Enhanced detection of reversible myocardial hypoperfusion by technetium 99m-tetrofosmin imaging and first-pass radionuclide angiography after nitroglycerin administration.

BACKGROUND: Reversal of ischemia after myocardial infarction by revascularization is worthwhile only if viability exists in a sufficiently large portion of the left ventricle. METHODS AND RESULTS: To determine myocardial hypoperfusion reversibility and its influence on segmental and global function, we studied 50 patients after myocardial infarction. Three technetium 99m-tetrofosmin scintigraphies were performed: 1 at rest, 1 after 0.6 mg sublingual nitroglycerin (NTG), and 1 after injection at peak stress. First-pass multigated radionuclide angiography was obtained at rest and after NTG. Each patient also underwent a stress redistribution-reinjection thallium-201 scintigraphy. During stress 99mTc-tetrofosmin, 104 segments had normal uptake, 51 showed moderately reduced uptake, and 186 had severely reduced uptake. Of these 186 segments, 33 (18%) improved at rest, and 41 (22%) improved only after NTG. Fifty-nine (79%) of these segments with improved uptake were also found to have reversible defects on 201TI imaging. In the 26 patients with ventricular dysfunction, a 73% agreement was found between the functional and 99mTc-tetrofosmin uptake post-NTG improvement, whereas a 69% agreement was found with thallium reinjection. No significant differences were seen between 99mTc-tetrofosmin and 201T1 imaging. CONCLUSION: Nitroglycerin administration during 99mTc-tetrofosmin scintigraphy improves the detection of myocardium with reversible hypoperfusion in patients with a previous myocardial infarction.

Kerosene aerosol induces guinea-pig airway hyperreactivity to acetylcholine.

Kerosene aerosol (32.5 mg/l; 20 min), when administered to guinea pigs 1 h before exposure to acetylcholine (Ach), induced potentiation of cumulative dose-response curve of this agonist on isolated tracheal strips as well as a decrease of the lethal doses of Ach. This enhanced response was absent or greatly reduced when kerosene aerosol was administered to guinea pigs 24 h previously or just before Ach challenge. This airway hyperreactivity was also lacking when carbachol or histamine were used as spasmogens instead of Ach. Possible explanations of these results are discussed.

[Effect of several antiasthmatic prophylactic drugs on bronchoconstriction induced by kerosene in rabbits]. / Efecto de varias drogas profilácticas antiasmáticas sobre la broncoconstricción inducida por keroseno en conejos.

Various authors have reported the protective effect of disodium cromoglycate (DSCG) against bronchoconstriction induced by cold air, exercise, sulfurdioxide and other agents. We also found in our experimental work the protective effect of DSCG, ketotifen and oxatomide against the contractile effect of various agonists such as histamine prostaglandin F2, acetylcholine and barium chloride on isolated guinea pig intestine and trachea. This suggests an additional effect of these drugs on cholinergic endings and/or directly on smooth muscle fibers in addition to their membrane stabilizing effects on mast cells as it has been suggested by other authors previously. To offer insight into these mechanisms we decided to evaluate the action of ketotifen, oxatomide, ICI 74917 and BRL 10833 using the model of kerosene-induced bronchoconstriction in rabbits. Here the parasympathetic pathways play an important role as it has been demonstrated by us using atropine or vagal section. Ketotifen (5 mg/kg i.v.) and oxatomide (5 mg/kg i.v.) were administered before kerosene aerosol exposure these significantly inhibited kerosene-induced bronchoconstriction, whereas ICI 74917 (10 mg/kg i.v.) and BRL 10833 (10 mg/kg i.v.) lacked this protective effect. These results support our hypothesis that an additional protective effect on smooth muscle and its innervation is involved in the mode of action of the prophylactic antiasthmatic drugs which have been clinically successful.

Studies on the effects of kerosine aerosol on airways of rabbits.

The effects of kerosine aerosol inhalation at a mean concentration of 32.5 mg/L on spontaneously breathing rabbits as well as on artificially ventilated rabbits were studied. Kerosine aerosol inhalation by spontaneously breathing rabbits during 4 minutes elicited an increase in total pulmonary resistance (RT) by 38 +/- 15 percent of control value (p less than 0.05). After atropine injection (0.2 mg/kg. I.V.) there was an immediate decrease in RT which was not significantly different from the control value after either, 1 or 5 minutes administration. Kerosine aerosol inhalation during 9 minutes elicited an increase in tracheal resistance by 45.5 +/- 8.2 percent of control value in artificially ventilated normal rabbits, while in vagotomized ones the increase was only by 21.2 +/- 6.9 percent of control value (p less than 0.05). It is concluded that inhalation of kerosine by spontaneously breathing or artificially ventilated rabbits elicit an acute increase in airways resistance which is mainly reflex and mediated by parasympathetic pathways.

Comparative study of ascorbic acid and disodium cromoglycate in some models of experimental anaphylaxis.

The pharmacological activity of vitamin C and the antiallergic drug disodium cromoglycate are compared in models of rat mast cell degranulation and histamine release, and in protracted anaphylactic shock in the guinea pig. Our results demonstrate that ascorbic acid has a very weak inhibitory effect on degranulation and histamine release from mast cells, and therefore cannot be considered a prophylactic antiallergic drug such as disodium cromoglycate.

Actions of diethylcarbamazine in experimental anaphylaxis.

Diethylcarbamazine citrate (DEC) is an anthelmintic drug which has been used recently, with varying results, in the treatment of bronchial asthma. We have examined the pharmacological activity of this drug in several in vivo and in vitro models of experimental anaphylaxis. DEC at doses of 25 and 50 mg per kg given intraperitoneally significantly reduced the mortality rate in sensitized guinea pigs during protracted shock phase but did not modify the time for the appearance of dyspnoea when antigen (egg albumin) was administered as aerosol. Nor did DEC at therapeutic doses inhibit the degranulation and histamine release from rat isolated peritoneal mast cells induced by phospholipase A, compound 48/80, and antigen respectively. It has been suggested that one possible explanation for the apparent effectiveness of DEC in asthma is its ability to antagonize prostaglandin F2 alpha. Our results using in vivo and in vitro models of bronchoconstriction in guinea pigs do not support this hypothesis to explain the inhibition of protacted shock by DEC.

Genetic polymorphism of ABO and Rh system in relation to bronchial asthma: preliminary report.

115 asthmatic children and 1001 healthy voluntary blood donors were studied in order to determine the distribution of blood groups among them. Gene frequencies were also calculated in asthmatic patients and controls. No difference was noted between Rh system in both groups; but the ABO system showed an excess of blood group A among asthmatic patients. Gene frequency of A (p) and gene frequency of O (r) was quite different too for asthmatics and controls. No difference was noted in blood groups B and AB; nor in the gene frequency of B(q). The difference in the distribution of blood group A and O between control and asthmatic groups was found to be highly significant (P less than 0.02) with the chi-square test.