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Biomedical subjects

J J Pailleret

Publications and source records attributed to J J Pailleret.

5 recordsLinked to original sources

Prevention with molsidomine of coronary artery spasm caused by alkalosis.

A provocative test of coronary artery spasm caused by alkalosis was used to evaluate a possible anti-coronary artery spasm effect of molsidomine. The rapid infusion of an alkaline buffer followed by maximal voluntary hyperventilation in 10 patients with angina at rest led to the appearance of anginal pain and significant, transient ischemic changes of the ST segment resulting from alkalosis-induced coronary spasm. A second provocative test was performed under the same conditions, 24 hours later, after the administration of 4 mg of molsidomine. Molsidomine prevented the development of coronary artery spasm in 8 of the 10 patients in the study group. These preliminary results justify further clinical evaluation of molsidomine in the treatment of vasospastic angina.

Alkalosis↗

[Classification and principles of the use of vasodilators in the treatment of left ventricular insufficiency].

Vasodilators have been widely used in recent years for the treatment of severe left ventricular failure (LVF). However, amongst these drugs, not all have the same therapeutic effects, but they differ from one another in molecular structures, cellular mechanisms, haemodynamic actions and modes of administration. A three tier classification is proposed with the single objective of facilitating the therapeutic choice: mechanism of action: this property distinguishes the alpha-blockers from the beta-2 sympathomimetics, calcium antagonists, angiotensin converting enzyme inhibitors and prostacyclin biosynthesis inducers. Some molecules such as hydralazine, whose mechanism of action remains unclear, cannot be classified in this way; haemodynamic effects: these effects can be used to distinguish vasodilators which act mainly on the venous sector from arterial and mixed vasodilators. The knowledge of the preferential site ol action of these molecules helps to adapt the choice of treatment to the initial haemodynamic profile of each patient; pharmacokinetics: these properties distinguish molecules active only by intravenous administration, better adapted for the treatment of acute LVF in the intensive care unit, from those active orally which can be used for long-term ambulatory therapy of chronic cardiac failure. Trinitrin and its derivatives occupy an intermediate position because of their relatively low bioavailability after oral administration: long-term administration is not always easy and may require special modes of administration (i.e. percutaneous). Vasodilators have been widely used in cardiac failure for about 5 years; the results of some medium term controlled therapeutic trials are now available and confirm the efficacy of these drugs but also define their limitations: variable therapeutic efficacy: the number of responders ranges from 30 to 60 p. 100 according to the molecule used.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium Channel Blockers↗

[Molsidomine prevention of coronary artery spasm caused by alkalosis].

A test provocation of coronary artery spasm by alkalosis was used to evaluate a possible anti-coronary artery spasm effect of molsidomine. The rapid infusion of an alkaline buffer followed by maximal voluntary hyperventilation in 10 patients with angina at rest led to the appearance of angina pain and significant, transient ischaemic changes of the ST segment, due to alkalosis induced coronary spasm. A second provocation test was performed under the same conditions, 24 hours later, after the prior administration of 4 mg of molsidomine. Molsidomine prevented the development of coronary artery spasm in 8 of the 10 patients in the study group. These preliminary results justify further clinical evaluation of molsidomine in the treatment of vasospastic angina.

Alkalosis↗

[Acquired B antigen: a new case].

A 86 year old woman, in good health but "Escherichia coli" urinary infection, was found to have an abnormality in blood group determination. 3 years ago, blood group of this patient was group A and now, precise determination shows the existence of an acquired B antigen. Disappearance of this acquired B Ag was obtained in 3 months after the urinary infection's treatment. The most cases of acquired B Ag result from neoplasic diseases or infection with enterobacteriacea. Physiopathology of acquired B Ag is secondary to the action of a deacetylase enzyme produced by enterobacteriacea, on group A1 erythrocytes.

ABO Blood-Group System↗