Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lidocaine-induced seizures have been reported after topical administration. A 30-year-old, 48-kg women with acquired immunodeficiency syndrome, chronic end-stage renal failure, anemia, congestive heart failure (CHF), cardiomyopathy, and increased liver function tests was admitted to the hospital with fever, chills, and dry cough. Bronchoscopy was performed to rule out Pneumocystis carinii pneumonitis; the patient experienced seizure activity after administration of a total dose of topical lidocaine 300 mg. Plasma drug concentration measured shortly after seizure, and at 4 and 22 hours after seizure were 12.0, 7.6, and 1.4 mg/L, respectively. A direct correlation exists between clinical symptoms and blood level of lidocaine; as the level increases to 8-12 mg/L the probability of seizure increases. The extent of absorption and bioavailability after airway administration depends on tissue vascularity, sites and techniques of application, patient's disease state, and, most important, the dose/unit body weight. The lidocaine dose should be titrated slowly and patients monitored for altered mental status. The dose often has to be decreased empirically in patients with liver disease or CHF. Efforts should be made to deliver minimum amounts of the drug to the lower respiratory tract, since its pharmacokinetics at that site are similar to those with intravenous administration.
 ...
PMID:Seizure after lidocaine for bronchoscopy: case report and review of the use of lidocaine in airway anesthesia. 843 71

The clinical course of congestive heart failure (CHF) and mitral valve stenosis (MVS) is accompanied by episodes of dyspnea, wheezing, and cough, symptoms also observed in patients with bronchial hyperreactivity. However, it is still controversial whether bronchial hyperreactivity is demonstrable in patients with chronic overload of the pulmonary circulation. In order to examine the effects of CHF on the respiratory function, we performed pulmonary function tests, titrated bronchial acetylcholine provocations, and left and right heart catheterization in 21 patients with impaired left ventricular function (mean ejection fraction, 37 percent, NYHA class 3), 5 patients with MVS, and 17 control patients with coronary artery disease (mean ejection fraction, 63 percent). Bronchial hyperresponsiveness was defined as an obstructive response to increased doses of inhaled acetylcholine. A 20 percent fall in forced expiratory volume in the first second (FEV1), a 100 percent increase in total airway resistance (Rtot), and a 60 percent reduction of pulmonary conductance (SGtot) were considered positive. Patients with impaired left ventricular function showed significantly higher airway resistance, and lower airway conductance at the maximal tolerated acetylcholine dose compared with control patients. Patients with MVS had a significant lower airway conductance. The induced bronchial obstruction was completely reversible upon inhalation of a beta 2-mimetic. We conclude that chronic overload of the pulmonary circulation is accompanied by bronchial hyperreactivity that may augment the symptoms of dyspnea in patients with CHF and MVS.
 ...
PMID:Bronchial hyperreactivity in patients with moderate pulmonary circulation overload. 848 30

Pharmacologic agents that attenuate the influence of the renin-angiotensin-aldosterone system are known to reduce systemic arterial blood pressure through vasodilatory action and enhanced renal clearance of sodium and water. Angiotensin-converting enzyme inhibitors are known to antagonize the renin-angiotensin-aldosterone system through their ability to inhibit conversion of angiotensin I to angiotensin II. A new class of antihypertensive agents, angiotensin-II receptor antagonists, has recently been developed. These agents specifically block the receptor for angiotensin II, thereby limiting angiotensin II-mediated vasoconstriction and reducing aldosterone secretion. These effects result in a reduction in systemic arterial blood pressure through reduced vascular tone and enhanced sodium and water clearance. Clinical trials have demonstrated the efficacy of these agents in reducing blood pressure. These new antihypertensive agents also have uricosuric actions and are well tolerated, with a low incidence of cough and angioedema, side effects that are seen with angiotensin-converting enzyme inhibitors. Clinical trials are underway to see if these drugs will be useful in the treatment of diseases other than hypertension, such as congestive heart failure and chronic renal disease.
 ...
PMID:Angiotensin-II receptor antagonists: a new class of antihypertensive agents. 862 40

Angiotensin II receptor antagonists represent a new class of drugs that provide a site-specific blockade of the effects of angiotensin II. Losartan potassium, the first compound of this drug class, has recently become available in the United States. The clinical experience with angiotensin II receptor antagonists has demonstrated that these drugs are safe and efficacious for the treatment of hypertension and, possibly, congestive heart failure. Unlike with angiotensin-converting enzyme inhibitors, the incidence of cough observed with angiotensin receptor antagonists is similar to that with placebo. Although several angiotensin receptors have been characterized, the effects of losartan and other angiotensin receptor antagonists under development are selective for the angiotensin II type 1 receptor. Unlike angiotensin-converting enzyme inhibitors, angiotensin receptor antagonists do not inhibit bradykinin metabolism or enhance prostaglandin synthesis. The antihypertensive efficacy of the angiotensin receptor antagonists has been documented to be similar to that of angiotensin-converting enzyme inhibitors. If the findings of clinical studies corroborate the initial reports on efficacy and safety, it seems likely that the angiotensin receptor antagonists will be added to the list of drugs that have been deemed suitable for first-line therapy in the treatment of hypertension and congestive heart failure.
 ...
PMID:Angiotensin II receptor inhibition. A new therapeutic principle. 882 49

One adverse effect of the angiotensin-converting enzyme (ACE) inhibitors used for treatment of hypertension and congestive heart failure is the production of dry coughs. Imidapril is a new type of ACE inhibitor with a very low incidence of coughs. The magnitude and the mechanism of cough potentiation of imidapril and other ACE inhibitors has been studied in guinea-pigs. In normal guinea-pigs single and repeated dosing of imidapril at 0.1 to 100 mg kg-1 had no effect on capasaicin- or citric acid-induced coughs. Single and repeated dosing of enalapril and captopril at 10 to 30 mg kg-1, respectively, significantly increased the number of capsaicin-induced coughs. Repeated dosing of 1 mg kg-1 enalapril also significantly augmented the capsaicin cough. In bronchitic guinea-pigs imidapril also had no effect on the coughs induced by the two stimulants. Enalapril and captopril significantly increased the number of coughs induced not only by capsaicin but also by citric acid. Lower doses of enalapril were enough to augment the capsaicin-induced coughs, whereas medium to large doses failed to augment the cough irrespective of the protocol of administration. Bradykinin-induced discharges of the vegal afferents from the lower airway were significantly increased by enalaprilat but not by imidaprilat. Capsaicin-induced discharges of the afferents were, on the other hand, significantly depressed by enalaprilat, but not by imidaprilat. Interestingly, enalaprilat depression of the discharges was significantly reversed by Hoe-140, a bradykinin B2 receptor blocker. In guinea-pigs pretreated with a low dose of enalapril, arterial infusion of bradykinin significantly potentiated the coughs induced by capsaicin. The results indicated that imidapril was less potent than enalapril and captopril in potentiating cough responses induced by capsaicin and citric acid in guinea-pigs, and further suggest that bradykinin might be a key substance in the mechanism of the potentiation of coughs associated with ACE inhibitors.
 ...
PMID:Studies on the magnitude and the mechanism of cough potentiation by angiotensin-converting enzyme inhibitors in guinea-pigs: involvement of bradykinin in the potentiation. 895 4

We examined the sputum of 114 subjects by noninvasive methods (voluntary coughing or induced cough with hypertonic saline) to determine whether sputum examination could be used to separate patients with episodic wheezing, dyspnea or cough of unknown origin into different diagnostic categories. An increased percentage of sputum eosinophils was seen in 92% (48/52) of asthmatics, 36% (9/25) of patients with chronic obstructive pulmonary disease (COPD) and 28% (7/25) of chronic coughers, but not in any of the 12 patients with congestive heart failure (CHF). Eight patients with combined symptoms of COPD and asthma (mixed COPD subgroup) showed above average diurnal peak expiratory flow variation (10.3 +/- 2.1% vs 2.5 +/- 1.4%, p < 0.05) and an above average percentage of sputum eosinophils (19.8 +/- 9.1 vs 2.1 +/- 3.2, p < 0.01) than those in the pure COPD group. After therapeutic corticosteroid trial, all of the mixed COPD patients and six of the 17 pure COPD patients were steroid responders. Seven of the 25 chronic coughers had sputum eosinophilia, but no asthmatic symptoms. The cough symptoms subsided in five of these seven patients after steroid treatment but not in the other 18 chronic coughers. Further study is indicated to determine if simple eosinophilic bronchitis is an early stage of asthma. In conclusion, sputum differential cell counting is a useful noninvasive diagnostic tool in differentiating diseases with episodic wheezing or chronic cough.
 ...
PMID:Importance of sputum differential cell counting in the diagnosis of airway diseases. 917 Aug 20

There are several theories on the cause of ACE inhibitor-induced cough, but the exact mechanism is not known. In many patients, if cough develops, the ACE inhibitor can be discontinued and a drug in another therapeutic class used in its place. However, in patients with CHF, diabetic nephropathy, and patients who have experienced a myocardial infarction, discontinuing the ACE inhibitor may not be in the best interest of the patient. In this patient population it would be reasonable to try cromolyn sodium to treat cough, while continuing the ACE inhibitor. Data are not available to support the efficacy of cromolyn sodium to treat cough in patients with diabetic nephropathy, but these patients clearly benefit from the use of an ACE inhibitor. Other factors not addressed in the case reports and the clinical trial such as patient adherence, cost, and quality of life should also play a role in the decision to use cromolyn sodium. Cromolyn sodium has been effective for the treatment of ACE inhibitor-induced cough in many case reports and has had mild success in one small clinical trial. Although none of the reports adequately assessed adverse effects, studies examining cromolyn for other indications have demonstrated a relatively benign adverse effect profile. It is difficult to recommend an exact dose to use because of the dosing variability in the case reports. The majority of the case reports and the one clinical trial used dosages similar to recommendations for bronchial asthma (i.e., 2 puffs [1.6 mg] 4 times daily via MDI or 20-mg capsules 4 times daily via breath-activated inhalation). At this time, the use of cromolyn sodium is a viable option, but more controlled studies are needed to fully elucidate its role in the treatment of ACE inhibitor-induced cough.
 ...
PMID:Cromolyn sodium for ACE inhibitor-induced cough. 918 21

Benazepril (BP), an angiotensin convertive enzyme inhibitor, was administered orally once daily for 4 weeks to 31 dogs with mild to moderate (NYHA functional classes II and III) congestive heart failure caused from mitral insufficiency (MI). There were no significant changes in clinical signs, electrocardiogram findings, radiographical observations and plasma biochemical results in 11 dogs treated with placebo for 4 weeks. In 31 dogs treated with BP, appetite increased, and mean scores of heart failure signs, such as activity, exercise tolerance, cough and respiratory effort, were significantly improved. No dog displays signs suggesting systemic hypotension. One dog died suddenly on the 26th day of treatment with BP. This dog had good vigor and appetite till the evening before the death, and cough and exercise tolerance had been gradually improving. The heart rate and ECG parameters of BP treated dogs did not change significantly, but length of long axis of the heart decreased. In plasma biochemical tests, plasma urea nitrogen (UN) levels did not change significantly, and plasma creatinine (CRE) levels increased slightly within the normal ranges during BP trial. Two dogs had higher plasma UN levels with slightly higher plasma CRE levels, but had normal general condition and other biochemical results. Plasma ACE activity decreased to 57.3% of pre-treatment level at 4 weeks after BP treatment. It is concluded that BP monotherapy was efficacious at least in dogs with relatively low grade congestive heart failure caused by MI.
 ...
PMID:Efficacy of monotherapy with benazepril, an angiotensin converting enzyme inhibitor, in dogs with naturally acquired chronic mitral insufficiency. 927 44

Nonpeptide angiotensin II type 1-receptor antagonists, AT1 receptor antagonists are newly developed and useful drugs for hypertension and congestive heart failure. In Japan, the efficacy and safety of losartan and candesartan cilexetil in patients with essential hypertension have been evaluated by the double-blind, parallel group-comparison study using enalapril as control drug. Both trials revealed that these drugs showed a hypotensive effect comparable to that of enalapril with a high safety since the adverse drug reaction of cough was recognized in very few patients. Furthermore, a recent randomised trial of losartan versus captopril in patients over 65 with heart failure, evaluation of losartan in the elderly study (ELITE), showed that losartan was associated with a lower mortality than that found with captopril. Further studies will clarify differences in protection of cardiovascular system with a long-term treatment between AT1, receptor antagonists and angiotensin-converting enzyme inhibitors.
 ...
PMID:[Angiotensin receptor antagonist for therapy of patients with hypertension]. 928 26

Whether any class of antihypertensive drugs has specific renoprotective effects above and beyond lowering of blood pressure is still debatable. The renin-angiotensin system (RAS) is both localized and has many actions within the kidney, on intrarenal hemodynamics, on the mesangial cell, as well as stimulating growth factors and cytokines. Angiotensin converting enzyme (ACE) inhibitors have been shown to ameliorate the progression of renal failure. How much of this beneficial effect is due to their hemodynamic effects, how much to non-hemodynamic effects and how much to their effects on bradykinin and other putative ACE substrates is still unclear. Experimentally it can be shown that inhibiting ACE but preventing the fall in systemic blood pressure by salt loading abolishes renoprotection. Bradykinin has been implicated in both the beneficial and the adverse effects of ACE inhibitors. Because of this and because ACE inhibitors may not provide complete blockade of the RAS, angiotensin receptor (AT1R) antagonists have been developed. Experimentally AT1R antagonists have been shown to reproduce most of the beneficial effects of ACE inhibitors. The experience in humans is more limited but they have been demonstrated to be efficacious in hypertension, to reduce proteinuria, and produce a favorable hemodynamic effect in congestive cardiac failure with a low incidence of adverse effects and without cough. Calcium channel blockers (CCB) also have additional properties that may provide renoprotection beyond lowering blood pressure. However, as the different types of CCB block different calcium channels their effects may differ substantially. The inconsistency of the data in the renoprotective effect of CCB may reflect these differences. Quantitatively probably the most important factor in preventing the progress of renal failure by antihypertensive drugs is strict control of blood pressure. Lowering blood pressure by drugs is most likely effective by both reducing physical and sheer stress damage, as well as turning off the signal for the activation and production of vasoactive peptides and cytokines.
 ...
PMID:Comparison of renin-angiotensin to calcium channel blockade in renal disease. 940 14


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>