Drugs online research references
Circulation. 1994 Aug;90(2):873-7.
Mechanism of 'inappropriate' sinus tachycardia. Role of sympathovagal balance.
Morillo CA, Klein GJ, Thakur RK, Li H, Zardini M, Yee R.
Department of Medicine, University of Western Ontario, London, Canada.
BACKGROUND: "Inappropriate" sinus tachycardia (IST) is an uncommon and poorly defined atrial tachycardia characterized by inappropriate tachycardia and exaggerated acceleration of heart rate with "normal" P wave. The mechanism of this tachycardia is unknown. The purpose of the present study was to determine the role of autonomic balance in the genesis of IST. METHODS AND RESULTS: Six female patients aged 23 to 38 years with IST and 10 age- and sex-matched control subjects were assessed with the following autonomic function tests: (1) sympathovagal balance to the sinus node assessed by calculating the LF/HF (low frequency/high frequency) ratio using power spectral analysis both in the supine position and after 10 minutes of head-up tilt to 60 degrees, (2) cardiovagal reflex assessed by cold face test (CFT), (3) beta-adrenergic sensitivity as determined by calculating isoproterenol dose-response curves and isoproterenol chronotropic dose 25 (CD25), and (4) intrinsic heart rate (IHR) assessed after autonomic blockade with atropine 0.04 mg/kg and propranolol 0.2 mg/kg administered as an intravenous bolus. No significant differences in the LF/HF ratio both in the supine position (2.8 +/- 0.3 versus 2.6 +/- 0.4) and during upright tilt (8.7 +/- 1.3 versus 8.5 +/- 0.5) were observed between control subjects and IST patients. Cardiovagal response to CFT was markedly depressed in all patients (6.3% IST patients versus 24.2% control subjects, P < .001). beta-Adrenergic hypersensitivity to isoproterenol was noted in all patients (mean CD25, 0.29 +/- 0.10 microgram IST patients versus 1.27 +/- 0.4 microgram control subjects; P < .001), and high IHR was noted in all cases. The patients were treated with high doses of beta-blockers with adequate short-term control. Radiofrequency catheter ablation of the sinus node area was performed in one drug-refractory patient. CONCLUSIONS: These findings suggest that the mechanism leading to IST is related to a primary sinus node abnormality characterized by a high IHR, depressed efferent cardiovagal reflex, and beta-adrenergic hypersensitivity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7913886&dopt=Abstract
Arch Int Physiol Biochim. 1979 Dec;87(5):887-97.
An alpha-adrenotropic study of the normal and diabetic rabbit kidney.
Costa e Forti A, Fonteles MC.
Rabbit kidneys from normal and alloxan-treated animals were isolated and perfused at 30 degrees C, with Krebs-Henseleit solution. Norepinephrine (NOR), 1 microgram/min, promoted an increase in perfusion pressure which was blocked by phentolamine. In diabetic kidneys NOR induced a sluggish increase in perfusion pressure and resistance, showing a decrease in sensitivity of the adrenergic receptors to the drug. Propranolol, a beta-blocker, was able to elicit an alpha adrenergic blockade in diabetic kidneys. These facts demonstrate an adrenergic receptor defect in diabetic animals, which was shown just three weeks after alloxan treatment.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=94820&dopt=Abstract
J Hepatol. 1994 Apr;20(4):548-52.
Hemodynamic effects of acute administration of furosemide in patients with cirrhosis receiving beta-adrenergic antagonists.
Sogni P, Soupison T, Moreau R, Le Moine O, Bacq Y, Hadengue A, Lebrec D.
Laboratoire d'Hemodynamique Splanchnique, Hopital Beaujon, Clichy, France.
In patients with cirrhosis, both beta-blockers and diuretics decrease the degree of portal hypertension. Since their mechanisms of action differ, the combination of these two substances should induce a more pronounced effect on portal pressure than one of these substances alone. Thus, the hemodynamic effects of furosemide were evaluated in ten patients with cirrhosis receiving beta-blockers. One hour after furosemide (0.75 mg/kg intravenously) administration, cardiac output decreased significantly from 6.2 +/- 0.6 to 5.2 +/- 0.3 l/min and blood volume from 8.0 +/- 1.6 to 5.3 +/- 0.5 l. Mean arterial pressure was not affected. Wedged and free hepatic venous pressures did not change significantly; nor did the hepatic venous pressure gradient (19.6 +/- 1.7 to 18.6 +/- 1.5 mmHg). Azygos blood flow was not affected (0.46 +/- 0.05 to 0.50 +/- 0.07 l/min). In conclusion, this study did not demonstrate that the addition of furosemide to propranolol further decreased portal pressure in patients with cirrhosis. The long-term effects of this combination are unknown and should be tested.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7914215&dopt=Abstract
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