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Biomedical subjects

L A Donovan

Publications and source records attributed to L A Donovan.

4 recordsLinked to original sources
PubMed1997

Malignant hyperthermia.

Malignant hyperthermia is a pharmacogenetic disease of skeletal muscle characterized by hypermetabolism that occurs on exposure to a triggering agent or agents. The most common agents are halogenated inhalational anesthetics and succinylcholine, a depolarizing muscle relaxant. Patients who experience malignant hyperthermia are generally transferred to the ICU for ongoing treatment and monitoring for secondary complications of the disorder. Critical care practitioners must be both knowledgeable and competent to prevent and treat perioperative episodes of malignant hyperthermia. A thorough preoperative interview should be done to determine risk factors and susceptible patients. This article provides critical care nurses with sound information on the pathophysiology of malignant hyperthermia, the ability to assess the disease properly and treat the patient both before and after the crisis, and the ability to provide support and teaching to patients and patients' families to prevent the recurrence of malignant hyperthermia.

Animals↗
PubMed1990

Differential desensitization of A1 adenosine receptor-mediated inhibition of cardiac myocyte contractility and adenylate cyclase activity. Relation to the regulation of receptor affinity and density.

Effects of chronic exposure of cultured atrial myocytes to R-N6-(2-phenylisopropyl)-adenosine (R-PIA) on the A1 adenosine receptor-mediated inhibition of adenylate cyclase activity and myocyte contractility were examined. Chronic exposure of atrial myocytes cultured from 14-day-old chick embryos to R-PIA desensitized the myocyte to the inhibitory effects of R-PIA on contractility and adenylate cyclase activity in a time- and dose-dependent manner. Desensitization of the negative inotropic response was only partial, whereas the adenosine receptor-mediated inhibition of adenylate cyclase activity was almost completely absent after 24 hours of R-PIA (1 microM) exposure. Furthermore, the contractile response to R-PIA desensitized more slowly than the desensitization of A1 adenosine receptor-mediated inhibition of adenylate cyclase (t1/2 = 11.4 +/- 0.7 hours versus 7.5 +/- 1 hours, mean +/- SEM, n = 12 and 6, respectively). Thus, the two A1 adenosine receptor-linked functional responses desensitized differently in response to chronic exposure of the myocyte to R-PIA. Binding of the antagonist radioligand [3H]-8-cyclopentyl-1,3-dipropylxanthine [( 3H]CPX) in membranes from myocytes preexposed to R-PIA demonstrated a time-dependent decrease in receptor density without any change in the affinity for the antagonist radioligand. Computer analyses of agonist competition with [3H]CPX binding in membranes from control and R-PIA-treated myocytes revealed a conversion of the high-affinity A1 adenosine receptor to a low-affinity form such that after 24 hours of 1 microM R-PIA exposure, all of the receptors were in a low-affinity form.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗