[The oculocardiac reflex in blepharoplasties]. / Der okulokardiale Reflex bei Blepharoplastiken.

The oculocardiac reflex (OCR) is a well-known phenomenon in ophthalmic surgery, but is rarely described in aesthetic blepharoplasty surgery. It was first mentioned in 1908 by Ascher and Dagnini. Since then, ophthalmologists and anaesthesiologists have regarded the onset of the oculocardiac reflex as a significant intraoperative problem, which is undermined by several case reports that describe dysrhythmias which have haved caused morbidity and death. Per definition the OCR is caused by ocular manipulation and involves intraoperative bradycardia by a change of 20 beats/minute compared to the preoperative heart rate or any dysrhythmia during the manipulation via a trigeminal-vagal-mediated reflex arc. Having operated on a 48-year-old, healthy woman in our clinic, who underwent a cardiac arrest during the blepharoplasty procedure, followed by a successful resuscitation, we investigated the onset of the OCR in our blepharoplasty patients within the last 3 years. The onset of the OCR was noted in 22 of 110 (20 %) blepharoplasty patients, mainly affecting younger, low-weighted patients operated under local anaesthesia. Awareness and treatment of this potentially life-threatening oculocardiac reflex are necessary. In most cases the onset of the reflex may be avoided by a gentle operation technique and by refraining from severe traction to the muscle or fat pad. The best treatment of a profound bradycardia caused by the OCR is to release tension to the muscle or fat pad in order to permit the heart rate to return to normal. Intraoperative monitoring is of utmost importance.

[Merkel cell carcinoma -- a case report with regard to the current treatment concepts]. / Das Merkel-Zell-Karzinom -- Eine Falldarstellung unter Berücksichtigung der aktuellen Behandlungskonzepte.

A 54-year-old female patient was admitted due to a slow growing, painless resistance on the dorsum of the left hand. The intraoperative aspect of the tumor showed a yellow to white doughy tissue mass infiltrating the metacarpal musculature and bone. After immunohistopathological staining, the diagnosis of a Merkel cell carcinoma was confirmed. A high frequency of local recurrences (25 to 77 %) and lymph node metastases (50 %) are characteristic features of Merkel cell carcinoma. In 30 % of the cases, the disease has a fatal outcome. In primary Merkel cell tumors, surgical excision is the basic therapy, although this carcinoma is highly radiosensitive. Thus, besides surgical treatment, radiation should be included into the treatment concept. In the presented case, after radical excision of the tumor and sentinel-lymphnode biopsy, the patient has been free of local recurrence and metastases for 13 months.

Angiotensin II induces apoptosis of human endothelial cells. Protective effect of nitric oxide.

Angiotensin II (Ang II) importantly contributes to the pathobiology of atherosclerosis. Since endothelial injury is a key event early in the pathogenesis of atherosclerosis, we tested the hypothesis that Ang II may injure endothelial cells by activation of cellular suicide pathways leading to apoptosis. Human umbilical venous endothelial cells (HUVECs) were incubated with increasing doses of Ang II for 18 hours. Apoptosis of HUVECs was measured by ELISA specific for histone-associated DNA fragments and confirmed by DNA laddering and nuclear staining. Ang II dose-dependently induced apoptosis of HUVECs. Simultaneous blockade of both the AT1 and AT2 receptor prevented Ang II-induced apoptosis, whereas each individual receptor blocker alone was not effective. Selective agonistic stimulation of the AT2 receptor also dose-dependently induced apoptosis. Ang II-mediated as well as selective AT2 receptor stimulation-mediated apoptosis was associated with the activation of caspase-3, a central downstream effector of the caspase cascade executing the cell death program. Specific inhibition of caspase-3 activity abrogated Ang II-induced apoptosis. In addition, the NO donors sodium nitroprusside and S-nitrosopenicillamine completely inhibited Ang II-induced apoptosis and eliminated caspase-3 activity. Thus, Ang II induces apoptosis of HUVECs via activation of the caspase cascade, the central downstream effector arm executing the cell death program. NO completely abrogated Ang II-induced apoptosis by interfering with the activation of the caspase cascade.

Shear stress inhibits apoptosis of human endothelial cells.

Physiological levels of shear stress alter the genetic program of cultured endothelial cells and reduce endothelial cell turnover in vivo. To test the hypothesis that shear stress interferes with programmed cell death, apoptosis was induced in human umbilical venous endothelial cells by growth factor withdrawal or incubation with tumor necrosis factor alpha (TNFalpha) for 18 h. Apoptosis was quantified by ELISA specific for histone-associated DNA fragments and confirmed by demonstrating the specific pattern of internucleosomal DNA fragmentation detected by electrophoresis and immunohistochemical staining. The TNFalpha (300 U/ml)-mediated increase in DNA fragmentation was completely abrogated by shear stress. Furthermore, shear stress dose-dependently reduced DNA fragmentation induced by growth factor withdrawal with maximal effect at 45 dyn/cm2. Inhibition of the CPP32-like proteases with Ac-DEVD-CHO (100 microM) revealed similar anti-apoptotic effects. In contrast, CPP32-independent induction of endothelial cell apoptosis by C2-ceramide (50 microM) was not prevented by shear stress. Thus, we propose that shear stress interferes with common cell death signal transduction involving the CPP32-like protease family and may contribute to endothelial cell integrity by inhibition of apoptosis.