During heat stress, increases in blood flow in nonglabrous skin in humans are mediated through active vasodilation by an unknown neurotransmitter mechanism. To investigate this mechanism, a three-part study was performed to determine the following: (1) Is muscarinic receptor activation necessary for active cutaneous vasodilation? We iontophoretically applied atropine to a small area of forearm skin. At that site and an untreated control site, we measured the vasomotor (laser-Doppler blood flow [LDF]) and sudomotor (relative humidity) responses to whole-body heat stress. Blood pressure was monitored. Cutaneous vascular conductance (CVC) was calculated (LDF divided by mean arterial pressure). Sweating was blocked at treated sites only. CVC rose at both sites (P < .05 at each site); thus, cutaneous active vasodilation is not effected through muscarinic receptors. (2) Are nonmuscarinic cholinergic receptors present on cutaneous arterioles? Acetylcholine (ACh) was iontophoretically applied to forearm skin at sites pretreated by atropine iontophoresis and at untreated sites. ACh increased CVC at untreated sites (P < .05) but not at atropinized sites. Thus, the only functional cholinergic receptors on cutaneous vessels are muscarinic. (3) Does cutaneous active vasodilation involve cholinergic nerve cotransmission? Botulinum toxin was injected intradermally in the forearm to block release of ACh and any coreleased neurotransmitters. Heat stress was performed as in part 1 of the study. At treated sites, CVC and relative humidity remained at baseline levels during heat stress (P > .05). Active vasodilator and sudomotor responses to heat stress were abolished by botulinum toxin. We conclude that cholinergic nerve activation mediates cutaneous active vasodilation through release of an unknown cotransmitter, not through ACh.

We report five cases of post-extracapsular cataract extraction infection in which subsequent pathologic analyses identified the organisms and found the infection to be localized or confined to the lens capsular sac. The most common offending organisms were gram-positive pleomorphic bacilli. In one case, we were able to identify the bacteria as Propionibacterium acnes. We designate this condition a localized endophthalmitis. It should be considered any time a persistent, smoldering, postoperative inflammation occurs, and in the differential diagnosis of phacoanaphylactic endophthalmitis. The condition itself is not new, but undoubtedly many such cases have gone unrecognized or have been misdiagnosed as the so-called toxic lens syndrome. In localized endophthalmitis, a clinically visible inflammatory process may occur even when multiple diagnostic taps are negative, although when the cases first appeared, the surgeons were not aware of the entity and anaerobic cultures were not always obtained. A negative tap may be explained by the fact that metabolic products from the organisms are released from the bag into the anterior segment and vitreous. A synergistic reaction may occur between these organisms and retained lens cortical remnants that may cause or exacerbate a hypersensitivity reaction. The condition may be worsened by Nd:YAG capsulotomy. The pathogenesis of localized endophthalmitis has nothing to do with the type of intraocular lens fixation (lens capsular sac or ciliary sulcus); rather, the simple presence of a capsular sac after extracapsular cataract extraction is the prerequisite for the clinical condition.

With early recognition and appropriate management of eyelid malignancies, an extremely favorable prognosis can be obtained. The management is twofold and consists of curing the patient of the malignancy and then restoring the form and function of the eyelid in order to save the eye if possible.

No abstract

Over a period of 27 months, November 1983 to February 1986, 75 eyes obtained postmortem with posterior chamber intraocular lenses (IOLs) were examined at the Center for Intraocular Lens Research, University of Utah Health Sciences Center. These IOLs were studied by histopathological techniques to determine the location of the loops. The most common combination, found in 47% of the specimens, was one loop in the lens capsular sac (bag) and one loop in the ciliary sulcus. In 32% of the specimens, both loops were in the capsular sac; in 17%, both loops were in the ciliary sulcus. Compared to results observed in other autopsy studies, in which capsular fixation was documented in less than 3% of cases, these findings reflect a trend toward capsular sac (in-the-bag) implantation of open-looped posterior chamber IOLs.