ABSTRACT
A comparative pharmacokinetic study of enrofloxacin (5 mg/kg, sc) was conducted in probenecid-pretreated (70 mg/kg, orally 1.5 h prior to enrofloxacin administration) lactating goats to assess the effect of probenecid on the kinetics of enrofloxacin. Concentration of enrofloxacin in plasma, milk and urine was estimated by microbiological assay using Escherichia coli (ATCC 25922). Minimum detection level of enrofloxacin was 0.01 microg/ml. The plasma log concentration versus time curve showed monophasic pattern and followed one compartment open model. Plasma drug concentration was significantly higher during 1-2 h in probenecid-pretreated group. Significantly higher drug concentration in milk was noted at most of the time points, while significantly lower urine drug concentration (0.083-1 h and 5-12 h) were obtained in probenecid-pretreated group. The kinetic parameters (A, B and 3) were significantly higher, while t(1/2)beta, MRT and Vd(area) were significantly lower in probenecid-pretreated group. Probenecid pretreatment decreased the urinary excretion of enrofloxacin, whereas enhanced excretion in milk which could be useful in cases of affections of udder in goats.
Subject(s)
Animals , Female , Fluoroquinolones/administration & dosage , Fluoroquinolones/analysis , Fluoroquinolones/pharmacokinetics , Goats/blood , Goats/physiology , Goats/urine , Injections, Subcutaneous , Lactation/drug effects , Milk/chemistry , Probenecid/administration & dosage , Probenecid/pharmacologyABSTRACT
Perfusion lung scan using macroaggregate of human serum albumin tagged with I131 was done in 7 patients with tropical pulmonary eosinophilia (TPE). In the 3 untreated patients perfusion defect of varying degree could be noticed, whereas in 4 other patients with history of chronic illness and previous treatment with multiple courses of diethylcarbamazine the lung scan was normal. Possible pathophysiology in light of above findings in TPE is discussed.
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Perfusion , Serum Albumin, Radio-Iodinated/diagnosisABSTRACT
(+) Propranolol is considered to prevent adrenaline-induced pulmonary edema (A.P.E.) due to the beta-adrenoceptor blockade. However, local anaesthetics also are known to prevent pulmonary edema. To assess the role of beta-adrenergic blockade in A.P.E., the effect of a beta 1-blocker possessing local anaesthetic action (+/- Metaprolol) and a beta 1-blocker possessing no local anaesthetic action (+/- practolol) was studied along with propranolol derivatives. The study revealed that (+), (-), (+/-) propranolol and (+/-) metaprolol completely prevented A.P.E. whereas (+/-) practolol did not. This shows that local anaesthetic action but not the-beta adrenergic blockade may be responsible for prevention of A.P.E.
Subject(s)
Adrenergic beta-Antagonists/pharmacology , Animals , Body Weight , Epinephrine/pharmacology , Female , Hemorrhage/physiopathology , Male , Mice , Organ Size , Propranolol/pharmacology , Pulmonary Edema/chemically inducedABSTRACT
A study has been carried out to examine the role of pulmonary surfactants in pulmonary oedema induced by head injury. Pulmonary oedema was induced by head injury in mice by the method of Mackay (5). There was no change in surface tension as well as total phospholipid concentration of the lung between control and test groups suggesting that there was no involvement of lung surfactant sytem in pulmonary oedema induced by head injury. Since the animals in the test group died within a few minutes, possibly there may not have been sufficient time for alteration of lung surfactant system.