Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hemodynamic, hormonal, and metabolic effects of chronic neutral endopeptidase (NEP) 24.11 inhibition and furosemide were compared in the pacing model of ovine heart failure (HF). Intravenous SCH 39370 induced a dose-related inhibition of NEP activity during 4-days treatment, in association with a transient increase in plasma atrial natriuretic peptide (ANP) and, at the higher dose, an increased mean level of plasma cyclic guanosine monophosphate. There was a significant and persistent decrease in left atrial pressure, a brief increase in cardiac output (CO), and a tendency for arterial pressure to be reduced. Significant dose-related diuresis and natriuresis were also observed. Furosemide induced a similar hemodynamic response, associated with greater diuresis and natriuresis. Both agents significantly reduced plasma aldosterone levels. Coinfusion of captopril on day 4 of treatment resulted in similar responses in both the SCH 39370- and furosemide pretreated groups. Chronic NEP inhibition significantly alters circulatory and renal function and appears to be as effective as furosemide in reducing cardiac preload in this model of congestive HF.
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PMID:Comparison of chronic neutral endopeptidase inhibition and furosemide in an ovine model of heart failure. 890 7

A 45-year-old Japanese woman presented with a high fever, a nonproductive coughing, and severe dyspnea, and was admitted to another hospital. During the week prior to hospitalization, she had been given Shosaikoto for treatment of liver dysfunction of unknown etiology. Mycoplasma pneumonitis was initially suspected, so she was treated with antibiotics (clindamycin and minocycline) and received oxygen therapy. Pulmonary insufficiency worsened rapidly, and she was transferred to our hospital. On admission, a chest roentgenogram revealed bilateral alveolar infiltrates predominantly in the medial lung fields. Furosemide and high-dose methylprednisolone were immediately administered, but hypoxemia increased. When the PaO2 was 55.7 Torr while the patient breathed 100% oxygen, mechanical ventilation with positive end-expiratory pressure (PEEP) was started. Arterial blood-gas values improved dramatically, and the chest roentgenogram became clear. Our diagnosis of noncardiogenic pulmonary edema is based on the chest-roentgenographic findings, infiltration of inflammatory cells as seen in two lung-biopsy specimens and bronchoalveolar lavage fluid, the lack of findings of heart failure on physical examination and electrocardiography, and the good clinical response to PEEP. A positive lymphocyte stimulation test in response to Shosaikoto implicated this non-traditional herbal medicine as an etiologic factor in the non-cardiogenic pulmonary edema. Shosaikoto has been identified as the cause of interstitial pneumonia or eosinophilic pneumonia, but pulmonary edema associated with Shosaikoto has not been previously described. This case suggests that methylprednisolone treatment may be insufficient for Shosaikoto-induced pulmonary edema, and that mechanical ventilation with PEEP is very effective.
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PMID:[Pulmonary edema associated with the Chinese medicine shosaikoto]. 986 80

It is sometimes necessary for the practitioner to transfuse the ruminant with whole blood or plasma. These techniques are often difficult to perform in practice, are time-consuming, expensive, and stressful to the animal. Acute loss of 20% to 25% of the blood volume will result in marked clinical signs of anemia, including tachycardia and maniacal behavior. The PCV is only a useful tool with which to monitor acute blood loss after intravascular equilibration with other fluid compartments has occurred. An acutely developing PCV of 15% or less may require transfusion. Chronic anemia with PCV of 7% to 12% can be tolerated without transfusion if the animal is not stressed and no further decline in erythrocyte mass occurs. Seventy-five percent of transfused bovine erythrocytes are destroyed within 48 hours of transfusion. A transfusion rate of 10 to 20 mL/kg recipient weight is necessary to result in any appreciable increase in PCV. A nonpregnant donor can contribute 10 to 15 mL of blood/kg body weight at 2- to 4-week intervals. Sodium citrate is an effective anticoagulant, but acid citrate dextrose should be used if blood is to be stored for more than a few hours. Blood should not be stored more than 2 weeks prior to administration. Heparin is an unsuitable anticoagulant because the quantity of heparin required for clot-free blood collection will lead to coagulation defects in the recipient. Blood cross-matching is only rarely performed in the ruminant. In field situations, it is advisable to inject 200 mL of donor blood into the adult recipient and wait 10 minutes. If no reaction occurs, the rest of the blood can probably be safely administered as long as volume overload problems do not develop. Adverse reactions are most commonly seen in very young animals or pregnant cattle. Signs of blood or plasma transfusion reaction include hiccoughing, tachycardia, tachypnea, sweating, muscle tremors, pruritus, salivation, cough, dyspnea, fever, lacrimation, hematuria, hemoglobinuria, collapse, apnea, and opisthotonos. Intravenous epinephrine HCl 1:1000 can be administered (0.2 to 0.5 mL) intravenously or (4 to 5 mL) intramuscularly (preferable) if clinical signs are severe. Pretreatment with antipyretics and slowing the administration rate may decrease the febrile response. Blood or plasma administered too rapidly will also result in signs of cardiovascular overload, acute heart failure, and pulmonary hypertension and edema. Furosemide and slower administration of blood or plasma should alleviate this problem. Administration rates have been suggested starting from 10 mL/kg/hr; faster rates may be necessary in peracute hemorrhage. Plasma should be administered when failure of absorption of passive maternal antibody has occurred or when protein-loosing enteropathy or nephropathy results in a total protein of less than 3 g/dL or less than 1.5 g albumin/dL. Plasma can be stored at household freezer temperatures (-15 to -20 degrees C) for a year; coagulation factors will be destroyed after 2 to 4 months when stored in this manner. To maintain viability of coagulation factors, plasma must be stored at -80 degrees C for less than 12 months. When administering plasma, a blood donor set with a built-in filter should always be used. When bovine plasma is thawed, precipitants form in the plasma and infusion of these microaggregates may result in fatal reactions in the recipient.
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PMID:Use of blood and blood products. 1057 16

Treatment of heart failure should include correction of the underlying cause. These causes include large left to right shunts, obstructive lesions, arrhythmias, primary myocardial disease etc. The main pharmacological therapy includes inotropic agents, vasodilators and diuretics. Inotropic agents increase myocardial contractility and include digoxin, intravenous dopamine, dobutamine and isoproterenol. Vasodilators improve cardiac pump performance by decreasing the vascular resistance and/or increasing the venous capacitance. Commonly used vasodilator agents include angiotensin converting enzyme inhibitors (captopril, enalapril etc.), hydralazine, prazosin hydrochloride etc. Diuretics inhibit salt and water reabsorption promoting their excretion. Furosemide, thiazide diuretics, aldactone, are commonly used diuretics. Electrolyte and acid-base imbalance can occur on chronic diuretic therapy. Cardiac transplantation is considered for patients where all medical management has failed.
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PMID:Recent advances in the treatment of congestive heart failure. 1077 42

Evidence suggests that, in addition to its diuretic property, furosemide also may exert direct vascular effects. Because thromboxane A2 (TXA2) has a role in the control of vascular tone, we investigated the effect of furosemide on the contraction induced by U46619 (a stable TXA2 mimetic) on isolated human internal mammary artery (IMA) and saphenous vein (SV). Concentration-response curves to U46619 were performed in the absence (vehicle) or the presence of furosemide (0.1-1 mM) on rings of IMA and SV. In addition, the relaxant effect of furosemide (0.1 microM-1 mM) also was evaluated on U46619-precontracted IMA and SV. The participation of cyclooxygenase derivatives was studied by pretreatment with indomethacin. Furosemide (0.1-1.0 mM) caused parallel rightward shifts of U46619 concentration-response curves without affecting the maximal responses in both IMA and SV. Treatment with indomethacin (1 microM) modified neither the inhibitory effect of furosemide on U46619-induced contractions, nor the relaxant effect of furosemide on U46619-induced contractions, nor the relaxant effect of furosemide on U46619-precontracted IMA and SV. In conclusion, furosemide at high concentrations inhibited U46619-induced contraction in human isolated IMA and SV and relaxed U46619-precontracted IMA and SV by mechanisms independent of the release of relaxant prostaglandins. These results suggest that blockade of TXA2 receptors by furosemide may contribute to explaining the therapeutic effects of furosemide in the treatment of severe heart failure.
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PMID:Furosemide inhibits thromboxane A2-induced contraction in isolated human internal mammary artery and saphenous vein. 1077 81

We describe the feasibility of chronic measurement of cardiac output (CO) in conscious mice. With the use of gas anesthesia, mice >30 g body wt were instrumented either with transit-time flow probes or electromagnetic probes placed on the ascending aorta. Ascending aortic flow values were recorded 6-16 days after surgery when probes had fully grown in. In the first set of experiments, while mice were under ketamine-xylazine anesthesia, estimates of stroke volume (SV) obtained by the transit-time technique were compared with those simultaneously obtained by echocardiography. Transit-time values of SV were similar to those obtained by echocardiography. The average difference +/- SD between the methods was 2 +/- 7 microl. In the second set of studies, transit-time values of CO were compared with those obtained by the electromagnetic flow probes. In conscious resting conditions, estimates +/- SD) of cardiac index (CI) obtained by the transit-time and electromagnetic flow probes were 484 +/- 119 and 531 +/- 103 ml x min(-1) x kg body wt(-1), respectively. Transit-time flow probes were also implanted in mice with a myocardial infarction (MI) induced by ligation of a coronary artery 3 wk before probe implantation. In these MI mice (n = 7), average (+/- SD) resting and stimulated (by volume loading) values of CO were significantly lower than in noninfarcted mice (n = 15) (resting CO 16 +/- 3 vs. 20 +/- 4 ml/min; stimulated CO 20 +/- 5 vs. 26 +/- 6 ml/min). Finally, using transfer function analysis, we found that, in resting conditions for both intact and MI mice, spontaneous variations in CO (> 0.1 Hz) were mainly due to those occurring in SV rather than in heart rate. These data indicate that CO can be measured chronically and reliably in conscious mice, also in conditions of heart failure, and that variations in preload are an important determinant of CO in this species.
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PMID:Chronic measurement of cardiac output in conscious mice. 1183 16

Extracellular matrix (ECM) remodeling and increased matrix metalloproteinase (MMP) expression and activity have been observed to be relevant in the development of heart failure (HF). We examined the effects of ramipril alone or with furosemide on ECM in a heart failure model. HF was induced by occlusion of the left coronary artery in spontaneously hypertensive rats (SHR). Rats were assigned to placebo (n=9), ramipril 1 mg/kg/day (n=11), furosemide 2 x 2 mg/kg/day (n=7) or both (1 mg/kg/day + 2 x 2 mg/kg/day n=8). LV-function, collagen content, MMP/TIMP (tissue inhibitor of matrix metalloproteinases) protein- and mRNA-expression were examined in non-infarcted LV tissue. MMP-2/TIMP-4 ratio was increased in HF. Ramipril reduced MMP-2 expression (active form), collagen type I mRNA expression and content and increased TIMP-4 levels associated with decreased left ventricular end diastolic pressure (LVEDP), mortality rate and increased LV pressure (LVP). Combination therapy with furosemide is less efficient with regard to collagen content and MMP-2 (active form) reduction but did not worsen beneficial effects of ramipril on LV function and mortality rate. Furosemide alone had no effect on MMP-2 (active form) expression, collagen content, LV function and mortality rate. Prevention of LV dilatation by ramipril was associated with decreased gelatinolytic activity and increased MMP-inhibition in heart failure SHR. Furthermore, ramipril reduced fibrosis by enhanced interstitial collagenase expression. Furosemide did not show the beneficial effects of ramipril on ECM remodeling but did not worsen LV function. Positive effects of furosemide treatment alone on LV remodeling and function were not observed.
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PMID:Effect of ramipril and furosemide treatment on interstitial remodeling in post-infarction heart failure rat hearts. 1185 55

A 26-year-old woman in the thirty-second week of her fifth pregnancy was admitted with diffuse sudden-onset abdominal pain. Examination revealed cervical dilation to 8 cm, a ruptured uterine cerclage and transverse presentation of the fetus, indicating a need for emergency cesarean section, which was performed under uneventful spinal anesthesia. Three days after surgery the patient presented signs consistent with acute pulmonary edema coinciding with blood transfusion. Echocardiography demonstrated left ventricular systolic dysfunction with an ejection fraction of 35%. The diagnosis was peripartum myocardiopathy with acute respiratory insufficiency due to heart failure. Furosemide and captopril were prescribed and the outcome was satisfactory. The discharge echocardiogram showed a left ventricle of normal size and thickness, and the ejection fraction was 55%. Peripartum myocardiopathy is a type of heart failure that develops during the third trimester or during the first six months after delivery, in the absence of signs of ventricular dysfunction or previous heart disease. Based on clinical presentation and echocardiographic findings, we believe that peripartum myocardiopathy was the cause of acute pulmonary edema in this patient.
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PMID:[Puerperal cardiomyopathy and pulmonary edema after cesarean section]. 1213 58

Elderly patients with heart failure are at risk of postprandial hypotension (PPH), orthostatic hypotension (OH), and concomitant cerebral oxygenation changes because of altered cardiovascular balance and the use of cardiovascular medications, such as furosemide and captopril. In 24 patients with heart failure (New York Heart Association class II to III, in stable condition, and receiving cardiovascular medication [aged 70 to 83 years]), blood pressure (BP) was measured by Finapres, and cortical concentrations of oxyhemoglobin and deoxyhemoglobin were measured using near-infrared spectroscopy during standing and after a 292-kcal carbohydrate meal. Tests were performed before and during therapy with furosemide 40 mg once daily (n = 11) or captopril 6.25 and 12.5 mg twice daily (n = 13) in a double-blind randomized trial. Before treatment, 13 of 24 patients had PPH, and 2 of 24 patients had OH. The first dose of furosemide significantly decreased postprandial systolic BP (p <0.05) and postprandial frontal cortical oxygenation (p <0.05), whereas the first dose of captopril did not. Furosemide and captopril did not significantly affect postprandial or orthostatic BP or cortical oxygenation after 2 weeks of treatment. Thus, PPH is a common phenomenon in elderly patients with heart failure, whereas OH is not. The first dose of furosemide 40 mg decreased postprandial systolic BP and frontal cortical oxygenation, in contrast with the first dose of captopril 6.25 mg and 2-week treatment with furosemide 40 mg once daily or captopril 12.5 mg twice daily. These findings indicate that initiating furosemide treatment worsens PPH, and furosemide is less safe in elderly patients with heart failure.
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PMID:Effects of furosemide versus captopril on postprandial and orthostatic blood pressure and on cerebral oxygenation in patients > or = 70 years of age with heart failure. 1223 Oct 83

Congestive heart failure is a disease state distinguished by the regular presence of both renal and hepatic abnormalities in drug handling. One such abnormality involves flaws in the process of drug absorption. In most instances, congestive heart failure-related abnormalities in drug absorption are of inconsequential significance. However, this is not the case with loop diuretics. Loop diuretic action ordinarily tracks the rate and extent of absorption if a sufficient amount of diuretic has been given to exceed the threshold for diuretic effect. In congestive heart failure, both the rate and absolute amount of loop diuretic absorbed can be reduced as a function of the heart failure state itself. In this setting, drug dissolution characteristics can assume added significance. Furosemide is the loop diuretic with the widest intra- and interpatient variability of absorption. Alternatively, the loop diuretic torsemide is rapidly and fairly completely absorbed independent of the heart failure state. This pattern of absorption establishes it as the preferred loop diuretic in the otherwise diuretic-resistant heart failure patient. However, the exact role of torsemide in the outpatient management of congestive heart failure remains to be determined.
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PMID:Pharmacotherapy in congestive heart failure: drug absorption in the management of congestive heart failure: loop diuretics. 1456 48


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