Corticosteroids and varicella. Six-year experience in an asthmatic population.
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Adolescent↗
Biomedical subjects
E F Ellis
Publications and source records attributed to E F Ellis.
Effect of oral aspirin dose on platelet aggregation and vascular prostacyclin (PGI2) synthesis in humans and rabbits.
Large doses of oral aspirin inhibit platelet aggregation and vascular synthesis of the antiaggregatory vasodilator prostaglandin I2 (PGI2) by irreversibly acetylating the cyclooxygenase enzyme. In order to determine if one can achieve selective inactivation of platelet cyclooxygenase using oral doses of aspirin, we studied human and rabbit platelet aggregation and rabbit aortic synthesis of PGI2 before and 3 hr after various doses of aspirin. In rabbits, lower doses of aspirin produced a major inhibition of platelet aggregation and a minor inhibition of PGI2 synthesis, while higher doses of aspirin inhibited both platelet aggregation and vascular PGI2 synthesis. In humans, we found that a dose equivalent to approximately 1/4 of one 300 mg aspirin tablet consistently produced a major inhibition of cyclooxygenase-dependent platelet aggregation in a pattern similar to the inhibition of rabbit platelet aggregation where the majority of rabbit PGI2 synthetic capacity was not inhibited. In another rabbit study, we found that it takes the vasculature over 24 hr to return to control PGI2 synthetic capacity following a single, high dose of oral aspirin. In conclusion, we speculate that approximately 1/4 of an aspirin tablet, which inhibits a major portion of cyclooxygenase-dependent human platelet aggregation, may not inhibit a major portion of vascular cyclooxygenase-dependent PGI2 synthesis and may be more efficacious as an antithrombotic agent in man than are higher doses of aspirin.
Adult↗
Inhibition of bradykinin- and kallikrein-induced cerebral arteriolar dilation by a specific bradykinin antagonist.
We have previously shown that topical brain application of kallikrein, an enzyme which converts kininogen to bradykinin, induces rabbit pial arteriole dilation. The purpose of the present investigation was to utilize a newly developed competitive kinin receptor antagonist to test the hypothesis that kallikrein-induced dilation was due to the conversion of brain kininogen to vasoactive kinins. As in our previous study, we measured rabbit pial arteriole diameter with a microscope using the closed cranial window technique. The kinin antagonist (6 microM) reduced the dose-dependent dilation produced by bradykinin and blocked the dilation induced by kallikrein. In addition, the kinin antagonist was specific since it did not alter the cerebral arteriole dilation produced by adenosine, acetylcholine, or vasoactive intestinal polypeptide. These experiments provide further evidence for a possible role of the endogenous brain kallikrein-kinin system in the modulation of the cerebral circulation and provide the necessary pharmacologic foundation for future use of this antagonist in testing the role of kinins in the normal or altered cerebral circulation.
Amino Acid Sequence↗
Effect of the thromboxane A2 mimetic U 46619 on pial arterioles of rabbits and rats.
Our previous experiments have shown that thromboxane A2 is a strong contractor of cerebral arterial smooth muscle strips. The objective of these experiments was to determine if U 46619, a stable thromboxane A2 mimetic, affects the cerebral microcirculation in vivo. Pial arteriole diameter in rabbits and rats was measured with a microscope using the closed cranial window technique. Topical application of 10(-11) to 10(-6) M U 46619 induced dose-dependent arteriole vasoconstriction in both species. In rabbits and rats the maximum vasoconstriction was 9.7 +/- 1.3% (mean +/- SEM) and 14.0 +/- 0.5%, respectively. In rats, 10(-7) and 10(-6) M U 46619 induced intravascular platelet aggregation accompanied by a further decrease in diameter and transient occlusion of the arterioles and venules. U 46619 had no significant effect on rabbit pial arterioles that were predilated by hypercapnia or hypercapnia plus hypoxia. Our data suggest that in animals with a normal vasculature, thromboxane A2 may be a moderate constrictor of cerebral arterioles and that this constrictor effect is prevented by hypercapnia and hypoxia.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
Cerebral arterial smooth muscle contraction by thromboxane A2.
The contractile effects of thromboxane A2 (TxA2), a labile arachidonic acid metabolite, were studied in arterial smooth muscle strips. TxA2 was generated upon the addition of 255 nM prostaglandin cyclic endoperoxide H2 to human platelet particles in the muscle bath. Using the isometric contaction produced by 40 mM K+ in isotonic saline as the reference contraction, bovine middle cerebral artery strips contracted to 153 +/- 14% of the reference response while bovine coronary and porcine coronary, renal and common carotid strips contracted to 47 +/- 3, 26 +/- 5, 43 +/- 2 and 2 +/- 1% of reference, respectively. The cerebral artery response to the TxA2 generating system was as great as the maximum response to prostaglandin F2alpha and two times the maximum response to 5-hydroxytryptamine. Because TxA2 is formed by brain tissue and released from aggregating platelets, it may be important in the pathogenesis of spasm associated with injured brain tissue or pathologic changes leading to platelet aggregation.
Animals↗
Use and acceptance of ventolin Rotacaps and the Rotahaler in 1235 asthmatic patients.
This open-label study was performed to characterize the acceptance, reliability, and adverse event profile of a dry powder delivery system for albuterol. A total of 1235 asthmatic outpatients, aged 11 to 84 years, were studied for 1 month. Each patient enrolled was documented as having a specific complaint concerning the use of a standard metered-dose inhaler. At the end of 4 weeks of treatment, the patients completed a questionnaire to record their opinions and preferences. The results were as follows: 93% stated that Rotacaps were easy to use; 92% that they could use Rotacaps during an asthma attack; 99% that they had no problems with breakage of the device; 94% that the drug tasted pleasant or had no taste; 70% that they could inhale a full dose with one breath; and 79% that Rotacaps were at least as effective as the metered-dose inhaler they had used previously. Drug-related adverse events were reported by 6% of the patients; no single event was reported by more than 1% of the patients. The results indicate that Rotacaps are a safe, effective, and well-accepted alternative to metered-dose inhalers in asthmatic patients.
Administration, Inhalation↗