Endothelial cell dysfunction after ischemic arrest and reperfusion: a possible mechanism of myocardial injury during reflow

To determine the mechanism(s) responsible for decreased coronary flow after global cardiac ischemia and reperfusion, we studied 40 isolated rabbit hearts before and after 30 minutes of normothermic ischemic arrest and reperfusion. In the control group (n = 10) we evaluated the time course of recovery of coronary flow, vascular reactivity, and myocardial function. In experimental groups A (n = 10) and B (n = 10), metabolic control of autoregulation was assessed by plots of myocardial oxygen consumption versus coronary flow generated by incremental increases in heart rate. The slope and intercept of these plots suggested that autoregulation of coronary flow was maintained after ischemia. In group B hearts (n = 10) hyperosmolar reperfusion with mannitol decreased myocardial water by 2% (p less than 0.01) but did not increase coronary flow. Endothelium-dependent function was assessed in group C (n = 10) by the administration of an endothelium-dependent vasodilator (serotonin) and a smooth muscle vasodilator (adenosine). Coronary artery smooth muscle function was comparable in hearts before and after ischemia. However, endothelium-dependent increases in coronary flow to serotonin were significantly impaired after ischemia (p less than 0.01), and this was accompanied by a significant decrease in prostacyclin synthesis by the endothelium (p less than 0.001). Global cardiac ischemia and reperfusion damages coronary artery endothelium, causing increased coronary vasomotor tone; this may be an important mechanism of decreased coronary perfusion and subsequent myocardial injury during reflow.     

Estimating amoxicillin influx/efflux in chinchilla middle ear fluid and simultaneous measurement of antibacterial effect

Understanding the transport process and the factors that control the influx/efflux of antibiotics between plasma and middle ear fluid is essential in optimizing the antimicrobial efficacy in the treatment of acute otitis media. In this study, an experimental chinchilla model with the application of a microdialysis technique was utilized to evaluate amoxicillin middle ear distribution kinetics. Amoxicillin solutions at various doses were instilled into the middle ear with a simultaneous intravenous bolus dose. Unbound amoxicillin levels were monitored by microdialysis in both ears. Serial phlebotomy provided samples for the measurement of unbound amoxicillin concentration in plasma ultrafiltrates. In infected chinchillas, discrete middle ear fluid samples were plated and cultured to characterize Streptococcus pneumoniae growth-kill kinetics. Noncompartmental analysis was used to estimate distributional and elimination clearances assuming linear pharmacokinetics. A nonlinear Michaelis-Menten equation was also used to determine the efflux clearance (from middle ear fluid to plasma) in a mammillary compartment model. No difference was observed in amoxicillin pharmacokinetics between control and infected chinchillas. Influx clearance was (4.6 +/- 2.4) x 10(-3) ml/min-kg and significantly lower than the efflux clearance estimated as (19.2 +/- 9.7) x 10(-3) ml/min-kg (P < 0.002). Nonlinear kinetics was observed in the locally dosed ear. The microdialysis procedure did not interfere with the bacterial growth-kill profile, thereby enabling pharmacokinetic and pharmacodynamic evaluation concurrently. In conclusion, the results suggested that the distribution equilibrium of amoxicillin in the middle ear favors efflux to plasma over influx. An active transport mechanism across middle ear mucosal epithelium may be involved in amoxicillin distribution.     

Blood plasma fluoride in haemodialysed patients

Blood plasma fluoride was determined in 15 chronic haemodialysed patients (60.2 +/- 7.2 yr old) before and after a 4-h dialysis using dialysates with very low fluoride level, and in two control groups, the first of 20 healthy younger subjects (45.9 +/- 3.4 yr old), the second of 8 healthy older subjects (69.1 +/- 6.8 y old). Before haemodialysis the fluoride concentration (1.31 +/- 0.31 mumol/l; 24.8 +/- 5.9 micrograms/l), was higher than in both control groups (0.35 +/- 0.16 mumol/l; 6.6 +/- 3.1 micrograms/l and 0.44 +/- 0.16 mumol/l 8.4 +/- 3.0 micrograms/l, respectively). During dialysis, the mean fluoride concentration fell to 0.94 +/- 0.26 mumol/l, remaining however, significantly higher than in control subjects. The use of fluoride-free dialysates seems to partially compensate the effect of renal impairment since plasma fluoride is only moderately increased in these patients.     

Cushing syndrome with food-dependent periodic hormonogenesis

Periodic hormonogenesis has been described in patients with ACTH-dependent hypercorticism, and fluctuations of cortisol secretion have also been observed in patients with adrenal tumors. In this report, we studied a 41-year-old white male who presented with hypertension, central obesity, and muscle weakness of 2-years duration. His plasma cortisol was low (4.5 micrograms) in the morning and high in the evening (29.3 micrograms). Urinary free cortisol was 750 micrograms/day. A 24-hour cycle demonstrated highest values at noon and in late afternoon. This pattern was not suppressed by dexamethasone. When the patient was kept fasting, plasma cortisol remained low all day, and became elevated immediately after meal administration overnight. A left-sided adrenal mass was demonstrated and removed. In vitro, the adenylate cyclase activity of tumor tissue demonstrated more significant response to vasopressin than to ACTH; other tested peptides were inactive. We propose that a humoral factor induced by eating was responsible for the periodic hormonogenesis, directly stimulating the adrenal secretion of cortisol.     

Lipoma widened to both lobes of the parotide gland: an exceptional entity. Case report

The authors report a very rare case of lipome extended to the superficial and deep lobes of parotid gland. MRI remains the best complementary examination to direct the diagnosis; however only the surgery will bring a histological proof formal.     

Treating facial overfilled syndrome with impaired facial expression—Presenting clinical experience with ultrasound imaging

Background

Facial overfilled syndrome is an adverse event following minimally invasive soft tissue filler injections. It presents in most cases as excess midfacial volume and/or as unnatural smile which is difficult to detect due to the absence of standardized evaluation methods.

Objective

To showcase how to identify, evaluate, and treat facial overfilled syndrome by utilizing facial ultrasound and simultaneous hyaluronidase injections.

Methods

Twenty-eight consecutive patients (26 females, 2 males) were enrolled in this study in which facial ultrasound was performed to evaluate the location previously implanted filler material. The position of the oral commissure was objectively measured in relation to bony landmarks, and the severity of lateral canthal lines was assessed by independent and blinded raters.

Results

The material was identified in 35.7% inside the subdermal fatty layer, in 28.6% inside the deep supra-periosteal fatty layer, in 10.7% inside the fibrous layer deep to the subdermal fatty layer, whereas in 25.0%, the product was not possible to locate clearly inside one specific layer. On average, 81.6 I.U. [range: 75–150] of hyaluronidase were injected. Lateral canthal line severity was before the treatment 2.28 (1.4) and was after the hyaluronidase treatment 2.02 (1.3) with p = 0.578. The position of the oral commissure increased by 0.60 cm in vertical and by 0.30 cm in horizontal directions (both p < 0.001).

Conclusion

Facial overfilled syndrome following aesthetic soft tissue filler injections can present as excess midfacial volume but also as unnatural smile. Targeted hyaluronidase injections into the culprit pockets inside the midfacial soft tissues have shown to re-establish a natural smile, to reduce excess midfacial volume, and to decrease lateral canthal line severity.     

Fatal ischemic stroke related to nonpermissive peripheral artery access for percutaneous aortic valve replacement.

This report describes an 85 year-old man who underwent percutaneous aortic valve replacement (PAVR). With a logistic euroSCORE of 37%, the patient had been refused surgical aortic valve replacement because of an unacceptably high peri-operative risk. During the PAVR procedure, severe resistance was encountered when advancing the 21 Fr delivery catheter through the left iliac artery despite pre-dilatation with a 7 mm balloon. Following this, PAVR was promptly achieved without difficulty, with excellent valve positioning, no peri-valvular leak and good hemodynamics. However, transesophageal echocardiography revealed a mobile echogenic mass within the outflow tract of the left ventricle. The mass was retrieved with a cardiac bioptome manipulated via the left femoral artery through a 9 Fr sheath. A right cerebral ischemic stroke manifested shortly after the post-procedure and the patient died on the fourth post-operative day. Post-mortem findings revealed a left subclavian artery occlusion by iliac vascular tissue. This report highlights the imperative for device-specific vascular access screening criteria and the need to minimize device size in order to safely accomplish PAVR.