Chloroform extracts of stem and root of Punica granatum and Artrmisia siversiana, used in ancient Indian Medicine as anthehnintics, were investigated for any activity.against Syphacia obvelata, Nippostrongylus brasiliense and Hymenolepis nana in vivo. Both extracts were able to eliminate H.nana from mice. Their potency was less as compared to Quinacrine. It is suggested that these drugs should be tried for tapeworm infestations in man and domestic animals.

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Digoxin was given intravenously in anaesthetized dogs in the dose of 25 'g/kg every 15 min till the animals died. ECG and carotid blood pressure were continuously monitored. Digoxin produced dose-dependent bradycardia. In physostigmine pretreated animals, the negative chronotropic activity of digoxin appeared to be slightly more than in the control animals. While atropine pretreatment did not appear to significantly affect the negative chronotropic activity of digoxin, but the negative chronotropic activity was found than to be less in vagotomized dogs than in the control dogs. These results indicate that part of the negative chronotropic activity of digoxin was mediated through cholinergic activation. Blockade of the adrenergic system, especially with the use of beta-adrenergic blocking agents, enhanced the negative chronotropic activity of digoxin. In this respect adrenal gland was not found to have any significant role. Propranolol pretreatment potentiated the negative chronotropic activity while adrenalectomy had no significant effect. It appeared that functional adrenergic activity partly offsets the negative chronotropic activity of digoxin. Continued administration of digoxin produced varieties of arrhythmias-bradyarrhythmias and tachyarrhythmias. Both types of arrhythmia were found to be present in the same dog in many of the cases.Terminal event was evoked in the form of ventri -cular fibrillation (VF) or cardiac arrest.The incidence of bradyarrhythmiar was found to be more in propranolol or physostigmias pretreated animals,On the other hand, the incidenece of bradyarrhythmine was low in vagotomized animals. Digoxin-induced tach arrhythmias were slightly but not significantly reduced by physostigmine or propranolol pretreatment, or in adrenalectomized dogs. It appeared that bradyarrhythmias were facilitated by cholinergic activity while tachyarrhythmias were not significanty affected by autonomic nervous system (ANS). In digitalized dogs, nearly half of the animals ended with VF and the other half in the cardiac arrest. None of the prapranolol pretreated dogs died of VF while all the vagotomized dogs died of VF. Physostigmine pretreatment reduced the incidence of VF. It seemed, therefore, that adrenergic activity potentiated digitalis-induced VF, while cholinergic activity had a protective role. Sub epicardial administration of digoxin in the concentration of 50 to 250 'g/ml at the rate of 10 'l/min for 5 min produced a unifocal ventricular extrasystole, the frequency of which was dependent on the concentration used. In none of the experiments, there was VF. These arrhythmias were always reversible. It was concluded that systemic administration of digoxin is more arrhythmogenic than the local administration, possibly because of activation of central and autonomic system along with the global effects digoxin on the heart whein given systemically. These focal arrhythmias could also be antagonized when administered along with propranolol.

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A simple and sensitive colorimetric method of assay of heparin sodium based on the comparative determination of anticoagulant activity of the test preparation with that of the standard has been deveIoped. The method involves the assessment of the quantity of heparin required to prevent 50 percent clotting (ED50) of a fixed amount of citrated goat plasma in presence of calcium ions. The method is more precise and rapid than and comparable in accuracy and reproducibility with the USP method. It has the further advantage that the subjectivity inherent in the existing bioassay methods is eliminated.

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Goat isolated trachea contracted to acetylcholine, histamine and barium chloride in a dose-dependent manner and to 5-hydroxytryptamine in a narrow dose range. Pheniramine blocked contractions to histamine while cimetidine potentiated. Atropine and cyproheptadine antagonised the contractions of acetylcholine and 5-hydroxytryptamine respectively. The relaxatory responses to epinephrine and isoprenaline were blocked by propranolol. These observations suggest the presence of both H1-excitatory and H2-inhibitory receptors for histamine, excitatory tryptamine and muscarinic receptors for 5-hydroxytryptamine and atropine and á-adrenergic receptors.

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Fifty patients attending Dental College and Hospitals (including private clinics ) at Ahmedabad. having gingivitis and bleeding gums, were advised to massage the gums with alcoholic extract of Chicorium intybus (chicory) roots, twice a day for three weeks.The gingival inflammation index was noted for each patient before starting the use of chicory extract and at the end of each week for three weeks. The analysis of the 42 turned up cases indicates the relief in the inflammatory and bleeding conditions of the gums consistently from day by day and week to week.

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The cbolioesterate (ChE) inhibitory activity of different groups of anti-arrhythmic drugs were investigated in vitro these drugs were found to be more potent in inhibiting the plasma (pseudo) ChE than RBC (true) ChE enzymes. On the basis of the potency as pseudo ChE inhibitor, these drugs could be divided into potent inhibitors like quinidine, UM-272 (the quaternary methyl analogue of propranolol), moderate inhibitors like racemic propranol, chloroquine quinine and procainamide and weak inhibitors like lignocaine, timolol and sotalol, Both racemic propranolol and UM-272 were found to reverse ouabain-induced arrhythmias in dogs where as timolol was found to have no such property. A good correlation exists between the in vitro inhibition of pseudoChE enzyme and the antagonism of ouabin arrhythmias in dogs.

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Sodium Fluorocetate (Na FAC, 20 'g to 320 'g) and dobutamine (.5 'g to 8 pg) produced dose dependent positive inotropic effect in isolated frog heart preparation, without affecting the heart rate. The responses to Na FAC and dobutamine were inhibited when calcium chloride (CaCl2) concentration was increased from 1.58 mM to 3.17 mM in frog Ringer solution. When Ca Cl2 concentration was reduced the responses to both Na FAC and dobutamine were potentiated. By reducing the potassium chloride (Kcl) concentration in the perfusion fluid (from 1.8 mM to 0.9 mM) the responses to Na FAC were potentiated, while increasing the concentration (from 1.8 mM to 3.6 mM) the responses were inhibited. However, the responses to dobutamine were unchanged by changing the Kc1 concentration in perfusion fluid. The decrease in sodium chloride (Na Cl) concentration (from 110mM to 55mM) in frog Ringer solution, inhibited the responses to Na FAC while increase in Na Cl chloride concentration (from 110mM to 165mM) potentiated the responses to Na FAC. However the responses to dobutamine were unchanged when Na Cl concentration in perfusion fluid were altered. It is suggested from the date that Na FAC induced positive inotropic effects were probably due to sodium extrusion mechanism leading to facilitation of calcium uptake, Dobutamine may be acting directly through the mechanism independent of extracellular ions.

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The effect of hyaluronidase on the myocardial infarction induced by the administration of isoprenaline (IP) was investigated in rats. Hyaluronidase, administered intravenously following the IP injection, failed to alter the severity of myocardial lesions, as judged by ECG recordings, serum CK estimations and histology. These findings differ from the reported beneficial effects of hyaluronidase in myocardial infarction produced after coronary ligation. This discrepancy may be due to a different mechanism of production of myocardial infarction by the present method and better penetration of IP in the myocardial cells, thereby enhancing rhe toxicity of its higher doses.

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( piperidiao-1 (p-bromophenyl) propiophenone HCI exhibited specific H, but not H2 antihistaminio activity in vitro and in vivo. At the in vivo antihistaminic dose, except for a nonspecific transient hypotension, it was devoid of any other significant pharmacological activity.

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