Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep apnea (SA) is associated with increased morbidity of the cardiovascular system, the interaction between the disordering of respiratory coordination and cardiovascular regulation being largely unknown. In 64 patients (age: mean = 54.1; range: 35-67 years) with an increased apnea index (AI greater than 10), a cardiac catheterisation investigation was performed to exclude coronary heart disease (CHD) or cardiomyopathy. CHD was excluded in 39 patients, 6 patients had coronary single-vessel disease, 9 patients coronary two-vessel, and 10 three vessel disease. In 10 patients, cardiomyopathy was detected, while high-grade impairment of the left ventricular ejection fraction (greater than 30%) was observed in five patients. With the exception of a single patient, CHD was observed only in patients in the over-fifty age group. Arterial hypertension was seen in 84% of the patients with, and in 69% of the patients without, CHD. The patient groups with and without coronary heart disease did not differ with respect to apnea index, ten minute index, or the average duration of the 30 longest apneic episodes. Anginal complaints, observed in a total of 72% of the patients, were one of the major indications for coronary angiography. These results do not support the assumption that SA is primarily a consequence of underlying cardiac disease, but do indicate that SA must be considered a cardiac risk factor, especially in view of the fact that pronounced nocturnal changes in blood gases and haemodynamics, together with malignant arrhythmias, are found in conjunction with this disturbance of breathing.
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PMID:[Results of left heart catheterization study in 64 patients with nocturnal disorders of respiratory control (sleep apnea)]. 260 54

The multidrug efflux pump P-glycoprotein (Pgp) is upregulated in cardiomyocytes following chronic ischemia from infarction and hypoxia caused by sleep apnea. This report summarizes the molecular dynamic studies performed on eight cardiovascular drugs to determine their corresponding binding sites on mouse Pgp. Selected Pgp transport ligands include: Amiodarone, Bepridil, Diltiazem, Dipyridamole, Nicardipine, Nifedipine, Propranolol, and Quinidine. Extensive molecular dynamic equilibration simulations were performed to determine drug docking interactions. Distinct binding sites were not observed, but rather a binding belt was seen with multiple residues playing a role in each studied drug's stable docking. Three key drug-protein interactions were identified: hydrogen bonding, hydrophobic packing, and the formation of a "cage" of aromatic residues around the drug. After drug stabilization, water molecules were observed to leak into the binding belt and condense around the drug. Water influx into the binding domain of Pgp may play a role in catalytic transition and drug expulsion. The cytoplasmic recruitment theory was also tested, and the drugs were observed to interact with conserved loops of residues with a strong affinity. A free energy change of astronomical value is required to recruit the drug from the cytoplasm to the binding belt within the transmembrane domain of Pgp.
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PMID:Characterizing the binding interactions between P-glycoprotein and eight known cardiovascular transport substrates. 2572 81