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Biomedical subjects

V S Murthy

Publications and source records attributed to V S Murthy.

At least 55 records · Page 3Linked to original sources
PubMed1982

Pentobarbital-induced changes in vagal tone and reflex vagal activity in rabbits.

The effects of pentobarbital on heart rate, reflexly mediated vagal activity and the automaticity (intrinsic rate) of the sinoatrial (SA) node were investigated in rabbits. When administered in three cumulative doses (10 mg/kg i.v. each) at 15 min intervals, each dose produced transient hypotension which was not modified by prior muscarinic receptor blockade (MRB), beta-receptor blockade (BRB), or combined MRB and BRB. Subanesthetic doses (10 mg/kg) of pentobarbital produced tachycardia in normal rabbits, as well as in rabbits with prior BRB. After pentobarbital, MRB failed to increase the heart rate, indicating total loss of resting vagal tone. Failure to induce tachycardia in rabbits with prior MRB indicated the absence of sympathetic stimulation in pentobarbital-induced tachycardia. In rabbits with prior BRB, pentobarbital enhanced the hypotensive effects of acetylcholine and nitroglycerin and abolished nitroglycerin-induced tachycardia without significant effects on the magnitude of reflex bradycardia produced by norepinephrine. Pentobarbital had minimal, transient depressant effects on the intrinsic rate of the SA node. These results indicate that pentobarbital produces total loss of resting vagal tone without major impairment of reflex vagal activation.

Animals↗
PubMed1982

Reversal of bradykinin-induced reflex tachycardia to bradycardia by captopril; evidence for prostacyclin involvement.

In conscious male New Zealand rabbits, bradykinin caused dose-dependent (0.03-1 microgram/kg i.v.) hypotension and reflex tachycardia. After inhibition of angiotensin converting enzyme (ACE, also known as kininase II) with captopril (1 mg/kg i.v.), the hypotensive effect of bradykinin was enhanced in magnitude and duration but the normally observed tachycardia was reversed to bradycardia. In rabbits treated with indomethacin to inhibit cyclooxygenase and then given captopril, the bradycardia to bradykinin reverted to tachycardia whereas the magnitude of the initial hypotensive effect was unchanged. However, inhibition of thromboxane synthetase with SQ 80,338 (1-[3-phenyl-2-propenyl]-1H-imidazole) was without effect on either bradykinin-induced hypotension or bradycardia in captopril treated rabbits. Infusion of nicotine to inhibit prostacyclin synthetase completely reversed the bradycardia induced by bradykinin in captopril-treated rabbits, an effect unrelated to ganglion blockade by nicotine since mecamylamine had no effect on the actions of bradykinin. beta-Adrenoceptor blockade with nadolol did not modify the bradycardia caused by bradykinin in captopril-treated rabbits whereas atropine methylnitrate caused a marked reduction. Captopril had no inhibitory effect on reflex tachycardia caused by nitroglycerin or acetylcholine and only reduced that caused by eledoisin. Hypotension and bradycardia resulted from giving rabbits prostacyclin (100 microgram/kg i.v.). These results suggest that the bradycardia observed in conscious rabbits to bradykinin after captopril treatment is the result of an increase in circulating bradykinin due to ACE (kininase II) inhibition leading to a vago-vagal reflex induced by the synthesis of prostaglandins, probably prostacyclin.

Acetylcholine↗
PubMed1982

Cerebral gumma.

Explore the source record for details and available documents.

Adult↗
PubMed1981

Influence of tricarboxylic acid cycle intermediates and related metabolites on the biosynthesis of aflatoxin by resting cells of Aspergillus flavus.

Resting cells of Aspergillus flavus synthesized aflatoxin from acetate as the sole carbon source after 36 h of incubation. Addition of pyruvate (5.5 mg/m) as cosubstrate to [1-14C]acetate and unlabeled acetate considerably reduced toxin production but increased the radioactivity on the tricarboxylic acid intermediates. This suggests that high tricarboxylic acid activity drastically affected toxin synthesis.

Acetates↗
PubMed1981

Antihypertensive activity of captopril (SQ 14,225), an orally active inhibitor of angiotensin converting enzyme in conscious two-kidney perinephritic hypertensive dogs.

Conscious dogs made hypertensive by wrapping both kidneys with cellophane were treated daily with a single dose of captopril (31 mg/kg p.o.), an inhibitor of the angiotensin converting enzyme, or with placebo (lactose, 31 mg/kg p.o.) for a period of 13 weeks. Blood pressures were recorded indirectly from a forepaw by using a Roche ultrasonic pressure transducer (Arteriosonde). Treatment with captopril resulted in decreases in blood pressure (25-30 mm Hg) that were maximal at 3 to 6 hr with no associated changes in heart rate. The captopril-induced hypotensive effect was maintained throughout the 13-week treatment period, and after the termination of captopril dosing, pressure rose slowly over the next 72 hr to a level not significantly different from placebo-treated dogs. Plasma renin activity (PRA) in the hypertensive dogs at the time treatment was initiated was not different from the same animals when they were normotensive. In captopril-treated animals, PRA increased 3- to 4-fold after each dose of the drug was given, reaching a maximum at 3 to 6 hr, a time corresponding to the maximal blood pressure decrease. PRA gradually declined but did not reach control levels before the next dose of captopril was administered. In animals treated with placebo, PRA remained at levels not significantly different from normotensive dogs during the entire treatment period. After termination of captopril administration, PRA slowly returned to pretreatment levels; the return of PRA paralleled the recovery of blood pressure. The results indicate that captopril is effective in reducing blood pressure for an extended period of time in a hypertensive model in which the level of activity of the renin angiotensin system is not elevated.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1980

The central canal of the filum terminale in communicating hydrocephalus.

Lumbar thecoperitoneal shunting was carried out in patients with communicating hydrocephalus due to long-standing tuberculous meningitis. At the time of this surgical procedure, the filum terminale was excised to achieve filum terminostomy. The central canal of the excised filum terminale in seven hydrocephalic children and an equal number from control cases was studied histologically. These observations indicate that the central canal of the filum terminale dilates in communicating hydrocephalus, and the dilatation is proportionate to the lateral ventricular enlargement.

Child↗
PubMed1980

Chronic subdural hematoma in the cerebellopontine angle.

A 32-year-old man had the clinical and radiological features of a mass lesion in the left cerebellopontine angle. Surgical exploration revealed a cyst containing 20 ml of altered blood. Microscopic examination of the cyst wall showed the structure of an organizing hematoma in the subdural space. The patient, on repeated questioning, denied a history of head injury.

Adult↗
PubMed1979

Hypotensive and other cardiovascular effects of arachidonic acid in rabbits.

Intravenous administration of arachidonic acid lowers systemic arterial pressure in conscious and anesthetized rabbits. This hypotensive response does not show tachyphylaxis and is blocked by aspirin. The hypotension on i.v. administration is due to both a decrease in cardiac output and a decrease in systemic vascular resistance. The decrease in cardiac output is accompanied by a severe pulmonary hypertension and right ventricular failure. Upon i.a. arachidonic acid administration, the hypotension is due to a decrease in systemic vascular resistance. It is proposed that arachidonic acid is transformed predominantly into a vasoconstrictor metabolite in the pulmonary vascular bed and vasodilator metabolite in the systemic vascular bed. The nature of the metabolite remains to be established.

Animals↗
PubMed1978

Hypotension induced by inhibition of angiotensin-converting enzyme in pentobarbital-anesthetized dogs.

The mechanism of the hypotensive response produced by inhibition of the angiotensin converting enzyme was studied in pentobarbital anesthetized dogs. A recently developed potent inhibitor of the converting enzyme, SQ 14,225 (D-3-mercapto-2-methyl propanoyl-L-proline), administered i.v. to intact dogs resulted in a rapid marked decrease in blood pressure. In nephrectomized dogs, SQ 14,225 retained significant hypotensive activity, although the absolute magnitude of the decreases in blood pressure were less than had been observed in dogs with intact kidneys. SQ 14,225 also lowered blood pressure when administered to intact dogs in which angiotensin II receptors had been blocked with the receptor antagonist Sar1,Ala8-angiotensin II. This apparent ability of SQ 14,225 to decrease blood pressure in the absence of a functional renin angiotensin system was shared by a structurally dissimilar, nonapeptide, angiotensin converting enzyme inhibitor, SQ 20,881 (Glu-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro). SQ 20,881 also produced significant decreases in blood pressure in nephrectomized dogs. These findings indicate that the angiotensin converting enzyme inhibitors, SQ 14,225 and SQ 20,881 may lower blood pressure in anesthetized normotensive dogs via a mechanism unrelated to either the renin angiotensin system or the renal kinin system.

Anesthesia↗
PubMed1978

Transitory block of the arachnoid granulations following subarachnoid haemorrhage. A postmortem study.

The arachnoid granulations of the superior sagittal sinus were examined for blockage by erythrocytes in 43 cases of subarachnoid haemorrhage. Ten cases had survived for more than two weeks after the haemorrhage. Among 33 cases with acute haemorrhage, 17 had evidence of blocking of the granulations. The severity of the block varied from complete clogging of nearly all granulations to slight filling of a few of them. Cases with some days' survival showed evidence of phagocytosis of the entrapped erythrocytes by macrophages. Several of the cases with old haemorrhage had groups of haemosiderin macrophages in the granulations but none showed fibrosis (except for one single villus). It is concluded that clogging of the arachnoid granulations may contribute to the raised intracranial pressure in some cases of acute subarachnoid haemorrhage. However, the observations do not support the hypothesis that the haemorrhage may lead to fibrosis or scarring of the granulations with chronic impairment of the cerebrospinal fluid resorption and subsequent hydrocephalus.

Acute Disease↗
PubMed1978

Studies on xylan hydrolases from different strains of Streptomyces and their mutual influences in the breakdown of xylan.

A good proportion of Sreptomyces isolates from natural sources produced extracellular xylan hydrolase. Nineteen isolated showing high activity were able to completely or partially degrade wheat bran in the growth medium. Chromatographic analysis of commercial xylan degradation products suggested that the isolates produced either endo- or exo-xylan hydrolases or their mixtures. Mixed additions of culture fluids showed a highly synergistic effect, up to an increase by 200%. In a few cases antagonism was seen which, however, could be removed by dialysis of the culture fluid.

Glycoside Hydrolases↗
PubMed1978

Alterations in brain and muscle oxygenation during hypovolemia and replacement with plasma substitutes in rats.

A study was conducted on the effects of mild hemorrhage-induced hypovolemia and subsequent replacement with lactated Ringer's dextran or hemoglobin solution in 52 pentobarbital-anesthesized rats. Blood loss of 1.25% of body weight had no significant effect on the blood flow or relative tissue PO2 of the white matter of the cerebral cortex. Blood flow and relative tissue PO2 of the biceps brachii muscle were lowered during hypovolemia. Volume replacement with any of the three plasma substitutes had no effect on blood flow or relative tissue PO2 of cortical white matter. They all caused partial restoration of blood flow and relative tissue PO2 in the biceps brachii muscle. Full return in the muscle was not achieved, nor were there any significant differences between the treatment groups.

Animals↗
PubMed1977

Inhibition of angiotensin converting enzyme by SQ 14,225 in conscious rabbits.

The cardiovascular pharmacology of SQ 14,225 (D-3-mercapto-2-methylpropanoyl-L-proline), a new orally effective inhibitor of angiotensin-coverting enzyme (ACE) was investigated in conscious normotensive rabbits. Intravenous administration of SQ 14,225 (3.1-310.0 microgram/kg) resulted in a dose related inhibition of the pressor responses to 310 ng/kg, i.v. of angiotensin I (AI) without diminishing the pressor responses to 100 ng/kg, i.v. of angiotensin II (AII). In fact, the responsiveness of the rabbits to AII was significantly enhanced by higher doses of SQ 14,225. This enhancement of the pressor effects of AII was found to be related to the inhibition of ACE and the resulting decrease in the levels of endogenous AII. In addition, SQ 14,225 (1.0 mg/kg, i.v.) markedly potentiated the magnitude and duration of the vasodepressor responses elicited by bradykinin (1.0 microgram/kg. i.v.). At a dose of 1.0 mg/kg. i.v., SQ 14,225 had no effect on the vasodepressor effects of intravenously administered isoproterenol (0.4 microgram/kg), acetylcholine (1.0 microgram/kg) or prostaglandin E2 (3.0 microgram/kg, i.v.). The pressor responses to norepinephrine (3.0 microgram/kg, i.v.) were similarly unaffected by SQ 14,225 (1.0 mg/kg, i.v.). In normal rabbits SW 14,225 (1.0 mg/kg, i.v.) caused a small but significant decrease in arterial pressure; it had no such effect in anephric rabbits. The observation of this study indicate that SQ, 14,225 is a specific inhibitor of ACE in conscious rabbits.

Angiotensin I↗