Left double lumen tube malposition.
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Humans↗
Biomedical subjects
D Coté
Publications and source records attributed to D Coté.
New landmarks improve the positioning of the left Broncho-Cath double-lumen tube-comparison with the classic technique.
PURPOSE: To compare a new technique (NT) for positioning the left modified Broncho-Cath double-lumen tube (LM- DLT) by fibreoptic bronchoscopy (FOB) to the classic technique (CT). METHODS: Sixty-one adult patients undergoing elective thoracic surgery with LM-DLT were randomly assigned to the NT or to the CT group. For the NT, the endoscopist confirms the left mainstem endobronchial intubation. The proximal edge of the blue bronchial cuff should not be visualized at the carina. Then, through the left bronchial lumen, by transparency across the wall of the tube, the position of the tube is adjusted so that the carina lies midway between the black radiopaque line and the top of the bronchial cuff. After this, the orifice of the left upper lobe (LUL) bronchus should be clearly seen. For the CT, the endoscopist uses the technique described by Benumof and Slinger. After lateral positioning of the patient, the LM-DLT was repositioned if the top of the endobronchial cuff was above the carina or when the LUL bronchus was obstructed. RESULTS: The incidence of proximal repositioning was significantly less in the NT compared to the CT (16% vs 43%, P=0.007). CONCLUSION: Using this new technique, the LM-DLT is inserted deeper in the left mainstem bronchus. This new landmark augments the range of movement that can be tolerated without requiring repositioning of the LM-DLT. This NT to position and to assess LM-DLT, by transparency across the wall of the tube with FOB, is better adapted to the LM-DLT and its recent modifications.
Bronchi↗
Paroxetine in the treatment of generalized social phobia: open-label treatment and double-blind placebo-controlled discontinuation.
We conducted an 11-week forced-escalation open-label study of paroxetine in the treatment of 36 patients with generalized social phobia. At the mean dosage of 47.9 +/- 6.2 mg/day, 23 of 30 completers (77%) were deemed responders on the basis of a clinician rating of either "very much improved" or "much improved" on the Clinical Global Impressions scale. Duke Social Phobia Scale ratings declined from 35.5 +/- 13.1 at baseline to 19.7 +/- 17.4 at week 11 (p < 0.0005), and Liebowitz Social Anxiety Scale ratings declined from 75.1 +/- 25.4 at baseline to 37.2 +/- 32.5 at week 11 (p < 0.0005). Sixteen responders were randomized to an additional 12 weeks of either paroxetine (with no dosage change) or placebo (after a taper period) on a double-blind basis. To the best of our knowledge, this is the first controlled medication-discontinuation study in social phobia. One of eight patients randomized to continue paroxetine relapsed versus five of eight patients randomized to placebo. These findings call for a double-blind, placebo-controlled treatment study of paroxetine in generalized social phobia. They also suggest that relapse rates are high if medication is discontinued early and that further study is needed to determine (1) the optimal duration of maintenance pharmacotherapy for social phobia and (2) if specific psychotherapeutic interventions before medication discontinuation may prevent relapse.
Adult↗
Pharmacy manager need not be pharmacist.
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Humans↗
Centrally mediated antihypertensive and bradycardic effects of methysergide in spontaneously hypertensive rats.
Methysergide caused dose-dependent reductions in systolic blood pressure and heart rate of unanesthetized SHR, whereas cyproheptadine was ineffective. In pithed SHR pretreated with methysergide or cyproheptadine, pressor responses to 5-HT were abolished. Responses to sympathetic nerve stimulation were unaltered by methysergide, whereas cyproheptadine slightly reduced them. Both drugs enhanced pressor responses to norepinephrine. Failure to identify a peripheral mechanism for the antihypertensive action of methysergide suggests that the effect may be centrally mediated but not reliant upon serotonin receptor blockade.
Animals↗
Tachycardia in spontaneously hypertensive and normotensive rats after fusaric acid and bupicamide.
1. The effects of the dopamine-beta-hydroxylase inhibitors bupicamide, fusaric acid, FLA-63 and U-14,624 on blood pressure and heart rate of spontaneously hypertensive rats were examined. 2. Bupicamide and fusaric acid caused marked tachycardia whereas FLA-63 and U-14,624 caused modest bradycardia; all drugs decreased blood pressure. 3. In normotensive rats, fusaric acid caused the same degree of tachycardia as in spontaneously hypertensive rats, but blood pressure was only slightly reduced. 4. Tachycardia after fusaric acid was not due to increased sympathetic activity or decreased parasympathetic activity but required intact catecholamine stores. 5. It is concluded that fusaric acid causes tachycardia by releasing catecholamines indirectly and that a metabolite of fusaric acid is also involved.
Animals↗