Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.4.1 (phosphodiesterase)
18,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiopulmonary bypass (CPB) produces an inflammatory response due to the interaction of blood with a foreign body surface. The lungs are most affected by this inflammatory response. Pentoxifylline (PTX), a phosphodiesterase inhibitor and an inhibitor of leukocyte activation, is used to minimize damage in lungs where leukocytes play an important role. Twenty patients with mitral valve stenosis with planned mitral valve surgery were included in the study. The ten patients receiving pentoxifylline (PTX group) were administered 400 mg PTX orally TID for 3 days preoperatively and, following anesthetic induction, a 300 mg PTX infusion was given. The ten patients receiving no PTX were the control group (CT). Platelet and leukocyte counts, mean pulmonary arterial pressure (mPAP), pulmonary capillary wedge pressure (PCWP), cardiac index (CI), pulmonary vascular resistance (PVR), alveolar-arterial PO2 gradient (AaDO2) were measured just before and after CPB, and 2 h postoperatively. The number of the leukocytes increased in the blood samples drawn 15 min after CPB in both groups and 2 h postoperatively showed no statistical change. The number of platelets had decreased significantly at the end of the CPB in both groups and, 2 h postoperatively, there was a further decrease in the blood count in the control group (P < 0.05). There was no significant difference in either the preoperative or postoperative PAP, PAWP, and CI. Pulmonary vascular resistance increased in both groups following the CPB (CT, before: 136 +/- 44, after: 177 +/- 94 dyne. sec.cm-5; PTX, before: 151 +/- 82, after 182 +/- 43 dynes.sec.cm-5). Two hours postoperatively, a considerable increase continued in the control group (CT 219 +/- 170 dynes.sec. cm-5), while there was an insignificant increase in the PTX group (PTX 193 +/- 51 dynes.sec.cm-5) (P < 0.05). The alveolar-arterial PO2 gradient increased after the CPB in both groups but a moderate decrease was observed 2 h postoperatively. In lung biopsy specimens taken before and after the CPB, there was marked leukocyte sequestration in the control group, whereas the number of leukocytes was seen to be insignificant in the PTX group (P < 0.005). This dosage regimen of PTX inhibits the postoperative increase in PVR and greatly minimized leukocyte sequestration in the lung due to CPB.
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PMID:The effect of pentoxifylline on the lung during cardiopulmonary bypass. 873 90

Pulmonary hypertension (PHT) is a rare entity that is difficult to treat. Prognosis is poor. Sildenafil, a selective inhibitor of type 5 phosphodiesterase, has been proposed among the many treatments available for primary and secondary pulmonary hypertension. We report our experience with an infant with pulmonary hypertension due to congenital mitral stenosis and persistent ductus arteriosus, who developed congestive cardiac failure with persistent PHT despite surgical correction. Conventional treatment was unsuccessful and the patient was treated with sildenafil. The clinical course was satisfactory, allowing extubation and withdrawal of vasoactive drugs; pulmonary and left atrial pressure decreased and the patient was discharged. She is currently being treated on an outpatient basis with oral sildenafil and shows satisfactory hemodynamic status. We review alternatives to conventional treatments for pulmonary hypertension with special reference to pediatrics.
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PMID:[Sildenafil in the treatment of pulmonary hypertension]. 1288 79

A 57-year-old man with mitral stenosis underwent mitral valve plasty under general anesthesia. He had a history of cerebral infarction. Although he was with atrial fibrillation, his left ventricular function was good. Preoperative coronary angiography revealed no significant coronary stenosis. Induction of anesthesia and the surgical procedure had been uneventful, but the patient had difficulty to wean the patient from cardiopulmonary bypass because of unexpected low cardiac output syndrome. O1-prinone hydrochloride, a newly developed phosphodiesterase III inhibitor, was initiated in addition to high doses of dopamine and dobutamine. This increased the amplitude of the electrocardiogram and caused ST elevation of the lead II. A full dose of isosorbide dinitrate was administered intravenously to differentiate coronary artery spasm from coronary air embolism. This drastically improved the ventricular function and mixed venous oxygen saturation, and weaning from CPB was finally accomplished. The heart showed hypercontraction and inotropes were tapered gradually without further cardiac events. Although there are various etiologies for low cardiac output syndrome after CPB, the possibility of myocardial ischemia must be the first consideration. Full pharmacological support must be tried before initiating a mechanical assist modality. Coronary dilators, nitrates in particular, and phosphodiesterase III inhibitors are promising agents in such cases.
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PMID:[Successful management of a patient for cardiac surgery with difficulty in weaning from cardiopulmonary bypass by using both isosorbide dinitrate and olprinone hydrochloride]. 1529 45

A 1-year and 11-month-old girl with congenital mitral stenosis (MS) and patent ductus arteriosus (PDA) underwent mitral valve replacement (CarboMedics 16 mm) and ligation of PDA. Though she had suffered from severe postoperative pulmonary hypertension crisis, the inhalation of nitric oxygen (NO) with intravenous use of phosphodiesterase (PDE) III inhibitor and prostaglandin I2 (PGI2) was useful for the postoperative management. Severe pulmonary hypertension is the one of critical postoperative complications for congenital MS with PDA cases. Therefore adequate treatments, such as the combination of NO, PDE Ill inhibitor and PGI2, should be important for those cases. In our case, cardiac catetherization revealed a remaining of pulmonary hypertension under medication of beraprost sodium. Further observation should be necessary for the patient including new medicine, such as sildenafil citrate.
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PMID:[Postoperative management for severe pulmonary hypertension in a patient with congenital mitral stenosis and patent ductus arteriosus]. 1652 92

Pulmonary hypertension is a serious disorder, difficult to treat especially in the severe forms. The treatment consists mainly of calcium channel blockers, anti-coagulation, intravenous epoprostenol, inhaled nitric oxide and recent agents as bosentan and sildenafil. Sildenafil, a phosphodiesterase 5 specific inhibitor, has been largely evaluated in primary pulmonary hypertension, and in some cases of secondary pulmonary hypertension including parenchymal and thromboembolic diseases; it has not yet been evaluated in severe pulmonary hypertension with elevated pre-capillary resistance in operated mitral stenosis. We report the cases of two patients operated from mitral valve replacement for severe mitral stenosis with elevated pre-capillary resistance, where oral sildenafil, introduced empirically immediately after the surgical procedure at the dose of 50 mg/d, permitted a significant decrease in pulmonary pressures and resistances, allowing a rapid withdrawal of nitric oxide and reducing therefore hospitalization time in the intensive care unit. We think that this simple treatment, with or without association to nitric oxide, should be generalized to persistent pulmonary hypertension following cardiac surgery.
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PMID:[Beneficial effect of sildenafil following surgery for mitral stenosis complicated by pre-capillary pulmonary hypertension: report of two cases]. 1707 67

The phosphodiesterase inhibitor milrinone is usually preferred in patients with pulmonary hypertension and myocardial dysfunction after cardiopulmonary bypass. We investigated the effects of low-dose milrinone on pulmonary hypertension in the immediate pre- and postoperative period. Forty-seven patients were randomized to the control and milrinone groups. All patients had mean pulmonary artery pressure greater than 30 mmHg and pulmonary capillary wedge pressure greater than 20 mmHg and were candidates for mitral valve replacement for rheumatic mitral stenosis. Twenty-four patients received a loading dose of milrinone 25 microg/kg(-1) during weaning from cardiopulmonary bypass, followed by a maintenance dose of 0.25 microg/kg(-1)/min(-1) to the end of the surgery. Cardiac output and other hemodynamic variables were noted at induction, weaning from bypass, and postoperative 1 h. Pulmonary artery pressure, capillary wedge pressure, and central venous pressure were significantly lower in the milrinone group during weaning after cardiopulmonary bypass, while other variables were roughly similar. However, patients in the control group required higher doses of vasodilators, inotropes, and antiarrhythmic agents. Mean arterial pressure in the milrinone group was significantly lower at 1 h postoperatively than in the control group; however, the patients did not need many more vasopressors. Fluid restriction and diuretic agent use were more significant in the control group. Systemic arterial hypotension and vasopressor requirements with milrinone use at inotropic doses were not observed at the doses used for the study. A total of 21.7% of the patients in the control group required vasopressors in the perioperative period. Both groups demonstrated similar hematologic variables except that the hemoglobin level in the control group was significantly lower during postoperative days 1 and 7. Low-dose milrinone for a short-term during weaning from cardiopulmonary bypass may be used in patients with mitral stenosis and pulmonary hypertension for its effects on pulmonary artery pressures, less inotropic and vasopressor requirements, and fluid balance.
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PMID:Effects of low-dose milrinone on weaning from cardiopulmonary bypass and after in patients with mitral stenosis and pulmonary hypertension. 1726 58

Left heart disease (LHD) is probably the most frequent cause of pulmonary hypertension (PH). Although rheumatic mitral valve stenosis has been in the past the most common cause of this condition, PH-LHD mainly results from heart failure related to systolic and/or diastolic dysfunction of the left ventricle and is associated with elevated left-sided cardiac filling pressures. Most patients have passive increase in pulmonary arterial pressure because of backward transmission of the elevated left atrial pressure, whereas a small subset develop severe PH with elevated transpulmonary gradient and pulmonary vascular resistance. When present, PH is usually associated with a poor prognosis and increased mortality. Optimizing heart failure regimens and corrective valve surgery are the cornerstones of the treatment of PH in LHD. Although PH-LHD may evolve to right ventricular failure and is associated with some changes in the pulmonary vascular bed similar to pulmonary arterial hypertension (PAH), there is no evidence-based data to support the use of PAH-specific therapies in the setting of PH-LHD. However, recent studies suggest the usefulness of sildenafil, a phosphodiesterase-5 inhibitor. This review addresses the epidemiology, pathophysiology, risk factors, and treatment controversies of PH due to LHDs.
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PMID:Pulmonary hypertension associated with left heart disease. 2403 33

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