Penetrating injury to the carotid artery. A reappraisal of management

Penetrating trauma remains the most common cause of cervical carotid artery injury. Controversy persists regarding proper management of these injuries, especially in the presence of a neurologic deficit. Recent experience with 24 patients over a 5-year period is reviewed. In patients with preoperative neurologic deficits, neither repair nor ligation of the injured vessel altered outcome. Outcome correlated only with preoperative neurologic status. All patients without preoperative neurologic deficits should have repair attempted when technically feasible. Although controversial, this study supports carotid artery repair except in comatose patients who have profound neurologic deficits.     

Ocular and systemic findings in the Aarskog (facial-digital-genital) syndrome

The Aarskog (facial-digital-genital) syndrome is an X-linked disorder in which short stature is accompanied by hypertelorism, digital anomalies, and shawl scrotum. Except for hypertelorism and blepharoptosis, ophthalmic abnormalities have been rarely noted in this condition. We examined four patients who had Aarskog syndrome and unilaterally or bilaterally decreased vision on initial examination. Three family members had V-pattern esotropia, latent nystagmus, inferior oblique overaction, and amblyopia. A fourth patient had bilateral blepharoptosis and severe astigmatism. Other ocular features included hyperopia, anisometropia, deficient ocular elevation, blue sclerae, and posterior embryotoxon. These findings underscore the need for ophthalmic examination in asymptomatic patients with Aarskog syndrome to rule out treatable causes of visual loss.     

Hypothalamic Na and Ca ions and temperature set-point: New mechanisms of action of a central or peripheral thermal challenge and intrahypothalamic 5-HT, NE, PGE1, and pyrogen

The effects of changes in ambient and central temperature, amines, PGE₁ and pyrogen were investigated with respect to the mechanism of Na⁺−Ca⁺⁺ ratio in the posterior hypothalamus of the unrestrained cat. Guide tubes were implanted bilaterally above the posterior hypothalamic area of 23 cats so as to accommodate push-pull cannulae. After a Na⁺ or Ca⁺⁺ sensitive site was identified by perfusion at 50 μ1/min of an artificial CSF containing 10.4 mM excess Ca⁺⁺ ions or 13.6 mM excess Na⁺ ions, several types of experiments were undertaken with the results summarized as follows: if the cat was exposed to a cold or warm environmental temperature as the posterior hypothalamus was perfused with excess cation, the typical hypothermia was produced by Ca⁺⁺ and hyperthermia by Na⁺ ions. However, if the cat was exposed to peripheral cooling or warming 30 min prior to the perfusion, the fall or rise produced by Ca⁺⁺ or Na⁺ was attenuated or prevented. In other experiments, 1.0 μCi ^{4 5}Ca⁺⁺ was injected in the ion sensitive site in the posterior hypothalamus to label stores of the cation. Raising of ambient temperature caused a retention of ^{4 5}Ca⁺⁺ in this hypothalamic area, whereas a cold environmental temperature enhanced the efflux of ^{4 5}Ca⁺⁺ at the same perfusion site. The magnitude of change in ^{4 5}Ca⁺⁺ efflux depended upon the intensity of the thermal challenge. Similarly, warming of the anterior hypothalamic, preoptic area by means of implanted thermodes caused an immediate diminution in ^{4 5}Ca⁺⁺ efflux in the posterior hypothalamus, whereas cooling of this anterior region augmented the extrusion of ^{4 5}Ca⁺⁺ ions from the posterior area. When substances which produce a temperature change were applied to the same thermosensitive zone, the direction of shift in ^{4 5}Ca⁺⁺ flux in the posterior area corresponded to the signal for heat production or heat loss. That is, the microinjection of 5-HT, PGE₁, or Salmonella typhosa into the anterior hypothalamus enhanced the efflux of ^{4 5}Ca⁺⁺ in the posterior hypothalamus as hyperthermia developed, whereas a similar microinjection of norepinephrine reduced the ^{4 5}Ca⁺⁺ output from the same sites. Finally, locally anesthetizing the cells of the anterior hypothalamus by the nerve blocker, procaine, prevented the cold and heat-induced ^{4 5}Ca⁺⁺ efflux and retention, respectively. These results suggest that if the Na⁴−Ca⁺⁺ ratio in the posterior hypothalamus establishes and maintains the set-point for body temperature of 37°–38°C, the mechanism of lability of Ca⁺⁺ through changes in binding characteristics, transport, or metabolism of the cation serves two purposes: (1) the active defense of the set-point temperature through gradations in ion shifts; and (2) the upward or downward change in set-point value, pathological or normal, triggered by virtue of impulses relayed from the anterior hypothalamus.     

Tritiated-6-beta-fluoro-6-desoxy-oxymorphone ([3H]FOXY): a new ligand and photoaffinity probe for the mu opioid receptors

6-Beta-fluoro-6-desoxy-oxymorphone (FOXY) is a fluorinated derivative of oxymorphone originally developed as a potential PET scanning ligand. Preliminary work (Rothman et al., Neuropeptides 4: 311-317, 1984) demonstrated that [3H]FOXY selectively labeled mu opioid binding sites with low levels of nonspecific binding. In this study the opiate receptor subtypes labeled by [3H]FOXY and [3H]D-ala2-MePhe4, Gly-ol5-enkephalin ([3H] DAGO) were compared using site directed acylating agents and binding surface analysis. Although the data indicated that both ligands selectively label mu opiate receptors, other experiments demonstrated that [3H]DAGO and [3H]FOXY labeled mu binding sites differently. Additional experiments demonstrated that [3H]FOXY can be used as a high yield photoaffinity label for the mu opiate receptor subtype.     

Copper-induced release of immunoreactive α-melanotropin from isolated hypothalamic granules

Previously, we demonstrated that copper chelates stimulate the release of luteinizing hormone releasing hormone (LHRH) from isolated hypothalamic granules. To assess the generality of the copper-stimulated release process, we determined the effects of copper on the release of immunoreactive α-melanotropin (α-MSH₁) from isolated granules. When granules were incubated with various copper complexes, CuATP stimulated α-MSH₁ release by 54 ± 6% (mean ± S.E.), Cu tartarate by 56 ± 4%, CuBSA by 32 ± 5% and Cu histidine by 29 ± 2%. CuATP-stimulated α-MSH₁ release from granules incubated under N₂ was 57% of that incubated under air. Furthermore, the reducing agent dithiothreitol (DTT) inhibited CuATP-stimulated α-MSH₁ release (p < 0.01), whereas oxidized DTT did not do so. Pretreatment of granules with the thiol-blocking reagents iodoacetic acid or 5, 5'-dithiobis-(2-nitrobenzoic acid) inhibited CuATP-stimulated α-MSH₁ release by 52 ± 3 and 38 ± 4%, respectively. Thus, chelated copper, rather than ionic copper, is the active form of the metal and the action of copper involves the oxidation of thiols. These data are similar to those previously observed for the copper-stimulated release of LHRH. Hence, the effects of copper on the permeability of granule membranes may be a generalized phenomenon which underlies susceptibility of storage granules to the reduction-oxidation status of the cellular milieu.