Our aim was to assess clinically whether there was any benefit in adding a single dose of sublingual nifedipine (a slow calcium channel blocker) to prazosin in the management of the cardiovascular manifestations of envenoming by the Indian red scorpion (Mesobuthus tamulus). A total of 163 patients stung by this species was admitted to hospital at Mahad between January 1991 and October 1993. Cardiovascular abnormalities were hypertension (59), of whom 42 had bradycardia and 17 had tachycardia; pulmonary oedema (14), of whom eight had hypertension and six hypotension; supraventricular tachycardia (eight), of whom three had hypotension and one died. Of the remaining patients, 78 demonstrated severe excruciating local pain at the site of sting but had no systemic involvement. Nineteen patients with hypertension and tachycardia were given a single dose of sublingual nifedipine plus prazosin on admission, then prazosin alone repeated 6 hourly. Five patients with massive life-threatening pulmonary oedema recovered after being given intravenous sodium nitroprusside. Prazosin alone helped to alleviate cardiovascular manifestations in the remaining 52 victims. One patient was admitted in a deep coma, 12 hr after the sting, and died. Eight victims whose blood pressure had been controlled in hospital by nifedipine plus prazosin developed acute pulmonary oedema necessitating additional doses of prazosin for recovery. Fifty-two victims treated with prazosin alone did not develop pulmonary oedema and the drug appeared to hasten the recovery. In the presence of high blood pressure, tachycardia, a murmur and impending myocardial failure, nifedipine appeared to contribute to cardiopulmonary instability and to augment myocardial oxygen consumption. In this situation calcium channel blockers should probably be avoided.

ConclusionIt is concluded that a relatively simple non-enzymatic substance, nicotinic acid, can induce fibrinolytic activity in vivo.

1. Observations were made on the physiological behavior of a compound in which the butyl side chain of phenylbutazone was replaced by a phenyl-thioethyl group. 2. Rate of biotransformation of this compound in man was greatly accelerated, with a biologic half life of only 3 hours compared to 70 hours for phenylbutazone. Such rapid disappearance might have some advantage in minimizing toxic manifestations but would pose the problem of maintaining therapeutic levels since the drug would have to be given at relatively frequent levels. 3. Like phenylbutazone, G-25671 exerted distinct antirheumatic effects but produced little or no sodium retention and consequently no hemodilution. These observations show that the antirheumatic and sodium-retaining properties in the phenylbutazone series may be dissociated. 4. The drug has a more marked uricosuric effect than phenylbutazone.

Adrenergic blocking with Dibenzyline measurably enhances the healing of ischemic ulcers. Eleven cases of obliterative arterial disease and two cases of Raynaud's disease were closely observed and are reported in detail. In six of the individuals suffering from obliterative arterial disease, changes in blood flow were documented by plethysmography. Dibenzyline measurably influenced intermittent claudication only after prolonged administration (three to four months) in four out of eight closely observed patients without ulcers. The results of the physiologic tests suggest that during the early phases of adrenergic blocking the increase in blood flow is mostly in the skin, while in the later phases increase in blood flow through the muscle predominates.

1.1. Phenylbutazone exhibits antirheumatic effects in rheumatoid arthritis which are comparable to those shown by cortisone and corticotropin.2.2. Like cortisone and corticotropin the drug causes urinary retention of sodium, chloride and water, and may reactivate peptic ulcers; but unlike cortisone it does not affect the excretion of potassium nor does it cause eosinopenia or increased ketosteroid excretion. It is concluded that the action of phenylbutazone is not mediated, directly or indirectly, through the adrenal cortex.3.3. During phenylbutazone therapy there is often a fall in red cell count, hemoglobin and hematocrit which is primarily the result of hemodilution and not of depression of the hematopoietic system.4.4. Plasma levels of phenylbutazone approach a limiting concentration as dosage is increased. This limiting concentration varies widely from patient to patient. Most subjects achieve plasma levels on 400 to 600 mg. daily that are only slightly lower than when 800 mg. are given.

The responses of the kidney and the lower extremities to single intravenous doses of six "hypotensive" drugs were measured in eight patients diagnosed as having essential hypertension. Use of Hexamethonium, Ilidar and Hydergine was followed by increase in the flow to the extremity and simultaneous decrease in renal blood flow. In contrast, the administration of Apresoline was followed by decrease in flow to the extremity and an increase in renal blood flow. Regitine produced no significant change in either. After the administration of protoveratrine, renal blood flow decreased but a significant change in blood flow to the extremity was not observed. Changes in arterial pressure which occurred with some of the drugs were not correlated with the changes in blood flow to the extremities or to the kidney.

D IFFICULTIES in the control of the hypothrombinemic effect of dicumarol@ in the treatment of thromboembolic diseases have led to the investigation of other coumarin derivatives. With one of these, tromexan@)t (3,3’-carboxymethylenbis [4-hydroxycoumarin] ethyl ester), the therapeutic effects take place more rapidly after administration of the drug and disappear more rapidly after discontinuance of the drug than is the case with dicumarol. These characteristics of tromexan are potential advantages in that they might be expected to permit more predictable control of induced hypoprothrombinemia. There was some confirmation of the early expectations1-5 but this has not been borne out in later studies.6*7 Previous works indicates that tromexan is rapidly and completely absorbed from the gastrointestinal tract, compared to the slow and sometimes incomplete absorption of dicumarol. Its biotransformation is rapid, the plasma concentration falling at an average rate of 25 per cent per hour, compared to dicumarol which falls at an average rate of about 40 per cent per day.g As with dicumarol the rate of metabolic transformation of tromexan varies widely in different subjects. The rapid disappearance of tromexan from the body is accompanied with a rapid return of the prothrombin time to pretreatment levels on discontinuing therapy. After a single dose the drug has almost disappeared from the body before the prothrombin response becomes evident, eight to twelve hours after drug administration.1 Single daily doses of the drug

ArticleMeasurement of Total Body Fat in Living Rats by Absorption of CyclopropaneGerson T. Lesser, Arnold G. Blumberg, and J. Murray SteeleGerson T. LesserFrom the Research Service, Third (New York University) Medical Division, Goldwater Memorial Hospital, Welfare Island, New York, and the Department of Medicine New York University College of Medicine, New York City, Arnold G. BlumbergFrom the Research Service, Third (New York University) Medical Division, Goldwater Memorial Hospital, Welfare Island, New York, and the Department of Medicine New York University College of Medicine, New York City, and J. Murray SteeleFrom the Research Service, Third (New York University) Medical Division, Goldwater Memorial Hospital, Welfare Island, New York, and the Department of Medicine New York University College of Medicine, New York CityPublished Online:01 Jun 1952https://doi.org/10.1152/ajplegacy.1952.169.3.545MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByTransient reduction of metabolic rate by food restrictionR. J. McCarter, and J. R. McGee1 August 1989 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 257, No. 2 More from this issue > Volume 169Issue 3June 1952Pages 545-553 Copyright & PermissionsCopyright © 1952 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1952.169.3.545PubMed14943844History Received 6 February 1952 Published online 1 June 1952 Published in print 1 June 1952 Metrics