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 determine the effects of coronary arterial occlusion on the contractile response of the heart to angiotensin II (ANG II) administration, large infarcts were surgically induced in Sprague-Dawley rats at 2 mo of age. Forty-eight hours later, hearts from experimental animals presented a hemodynamic profile indicative of left ventricular failure and right ventricular dysfunction and revealed a loss of mass of 49.3 +/- 10.8% of the left ventricle inclusive of the interventricular septum. Plasma renin activity was found to be decreased by 48% in animals with occlusion of the left main coronary artery. Left and right posterior papillary muscles removed from these same hearts were evaluated mechanically in the presence and absence of ANG II. Contractile performance was impaired in left ventricular myocardium from infarcted rats as evidenced by the inability to attain developed tension similar to that seen in control rats. In addition, peak rates of tension rise and decay were significantly depressed. A reduction in contraction duration was also found in experimental animals, limiting the active state of the myocardium. ANG II resulted in a depression in the force-generating ability of left and right papillary muscles of control and experimental animals. Importantly, the negative inotropic effect of ANG II affected the left and right myocardium from infarcted rats by nearly twofold and threefold more than the corresponding muscles from controls. Morphometric evaluation revealed the absence of damage in both papillary muscles from control hearts and in the right muscles from experimental animals. However, necrotic tissue comprised 28.3 +/- 9.8% of left papillary muscles obtained from infarcted ventricles. It is concluded that ANG II administration resulted in reduced mechanical performance of rat myocardium. Coronary arterial ligation potentiated this phenomenon, and such a negative effect may have implication in infarction induced heart failure in vivo.
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PMID:Alterations in ANG II responsiveness in left and right myocardium after infarction-induced heart failure in rats. 832 34

The past and present clinical history of 13 patients with hemodynamic and angiographic diagnosis of chronic thromboembolic pulmonary hypertension (CTPH) was reviewed in order to investigate the reasons for failure of resolution of acute pulmonary embolism (PE) and findings useful for diagnosis of CTPH. All patients had chest radiograph, ECG, arterial blood gas analysis and pulmonary perfusion scintigraphy performed. Clinical assessment demonstrated that no patient had diagnosis and treatment of the several retrospectively identified episodes of PE (from 1 to 8); the lack of diagnosis was due to underestimation of symptoms and signs such as dyspnea (85%), pleuritic chest pain (31%) or phlebitis (46%) that were present months or years earlier. Alternative diagnoses erroneously made were dyspnea of unknown origin (5 cases), left heart failure (4 instances) and pneumonia (2 cases). Once CTPH has developed, chronic dyspnea (92%) and substernal chest pain (100%) are almost always present: chest radiograph and ECG show signs of chronic hypertension such as enlargement of hila (100%), right heart sections (77%), azygos vein (46%) and P pulmonale (67%), T inversion on right precordial leads (75%), S-T segment depression (75%), respectively. Perfusion scintigraphy shows severe perfusion impairment (55.7% of the total vascular bed) paralleled by severe hypoxia (standard PaO2 = 49 +/- 14.1 mm Hg). In conclusion, patients with PE who develop CTPH are not diagnosed and thus untreated because clinical symptoms and signs of acute PE have not been recognized. If CTPH develops, clinical assessment (including simple and noninvasive techniques such as chest radiograph, ECG and blood gas analysis) may show a quite characteristic pattern useful for diagnosis.
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PMID:From not detected pulmonary embolism to diagnosis of chronic thromboembolic pulmonary hypertension: a retrospective study. 846 23

To determine whether the detrimental mechanical and anatomical changes that occur biventricularly with aging are associated with activation of DNA synthesis, flow cytometric analysis was performed on myocyte nuclei prepared from the left and right ventricles of rats at 4, 12, 20, and 29 months of age. Heart weight increased significantly with age, and this growth adaptation was associated with the development of left ventricular failure and right ventricular dysfunction. These phenomena were coupled with marked elevations in diastolic wall stress and increases in the percentage of myocyte nuclei in S+G2M in both ventricles. Linear regression analyses revealed a direct correlation between the fraction of myocytes that entered the cell cycle and diastolic pressure and wall stress. An inverse relation was found between the percentage of myocyte nuclei in S+G2M and +dP/dt and systolic wall stress. Thus the depression of hemodynamic performance coupled with alterations in the loading conditions contributes, at least in part, to increased DNA synthesis in cardiac myocytes with age.
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PMID:Myocyte DNA synthesis with aging: correlation with ventricular loading in rats. 849 94

Left ventricular hypertrophy (LVH) is associated with reinduction of the fetal program of gene expression. It is unclear whether this pattern of cardiac gene expression changes with the development of left ventricular decompensation and failure. To answer these questions, we quantified steady-state levels of mRNA by the polymerase chain reaction in the left ventricular myocardium of rats 8 and 20 weeks after ascending aortic banding. Clinical and hemodynamic assessment identified two distinct groups of animals 20 weeks after aortic banding. The first group (20-week nonfailed LVH) demonstrated substantial LVH but no depression in systolic developed pressure per gram left ventricular weight compared with the age-matched control group. In contrast, a second group of rats exhibited clinical signs of congestive failure as well as a marked diminution in left ventricular developed pressure per gram. Assessment of the levels of mRNA encoding a panel of cardiac proteins demonstrated a greater than twofold increase in beta-myosin heavy chain mRNA and an approximately sixfold increase in atrial natriuretic factor mRNA in left ventricular myocardium of all three groups (8-week LVH, 20-week nonfailed LVH, 20-week failed LVH) when compared with appropriate age-matched control groups. In contrast, Ca(2+)-ATPase mRNA levels were decreased by 50% only in the left ventricular myocardium of animals with both clinical signs and hemodynamic indexes consistent with cardiac decompensation (20-week failed LVH). These results suggest that in rats with ascending aortic banding the hypertrophic phenotype is associated with a selective reinduction of the fetal gene program, which persists even after the development of left ventricular failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Selective changes in cardiac gene expression during compensated hypertrophy and the transition to cardiac decompensation in rats with chronic aortic banding. 850 29

In modern anaesthesia various antagonists are used. They provide efficient tools to facilitate better control of pharmacological effects and side effects of drugs routinely used in anaesthesia. Naloxone is a competitive antagonist of opioids without any intrinsic activity. It counteracts respiratory depression, pruritus, sedation and analgesia caused by opioids. It is fast-acting with a duration of action of 45 to 90 min. Several investigators have reported severe side effects of naloxone including hypertension, tachyarrhythmias, left heart failure and cardiac arrest, and hence the use of naloxone must be carefully considered in every single patient. Flumazenil is a competitive antagonist of benzodiazepines. It is a remarkably safe drug and very effective to terminate all benzodiazepine effects in anaesthesia and intensive-care patients. Serious complications caused by flumazenil have been reported in patients receiving benzodiazepines in the treatment of seizure disorders and in patients with mixed intoxications. Neostigmine is one of several antagonists of neuromuscular blocking agents. Its side effects include bradycardia, increased bronchial secretions and increased peristalsis. Indication depends on the results of neuromuscular monitoring. Physostigmine is an unspecific antagonist of the central anticholinergic syndrome, an acute psychosis that may be caused by numerous drugs used in anaesthesia. Generally, antagonists should be carefully titrated. In emergency medicine the use of these antagonists is not recommended; the primary goal is to restore vital functions.
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PMID:[Antagonists in anesthesia]. 854 33

We report five patients who developed intraoperative myocardial ischemia but were treated successfully with nicorandil. Case 1; An 84 year-old male underwent emergent laparotomy and ileolysis under inhalational plus thoracic epidural anesthesia. During his emergence from anesthesia, arterial pressure and heart rate increased abruptly due to excitement, leading to ST-T depression on V5 lead. Bradycardia and hypotension developed subsequently. Immediately after i.v. injections of nicorandil 4 mg and atropine 0.3 mg, ST-T change and hemodynamics improved dramatically. Case 2; A 67 year-old male underwent esophagectomy under inhalational plus thoracic epidural anesthesia. Following the completion of surgery, elevation of ST-T developed suddenly on lead II, though hemodynamics were not compromised. ST-T elevation disappeared immediately after nicorandil 6 mg and continuous infusion of nitroglycerin (TNG) was initiated. Case 3; A 71 year-old female underwent aortic valve replacement under high-dose fentanyl anesthesia. Shortly after starting cardiopulmonary bypass (CPB), ST-T segment on leads II and V5 was elevated suddenly. This was accompanied by severe pulmonary hypertension suggestive of severe left ventricular failure. Shortly after nicorandil 4 mg via a pulmonary artery (PA) catheter, ST-T segment returned to the baseline and pulmonary arterial pressure was normalized. Case 4; A 61 year-old male underwent coronary revascularization under high-dose fentanyl anesthesia. During weaning from CPB, elevation of ST-T segment occurred on leads II and V5. ST change improved, responding to nicorandil 6 mg en bolus via a PA catheter. Case 5; A 67 year-old male underwent coronary revascularization under high-dose fentanyl anesthesia. He was unable to be weaned from CPB for several hours because of frequent and repeated attacks of ventricular tachycardia and ventricular fibrillation. The arrhythmia did not respond to various kinds of treatments including intra-aortic balloon pumping and continuous infusions of inotropes, anti-arrhythmic drugs and anti-anginal drugs. In spite of repeated intracoronary injections of TNG, graft flow to the left anterior descending branch remained low at 40 ml.min-1. After an intracoronary injection of nicorandil 1 mg, however, blood flow increased to 100 ml.min-1, resulting in a marked reduction in frequency of ventricular arrhythmia. The patient came off bypass successfully. In each case, intraoperative myocardial ischemia was treated successfully with nicorandil. Neither hypotension nor arrhythmia resulted from its bolus injection. Nicorandil might be a useful therapeutic tool for myocardial ischemia during anesthesia.
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PMID:[Successful treatment of intraoperative myocardial ischemia with nicorandil]. 912 27

The suggested role of oxidative stress in the pathogenesis of heart failure is largely based on utilizing left heart failure models. The present study on rats evaluated changes in antioxidants as well as oxidative stress in relation to hemodynamic function subsequent to the right heart failure induced by monocrotaline (50 mg/kg, i.p.). During the post-injection period, monocrotaline (MCT)-treated rats demonstrated a persistent growth depression. Two to three weeks after the injection, MCT-treated rats showed signs of fatigue, peripheral cyanosis and dyspnea. In these rats, right heart hypertrophy was confirmed by a significant increase in right ventricular weight as well as right ventricle to body weight ratio. In MCT-treated rats, there was also a significant increase in right ventricular systolic as well as end diastolic pressures. No change in lung and liver wet/dry weight ratios between MCT-treated and control animals was observed. Based on the hemodynamic data as well as other clinical observations, the functional stage achieved was compensated heart failure. Myocardial antioxidant enzymes, catalase, glutathione peroxidase and superoxide dismutase, in the MCT-treated rats were not different compared to control rats. Vitamin E levels were significantly depressed in the RV and there was no change in retinol levels. There was a significant increase in lipid hydroperoxide concentrations in MCT-treated rats as compared to the control group. These data provide evidence that right heart failure is associated with an increase in oxidative stress.
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PMID:Myocardial oxidative stress changes during compensated right heart failure in rats. 1044 2

Myocardial function is determined by preload, afterload, contractility and heart rate. Pathologic changes of these variables may result in decrease of blood pressure, acute heart failure or cardiogenic shock. Hyperdynamic septic shock is associated with systemic hypotension despite increased cardiac output. Mediators of sepsis induce both myocardial depression and pulmonary arterial hypertension. Moreover, sepsis is characterized by microcirculatory disturbances and dysbalance in regional oxygen delivery and consumption. Severe systemic hypotension is a symptom often requiring catecholamine therapy to restore systemic circulation and to avoid organ damage. As the use of catecholamines is not a causal therapy administration should be limited to an initial measure until correction of the underlying abnormalities can be achieved. Different etiologies of shock as well as diseases requiring specific interventions as pulmonary embolectomy, systemic lysis or coronary angioplasty have to be considered. First line intervention consists of optimizing preload by fluid resuscitation as appropriate and use of dopamine (4-12 micrograms/kg.min) as primary catecholamine to increase contractility and blood pressure. In acute left heart failure inotropic support with dobutamine (4-12 micrograms/kg.min) or epinephrine (0.05-1 microgram/kg.min) may be necessary, frequently combined with a vasodilator (sodium nitroprusside 0.2-5 micrograms/kg.min or nitroglycerine 0.5-2.5 micrograms/kg.min) or phosphodiesterase-III-inhibitor (milrinone 0.3-0.8 microgram/kg.min). In right heart failure norepinephrine is preferred to increase coronary perfusion pressure. Hyperdynamic septic shock with decreased vascular resistance is treated with norepinephrine to restore mean arterial pressure and to improve right ventricular dysfunction induced by pulmonary hypertension.
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PMID:[The basics of catecholamine therapy. 2. A guide to clinical use]. 1076 48

The average age of patients undergoing cardiac surgery has increased continuously during the last three decades due to a progressively increasing number of older people in the population and the advances in operative and perioperative treatment in open heart surgery. Consequently we have investigated the short- and long-term results of isolated myocardial revascularization in patients who are in their ninth decade of life. Between 1 January 1995 and 31 December 1998, 121 patients (51 women, 70 men, age 80 to 88 years, median: 82 years) underwent isolated coronary artery bypass grafting. As part of the revascularization, a unilateral internal mammary artery graft (IMA) was used in 87% of cases. The in-hospital mortality was 6.6%. Analysis of predictors of mortality unveiled the following factors: ejection fraction less than 50%; history of recent left ventricular failure; extent of coronary artery disease; perioperative use of an intraaortic balloon pump (IABP) and symptomatic pericardial effusion. Use of the IMA revealed no influence on in-hospital mortality. The median follow-up time was 20 months (range: 2-48 months). Survival rates after 1, 2, and 3 years were 93.1%, 87.3% and 73.7% for women and 86.9%, 82.5% and 65.1% for men. These survival rates were comparable with those of the entire 82 year old population. Predictors for late death were male gender, history of stroke, history of arterial embolism, and postoperative pulmonary failure resulting in mechanical ventilation. During the follow-up period myocardial infarcts were subsequently not observed. Freedom from angina after 1, 2 and 3 years was 90.1%, 82.6% and 78.1%, respectively. At an interval of 1 year after the operation 87.6% of patients had not been hospitalized as a result of cardiac disorders (2 years: 80.1%, 3 years: 73.2%). Permanent nursing care was not required 1 year after the operation by 94.3% of patients (2 years: 91.5%, 3 years: 91.5%). Four percent of the survivors suffered from permanent delirium, 3% from depression, 5% from lack of concentration, and 6% from vertigo. In summary this study has revealed that, in patients over eighty years of age suffering from ischemic heart disease, coronary artery bypass grafting has acceptable short- and long-term results. Yearly mortality rates during the first 3 years after the operation are comparable with the expected mortality rate in an age-matched population.
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PMID:[Isolated coronary bypass operation in the 9th decade of life]. 1113 Jan 92

The objective evidence of silent myocardial ischemia--ischemia in the absence of classical chest pain--includes ST-segment shifts (usually depression), momentary left ventricular failure, and perfusion defects on scintigraphic studies. Assessment of angina patients with 24-hour ambulatory monitoring may uncover episodes of silent ischemia, the existence of which may give important information regarding prognosis and may help structure a more effective therapeutic regimen. The emerging recognition of silent ischemia as a significant clinical entity may eventually result in an expansion of current therapy--not only to ameliorate chest pain, but to minimize or eliminate ischemia in the absence of chest pain.
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PMID:Controversies in cardiovascular care: silent myocardial ischemia. 1153 15


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