xylazine/kg followed in 10 minutes by 0.2 mg yohimbine/kg. The order of the 3 treatments in each sheep was randomized. Xylazine alone caused recumbency for 41.0 +/- 3.7 minutes (mean +/- SEM). Tolazoline and yohimbine shortened the xylazine-induced recumbency to 12.1 +/- 0.9 minutes and 18.1 +/- 1.5 minutes, respectively. Sheep given xylazine alone had head droop for 34.0 +/- 5.4 minutes after rising. Head drooping of sheep given tolazoline or yohimbine was reduced to 10.1 +/- 1.7 minutes and 14.2 +/- 1.7 minutes, respectively. Both tolazoline and yohimbine reversed the bradycardia and tachypnea that followed xylazine administration. No statistical differences in the rate and magnitude of the reversal were observed between the 2 drugs.
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PMID:Effects of tolazoline and yohimbine on xylazine-induced central nervous system depression, bradycardia, and tachypnea in sheep. 355 80

A single oral dose of levamisole hydrochloride given at the rate of 12 mg/kg was believed responsible for bradycardia, tachypnea, hypothermia, cerebrocortical depression, and diarrhea in a dog. Supportive treatment and symptomatic treatment for the bradycardia were required for 4 days. In addition to these previously reported abnormalities associated with levamisole toxicosis, cerebrocortical depression and multiple foci of irritation were characterized by electroencephalography.
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PMID:Levamisole toxicosis in a dog. 375 34

Pulmonary edema has been proposed as a stimulus for pulmonary C-fibers. Stimulation of pulmonary C-fibers causes depression of cardiovascular function and either tachypnea or apnea. Our objective was to determine whether pulmonary edema, induced by either increasing pulmonary vascular permeability with alloxan or hydrostatic challenges, would elicit depression of cardiovascular function or changes in frequency of inspiratory activity. Utilizing a preparation in which the left pulmonary vessels and left airway were isolated, we monitored systemic blood pressure (BP), heart rate (HR), and diaphragm contractions (DC) in 13 anesthetized dogs. Injection of alloxan into the left pulmonary artery (LPA) produced transient decreases in HR, BP, and frequency of DC within 20 s of injection with no subsequent cardiorespiratory changes up to 5 min. These alloxan injections also caused coagulation necrosis. Generation of hydrostatic pulmonary edema in the left lung caused no changes in HR, BP, or in the frequency and amplitude of DC. We conclude that alloxan does stimulate reflex cardiorespiratory depression consistent with C-fiber stimulation, but these reflex responses are probably caused by alloxan's caustic effect and not by the resultant edema. We also conclude that pulmonary edema induced by increased hydrostatic pressure does not evoke any reflex cardiovascular responses or changes in frequency of inspiratory activity.
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PMID:Pulmonary edema in dogs fails to cause reflex responses. 381 22

New glutarimide compounds were synthesized by incorporating piperidine (compounds 1 to 7), diethylamine (8 and 9), morpholine moities (10 to 13), and alkyl derivatives of 3,5 dicyanoglutarimide (14 to 20) at position -1 of the nitrogen atom. Only compounds 1 to 7 at a dose of 8 mg/kg i.p. caused hypermotility, ataxia, tachypnoea and mild tremors in mice. At higher doses (32 mg/kg i.p.), all compounds induced tonic and clonic convulsions, respiratory paralysis and death. The LD50 values of compounds 1 to 20 in mice range from 152 to 488 mg/kg i.p. and for compounds 21 to 23, the p.o. values are 484, 500 and 525 mg/kg. The relative toxicity of compounds 1 to 7 and 14 to 20 showed inverse ratio in their numbers. Basic compounds 21 to 23 at high dose levels (64 mg/kg i.p.) induced only hypnotic depression. No change was observed in organ-wise histopathological study except patchy necrosis at the site of injection of basic compounds. The CNS pharmacological studies were negative with reference to anti-convulsion, analgesic, antipyretic tests by conventional methods except at higher doses (32 or 64 mg/kg i.p.), which exhibited synergistic effects in mice and rats.
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PMID:Pharmacology of new glutarimide compounds. 387 5


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