Comorbid disorders in hospitalized bipolar adolescents compared with unipolar depressed adolescents

This study examined comorbid psychiatric disorders in adolescents with bipolar disorder. Hospitalized bipolar adolescents (N=10) were compared to hospitalized adolescents with unipolar depression (N=33), and to adolescents with nonaffective psychiatric disorders (N=11). Results showed conduct disorder, attention-deficit hyperactivity disorder, psychosis, and having any DSM-III-R psychoactive substance use disorder were all significantly more common in the bipolar group than the unipolar depressed group. Comorbid anxiety disorder was present in 40–45% of the subjects in the unipolar and bipolar groups, but in none of the control group subjects. This study is supported in part by a grant to Dr. Borchardt from the University of Minnesota Graduate School.     

Dexmedetomidine Produces Similar Alterations in the Determinants of Left Ventricular Afterload in Conscious Dogs before and after the Development of Pacing-induced Cardiomyopathy

Background: The authors tested the hypothesis that intravenous dexmedetomidine produces alterations in left ventricular (LV) afterload that are deleterious to cardiac performance in conscious dogs with pacing-induced cardiomyopathy.

Methods: Dogs (n = 8) were fitted with instruments for long-term measurement of LV and aortic blood pressure, aortic blood flow, and subendocardial segment length and received dexmedetomidine (1.25, 2.5, and 5 [micro sign]g/kg) in a cumulative manner before and after 19 +/- 3 (mean +/- SEM) days of rapid LV pacing. LV afterload was measured with aortic input impedance [Zin ([Greek small letter omega]) and quantified with a three-element Windkessel model. Hemodynamics and Zin ([Greek small letter omega]) were assessed under control conditions and 5 and 60 min after administration of each dose.

Results: Dexmedetomidine caused early and late decreases in heart rate, the maximum rate of increase of LV pressure, mean aortic blood flow, and stroke volume in dogs before and after pacing. Dexmedetomidine caused similar early increases in total arterial resistance and decreases in total arterial compliance in dogs before and after pacing. Early dexmedetomidine-induced increases in resistance and decreases in compliance caused similar reductions in mean aortic blood flow in cardiomyopathic compared with healthy dogs. Resistance and compliance returned to control values, and characteristic aortic impedance decreased late after dexmedetomidine in healthy dogs. In contrast, resistance remained elevated late after dexmedetomidine in dogs with dilated cardiomyopathy.     

Direct Inhibitory Mechanisms of Halothane on Human Platelet Aggregation

Background: Although halothane directly inhibits platelet aggregation, the mechanisms of this effect are still unknown. The current study aimed to clarify the inhibitory mechanisms of halothane on thrombin-induced human platelet aggregation by measuring (1) platelet-surface glycoprotein Ib expression, (2) the concentration of intracellular free Calcium2+ ([Calcium2+]i) measured simultaneously with aggregation, (3) the concentration of intracellular inositol 1,4,5-triphosphate, and (4) the concentration of intracellular cyclic 3',5'-adenosine monophosphate ([cAMP]i).

Methods: Washed platelet suspensions, obtained from healthy volunteers, were preincubated with halothane (0-2 mM) for 2 min and then exposed to 0.02 units/ml thrombin for 3 min. The glycoprotein Ib bound to fluorescein-labeled antibody was measured by fluorescence flow cytometry. [Calcium2+]i was measured, simultaneously with aggregation, in Fura-2 (Calcium2+ indicator)-loaded platelets by use of a fluorometer. Inositol 1,4,5-triphosphate and [cAMP]i were measured by radioimmunoassay.

Results: Halothane had no effect on glycoprotein Ib expression with or without thrombin. Halothane decreased the thrombin stimulated [Calcium sup 2+]i transient and inhibited platelet aggregation in a dose-dependent manner, both in the presence and in the absence of external Calcium2+. Isoflurane had no apparent effect on either platelet aggregation or [Calcium2+]i in the absence of external Calcium sup 2+. Halothane inhibited the increase in inositol 1,4,5-triphosphate induced by thrombin. Halothane moderately but significantly increased [cAMP]i, but the adenylate cyclase activator forskolin (which has the same inhibitory ability on aggregation as halothane) increased [cAMP]i to a much greater extent than did halothane.