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)

The intravenous infusion of sodium fluoride (2 mg/kg X min) into anesthetized rats caused a progressive fall in arterial blood pressure, cardiac output, heart rate and peripheral resistance. Respiratory rate increased during the first 20 min of infusion resulting in increased oxygen and decreased carbon dioxide blood concentrations. Total body oxygen consumption decreased after 30 min of NaF infusion by 29%, whereas the respiratory quotient (RQ) increased from 0.8 to 1.06. Death occurred after a mean dose of 79.6 +/- 4.6 mg/kg NaF. The terminal cardiac event before death was atrioventricular block followed immediately by asystole. Artificial ventilation did not influence the cardiovascular and the lethal effects of fluoride infusion. The plasma concentrations of total and ionized calcium decreased upon NaF infusion. The infusion of extra calcium did not prevent NaF-induced cardiovascular failure but decreased plasma fluoride levels and increased the lethal dose of NaF by 17% (not significant). In isolated atria and perfused hearts in vitro, NaF decreased the force of contraction in a dose-dependent manner. In conclusion, cardiovascular failure resulting from the direct cardiodepressive and vasodilatating effects of fluoride (and not from respiratory depression or hypocalcemia) accounts for the lethal outcome of fluoride intoxication.
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PMID:The pathophysiological profile of the acute cardiovascular toxicity of sodium fluoride. 692 49

To our knowledge, the clinical course of acute caffeine poisoning in neonates has not been previously reported. Three full-term infants manifested CNS irritability after the parenteral administration of large doses of caffeine and benzoate sodium injection in the delivery room for respiratory depression. The infants received caffeine in doses that ranged from 36 to 136 mg/kg. On arrival in a regional newborn center, they exhibited one or more of the following symptoms: tachypnea, fine tremor of the extremities, opisthotonus, tonic-clonic movements, and nonpurposeful jaw and lip movements. The overdose of caffeine produced a clinical picture that suggested neonatal seizures and prompted therapy with anticonvulsants. A fourth infant (premature) attained a high plasma caffeine concentration, but this infant's symptoms were altered by intraventricular hemorrhage. The combination of caffeine overdose and perinatal asphyxia may precipitate or increase seizure activity in the neonate. Recognition of the potential toxic effects of caffeine overdose should guide patient care and stimulate further study to establish appropriate use of caffeine in the newborn infant.
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PMID:Acute caffeine overdose in the neonate. 737 58

Acute intrinsic renal failure was diagnosed in a two-year-old, male, German shepherd dog following a Vipera aspis bite. Clinical signs included depression, hypersalivation, vomiting, tachypnoea, abdominal pain, splenomegaly, oliguria with haematuria and haemolysed serum. Leucocytosis with a shift to the left, thrombocytopenia, prolonged coagulation times (activated partial thromboplastin time, prothrombin time and thrombin time), hypofibrinogenaemia, azotaemia and hyposthenuria were the most prominent laboratory abnormalities. Histopathological evaluation of the kidneys showed a discrete glomerular hypercellularity, mesangial lysis and renal tubules filled with many hyaline casts and some necrotic cells.
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PMID:Acute intrinsic renal failure and blood coagulation disorders after a snakebite in a dog. 747 66

A major determinant of survival in patients with advanced viral or bacterial infection, or following severe trauma or burns complicated by multiple organ failure, is the combination of clinical signs termed the systemic inflammatory response syndrome (SIRS). SIRS is characterized by hypotension, tachypnea, hypo- or hyperthermia and leukocytosis as well as other clinical signs and symptoms, including a depression in myocardial contractile function. Heart failure complicating systemic sepsis or other causes of SIRS is usually not accompanied by coronary artery ischemia due to hypotension, myocardial necrosis, or marked cardiac interstitial inflammatory infiltrates, and thus the cause of cardiac contractile dysfunction in this syndrome has remained unclear. However, recent evidence has implicated an endogenous nitric oxide (NO) signalling pathway within cardiac myocytes and other cellular constituents of cardiac muscle, including the microvascular endothelium, as a possible contributor to the pathogenesis of heart failure in this syndrome. Cardiac myocytes are now known to express both constitutive NO synthase (cNOS) and inducible NO synthase (iNOS) activities. Activation of cNOS appears to modulate cardiac myocyte responsiveness to muscarinic cholinergic and beta-adrenergic receptor stimulation. Induction of iNOS by soluble inflammatory mediators, including cytokines, causes a marked depression in myocyte contractile responsiveness to beta-adrenergic agonists. Thus, inappropriate activation of cNOS or excessive or prolonged induction of iNOS in the myocardium may contribute to cardiac dysfunction complicating SIRS.
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PMID:Myocardial contractile dysfunction in the systemic inflammatory response syndrome: role of a cytokine-inducible nitric oxide synthase in cardiac myocytes. 753 82

We compared the ability of 2 alpha 2-adrenergic receptor antagonists, atipamezole and yohimbine, to reverse medetomidine-induced CNS depression and cardiorespiratory changes in lambs. Twenty lambs (7.8 +/- 2.6 kg) were randomly allotted to 4 treatment groups (n = 5). Each lamb was given medetomidine (30 micrograms/kg of body weight, i.v.), followed in 15 minutes by i.v. administration of atipamezole (30 or 60 micrograms/kg), yohimbine (1 mg/kg), or 0.9% NaCl (saline) solution. Medetomidine caused lateral recumbency in 1 to 2 minutes in all treated lambs. Medetomidine significantly (P < 0.05) decreased heart rate at 5 and 10 minutes after its administration. Heart rate remained above 120 beats/min, and severe bradycardia (< or = 70 beats/min) and other arrhythmias did not occur throughout the study. Medetomidine also induced tachypnea in all treated lambs. The tachypnea was abolished by atipamezole and yohimbine, but not by saline solution administration. The medetomidine-induced tachypnea did not significantly affect arterial pH and PaCO2. Arterial oxygen tension was within acceptable range (PaO2 = 71 to 62 mm of Hg), but was lower than expected. Administration of atipamezole, yohimbine, or saline solution did not change PaO2 significantly. Lambs treated with 30 or 60 micrograms of atipamezole/kg were able to walk unassisted in 2.4 +/- 0.4 and 2.3 +/- 0.7 minutes, respectively, whereas yohimbine- and saline-treated lambs did not walk unassisted until 15.6 +/- 2.7 and 73.0 +/- 6.8 minutes later, respectively. Results of this study indicated that medetomidine is a potent CNS depressant in lambs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of atipamezole and yohimbine on medetomidine-induced central nervous system depression and cardiorespiratory changes in lambs. 766 59

Carbon monoxide poisoning usually results from inhalation of exhaust fumes from motor vehicles, smoke from fires or fumes from faulty heating systems. Carbon monoxide has a high affinity for hemoglobin, with which it forms carboxyhemoglobin. The resulting decrease in both oxygen-carrying capacity and oxygen release can lead to end-organ hypoxia. The clinical presentation is nonspecific. Headache, dizziness, fatigue and nausea are common in mild to moderate carbon monoxide poisoning. In more severe cases, tachycardia, tachypnea and central nervous system depression occur. When carbon monoxide intoxication is suspected, empiric treatment with 100 percent oxygen should be initiated immediately. The diagnosis is confirmed by documenting an elevated carboxyhemoglobin level. Hyperbaric oxygen therapy is recommended in patients with neurologic dysfunction, cardiac dysfunction or a history of unconsciousness.
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PMID:Carbon monoxide intoxication. 769 50

Endotoxin (lipopolysaccharide, LPS) can induce shock, multiple organ failure, and death. A recombinant N-terminal fragment of bactericidal/permeability increasing protein, rBPI23, binds with high affinity to gram-negative bacterial LPS and neutralizes its biological activity. We sought to determine the effect of rBPI23 on LPS-induced respiratory dysfunction and cardiovascular depression in conscious rabbits. Rabbits were injected with Escherichia coli O113 LPS (6 micrograms/kg) and treated with rBPI23 (2 mg/kg), vehicle, or control protein after recovery from surgery performed to implant catheters for hemodynamic assessments and intravenous injections. LPS challenge caused respiratory dysfunction including tachypnea, significant decreases in arterial O2 tension (PO2), arterial oxygen content, and an increase in alveolar-arterial O2 gradient (A-aDO2). LPS administration also resulted in profound and prolonged decreases in mean arterial blood pressure and cardiac index. Treatment with rBPI23 prevented LPS-induced respiratory dysfunction and significantly ameliorated the cardiovascular depression. 5 of 16 LPS-challenged animals died of respiratory failure and acidosis, whereas none died in the rBPI23 treated group (p = .11). The results demonstrate that rBPI23 protects animals against LPS-induced cardiopulmonary depression in endotoxic shock.
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PMID:Protective effects of a recombinant N-terminal fragment of bactericidal/permeability increasing protein on endotoxic shock in conscious rabbits. 774 57

Septic shock is a common life-threatening problem, usually presenting with fever, tachycardia, tachypnea, and often a source of infection. The cardiac index is increased, with a decreased systemic vascular resistance, and a reversibly decreased ejection fraction with an increased end diastolic volume. The myocardial depression is most likely caused by a circulating humoral substance that depresses myocardial contractility. The initial treatment of septic shock is aggressive fluid resuscitation and antibiotic therapy, with vasopressors and inotropes being indicated in those patients who do not respond adequately to fluids. Therapy directed against the mediators of septic shock is theoretically promising, but to date has not been successful.
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PMID:New perspectives on the management of septic shock in the cancer patient. 880 20

A 61-year-old woman with chronic asthma sustained an episode of dyspnea and chest heaviness and was brought to the emergency department. Her examination revealed tachypnea, tachycardia, hypotension, and diffuse prolonged respiratory wheezing. Arterial blood gas analysis showed severe hypoxemia and hypercapnia. A 12-lead electrocardiogram showed marked, downsloping ST-segment depression, with deep, negative T waves in leads I, II, III, and aVF and precordial leads V3-V6. After 15 minutes of therapy with oxygen, beta-agonists, and corticosteroids, the electrocardiographic abnormalities subsided and 2 hours later they had disappeared. Subsequent coronary angiography and ventriculography revealed normal coronary arteries and good left ventricular ejection fraction. It is concluded that an acute asthmatic paroxysm may produce transient myocardial ischemia even with angiographically documented normal coronary arteries.
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PMID:Acute, reversible myocardial ischemia in a patient with an asthmatic attack. 891 9

Cardiovascular diseases, including atherosclerosis and myocardial ischemia, occur as a result of a complex set of genetic and environmental factors. During periodontitis, dental plaque microorganisms may disseminate through the blood to infect the vascular endothelium and contribute to the occurrence of atherosclerosis and risk of myocardial ischemia and infarction. Myocardial ischemia and infarction are often preceded by acute thromboembolic events. In an in vitro model of thrombosis, certain dental plaque bacteria induce platelets to aggregate. Aggregation of platelets is induced by the platelet aggregation-associated protein [PAAPJ expressed on plaque bacteria, including Streptococcus sanguis and Porphyromonas gingivalis. Intravenous infusion of S. sanguis into rabbits has been shown previously to cause changes in the electrocardiogram (ECG), heart rate, blood pressure, and cardiac contractility. These changes are consistent with the occurrence of myocardial infarction. The ECG changes are now shown to begin within 30 seconds after infusion of PAAP+ S. sanguis, followed by alterations in blood pressure and respiratory rate. These changes occurred intermittently over a 30-minute period and changed within one heartbeat to a normal pattern and suddenly back to abnormal. Intermittent ECG abnormalities were seen in 13 of 15 rabbits, including left axis deviation, ST-segment depression, preventricular contractions, alternans, and bigemnia. Dose-dependent thrombocytopenia, accumulation of 111Indium-labeled platelets in the lungs, and tachypnea also occurred. No changes occurred with the PAAp- strain. The data indicated that PAPP+ S. sanguis interacts with circulating platelets, inducing thromboemboli to cause the pulmonary and cardiac abnormalities. During periodontitis, therefore, PAAP+ S. sanguis and P. gingivalis bacteremia may contribute to the chance of acute thromboembolic events.
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PMID:Dental plaque, platelets, and cardiovascular diseases. 972 99


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