Drugs online research references
Pharmacol Biochem Behav. 1983 Aug;19(2):313-20.
Increased shock-induced fighting with supersensitive beta-adrenergic receptors.
Hegstrand LR, Eichelman B.
Adult male rats were treated chronically with haloperidol (1 mg/kg) daily or propranolol (10 mg/kg bid) and evaluated for changes in shock-induced fighting. Haloperidol suppressed fighting. Chronic propranolol facilitated fighting when rats were tested eight hours after injection. Acutely, either 5 or 10 mg/kg of d,1-propranolol suppressed shock-induced fighting. Chronic pindolol (10 mg/kg bid) and chronic 1-propranolol (5 mg/kg bid) administration increased fighting. Chronic d,1-propranolol, 1-propranolol or pindolol administration was associated with an increase in Bmax for beta-adrenergic receptors. No change in fighting or Bmax was observed with the chronic administration of d-propranolol (5 mg/kg bid) or metoprolol (10 mg/kg bid). This increase in shock-induced fighting appears to be a behavioral response developing as a consequence of increased beta-adrenergic receptors responding to endogenously released norepinephrine.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6314390&dopt=Abstract
Circulation. 1981 Oct;64(4):708-15.
Changes in ischemic blood flow distribution and dynamic severity of a coronary stenosis induced by beta blockade in the canine heart.
Buck JD, Hardman HF, Warltier DC, Gross GJ.
The effects of equipotent beta 1-receptor-blocking doses of propranolol, metoprolol and sotalol on distal coronary pressure, stenosis resistance and regional myocardial blood flow (endo/epi) were studied in anesthetized dogs with a severe noncircumferential stenosis of the left circumflex coronary artery. No significant differences between the three beta blockers were observed for overall hemodynamics and regional myocardial blood flow. After drug treatment, subendocardial blood flow (0.47 +/- 0.05 to 0.78 +/- 0.05 ml/min/g) and endo/epi (0.67 +/-0.04 to 1.18 +/- 0.04) increased significantly (p less than 0.05) in the ischemic region. These changes were associated with a marked increase in distal coronary perfusion pressure and a decrease in heart rate. Resistance across the stenosis decreased significantly (p less than 0.05) after beta-receptor blockade (3.2 +/- 0.3 to 1.4 +/- 0.2 units). Atrial pacing to control heart rate only partially attenuated these changes. These results suggest that a favorable redistribution of ischemic blood flow after beta blockade is the result of an increase in distal diastolic pressure-time index and an autoregulation-induced increase in distal bed vascular resistance due to a decrease in myocardial oxygen demand associated with beta blockade. The latter effect also resulted in a decrease in the dynamic severity of a proximal coronary stenosis.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6115724&dopt=Abstract
J Pharmacobiodyn. 1992 Jun;15(6):295-302.
Brain and cerebrospinal fluid distributions of metoprolol in rats.
Nakazono T, Murakami T, Sakai S, Higashi Y, Yata N.
Institute of Pharmaceutical Sciences, Hiroshima University School of Medicine, Japan.
The distribution of metoprolol tartrate (MPL) into the brain and cerebrospinal fluid (CSF) from plasma was determined at 2 different steady-state plasma concentrations (2 and 20 nmol/ml) and following intravenous bolus administration (100 nmol/kg) in rats. Under steady-state condition, no difference in the brain and CSF distributions of MPL was observed between 2 different plasma MPL concentrations, and the value of brain- or CSF-to-plasma partition coefficients were 5.7 and 1.5, respectively. Following intravenous administration, MPL distributed into CSF very rapidly and its initial uptake phase was not detected. On the other hand, MPL distribution into the brain was relatively slow with the uptake phase. Thus, the brain uptake of MPL from the plasma was pharmacokinetically analyzed using a modified 2-compartment model and deconvolution method, whereas the CSF distribution of MPL was not adequate for kinetic analysis because of the lack of uptake phase. The analysis of brain uptake of MPL by both compartment model and deconvolution gave the same results and the calculated brain Kp value of MPL was almost comparable with that of observed Kp value under steady-state plasma concentration. The distribution of MPL into CSF was considered mainly depending on the pH difference between the plasma and CSF, and the mutual transfer of MPL between CSF and the brain tissue was considered to be negligible from an in vitro study.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1432569&dopt=Abstract
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