Tension pneumothorax, pneumomediastinum, pneumoperitoneum, and subcutaneous emphysema in a 15-year-old Chinese girl after a double-lumen tube intubation and one-lung ventilation.
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Biomedical subjects
Publications and source records attributed to R Tio.
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Percutaneous coronary angioplasty (PTCA) is usually performed using concentric shaped balloon catheters with the guidewire passing through the center of the shaft. The Falconª balloon catheter features a guide wire lumen on the outside of the balloon so that an eccentric balloon catheter profile is obtained concentrating the dilating force on the wire supported side, allowing lower inflation pressures and potentially causing less vessel injury. The aim of this study was to evaluate the safety and efficacy of this new balloon catheter in patients with stable and unstable angina. In 95 prospectively randomized patients, 57 lesions were dilated with a concentric balloon and 51 with the eccentric balloon. Technical success in the two groups was similar (73.3% vs. 74.5% control vs. Falcon respectively). Procedural success was 96.5% vs. 96.1% in the control and Falcon groups respectively. The mean increase in minimum luminal diameter (MLD) was 1.01 +/- 0.41 mm in the control vs 0.85 +/- 0.45 mm in Falcon (p = 0.053). There was an increase in type A dissections in the Falcon group 18 (36.75%) vs. 10 (19.23%) in the control group (p = 0.07) with no difference in stent implantation, myocardial infarction, CABG or death between the two groups. All patients with a technically successful PTCA were followed up. Seventeen (43.6%) in the control and 11 (32.4%) in the Falcon had repeat coronary angiography (p = 0.38), 12 (30.8%) vs. 7 (20.6%) had repeat PTCA (p = 0.37) and time to PTCA was 116 +/- 70 days vs. 154 +/- 103 days respectively (p = 0.36). The Falcon performed technically as well as the concentric balloons. Despite a smaller MLD and increase in Type A dissections there was no associated increase in complications or reintervention for restenosis. Further investigation is required to evaluate the role of this mechanism of dilatation in restenosis.
This paper reviews the haemodynamic effects of angiotensin-converting enzyme (ACE) inhibitors in hypertension, focusing on their ability to cause a fall in systemic vascular resistance, with no change in cardiac output and no reduction and even an increase in blood flow to vital organs such as the brain, the kidney and the heart. The haemodynamic effects of ACE inhibitors are qualitatively similar in congestive heart failure, except that, in the presence of impaired cardiac function, the fall in resistance is accompanied by a pronounced increase in cardiac output and tissue perfusion. In both conditions ACE inhibition opposes sympathetic influences and enhances vagal influences and, in hypertension, this intervention is followed by a regression of left ventricular hypertrophy providing a multifold background for a cardioprotective action. The new ACE inhibitor quinapril appears to share the haemodynamic effects of other ACE inhibitors with an improvement of cardiovascular function in congestive heart failure.
In anaesthetized cats, a biphasic contraction of the urinary bladder, consisting of an initial spike followed by a longer-lasting contracture, was elicited by 5-hydroxytryptamine (5-HT) in doses of 3-30 micrograms/kg, i.a. Administration of MDL 72222 (30, 100 and 300 micrograms/kg, i.v.), which specifically antagonizes the M-type 5-HT receptors, selectively blocked the spike phase of the 5-HT response. Ketanserin (30, 100 and 300 micrograms/kg, i.v.), on the other hand, eliminated only the second phase of the 5-HT-induced bladder contraction. Injection of MDL 72222 (300 micrograms/kg) after ketanserin (300 micrograms/kg), or of 100 micrograms/kg of methysergide or cyproheptadine, or 300 micrograms/kg of ketanserin after MDL 72222 (300 micrograms/kg), led to blockade of both phases of the response to 5-HT. The contractile response to dimethylphenylpiperazinium (DMPP) remained unaffected. These results clearly show that the early and late phases of the cat urinary bladder contraction elicited by 5-HT are mediated by M and 5-HT2 receptors, respectively.