Aseptic necrosis of the first metatarsal.
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Biomedical subjects
Publications and source records attributed to J L Morris.
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The vasodilator potency of guinea pig VIP (gp VIP) on the guinea pig uterine artery was compared with the potency of porcine VIP (p VIP), which differs in amino acid sequence at four locations. When antioxidants were not used, the two peptides were approximately equipotent in causing relaxation of precontracted vessel segments. Use of the antioxidants ascorbic acid and dithiothreitol resulted in significantly increased potency of both peptides. Porcine VIP was 15 times more potent than gp VIP synthesized by the same method (tBoc), and gp VIP synthesized by tBoc methodology was 2 times more potent than gp VIP synthesized by Fmoc methodology. Therefore, care should be taken in the choice and handling of synthetic peptides when aiming to mimic actions of endogenous peptides.
Interactions between neuropeptides contained in autonomic vasodilator neurons supplying the guinea pig uterine artery were investigated in isolated segments of the artery precontracted with prostaglandin F2 alpha. Neither somatostatin-14 (10(-6) mol.l-1) nor dynorphin A(1-17) (10(-6) mol.l-1) had direct effects on vascular tone, and did not affect relaxations produced by guinea pig vasoactive intestinal peptide (gpVIP). Both the porcine and the guinea pig forms of neuropeptide Y (NPY; 10(-7)-10(-5) mol.l-1) caused transient contraction of the precontracted arteries. NPY also inhibited relaxations of the artery produced by gpVIP, an action which was not directly related to the NPY contractions. NPY caused both a concentration-dependent rightward shift in the gpVIP concentration-response curve, and a reduction in size of the maximum relaxation to gpVIP. NPY (10(-6) mol.l-1) also produced a rightward shift in the concentration-response curves for the vasodilators forskolin and glyceryl trinitrate, but did not reduce the maximum relaxations to these compounds. Thus NPY, which is colocalized with VIP in vasodilator neurons supplying the uterine artery, can greatly reduce the vasodilator potency of VIP.
The hamster cheek pouch and its retractor muscle have provided valuable insights into microvascular physiology of an epithelial tissue and striated muscle, respectively. Nevertheless, the innervation of these vascular beds has not been resolved. This study has investigated the nature of autonomic and sensory innervation of these vascular beds and has tested whether it varies within or between tissues. Multiple-labelling immunohistochemistry identified autonomic and peptide-containing sensory nerve fibres. Presumptive sympathetic vasoconstrictor axons with immunoreactivity (IR) for tyrosine hydroxylase (TH) and neuropeptide Y (NPY) innervated feed arteries and arterioles (but not veins or venules) of the retractor and anterior (muscular) cheek pouch; these axons were absent from the posterior (epithelial) region of the cheek pouch, as confirmed by catecholamine fluorescence. Presumptive autonomic vasodilator axons with IR for vasoactive intestinal peptide (VIP) consistently innervated feed arteries and proximal arterioles of the cheek pouch, but generally not those of the retractor muscle nor distal arterioles of either tissue. Sparse presumptive sensory axons with IR for calcitonin gene-related peptide (CGRP) and substance P were found near arterial and venous vessels in all regions of the cheek pouch and retractor muscle; CGRP-IR was also located in motor end plates associated with striated muscle fibres. Such regional differences in vascular innervation by autonomic and sensory neurons may selectively effect local and regional control of blood flow between and within vascular beds.
This study utilised catecholamine fluorescence histochemistry, multiple-labelling immunohistochemistry and retrograde axonal transport to determine the distribution and neuropeptide content of sympathetic neurons innervating veins in the dorsal skin of the guinea pig pinna. There was a dense plexus of sympathetic axons innervating the large central vein at the base of the ear and the adjoining maxillary vein. The density of the plexus decreased towards the distal margin of the ear and in smaller veins, and was very sparse in the lateral veins at the base of the ear. Small venules < 50-80 microns diameter were not innervated. Probably all noradrenergic axons in the large veins near the base of the ear contained immunoreactivity (IR) to neuropeptide Y (NPY), but the proportion of axons with NPY-IR decreased in large veins in more lateral regions of the ear, and in smaller veins (80-100 microns diameter). Injections of Fast Blue or DiI close to large veins in the ear resulted in retrograde labelling of tyrosine hydroxylase-IR neurons in the ipsilateral superior cervical ganglion, 64% of which contained NPY-IR. Nearly all (> 90%) of the TH-IR axons in small and large veins also contained IR to dynorphin-related peptides. Thus, sympathetic venoconstriction in the thermoregulatory bed of the guinea pig pinna is likely to occur predominantly in the large central veins towards the base of the ear. Furthermore, sympathetic constriction is likely to be qualitatively different in large cutaneous veins from that occurring in small veins, and absent altogether from small venules and some lateral veins.
This study set out to examine in detail the distribution of axons of sympathetic non-noradrenergic neurons innervating the arterial bed in skeletal muscles of the forelimb and hindlimb of guinea-pigs. The distribution of non-noradrenergic axons with immunoreactivity to vasoactive intestinal peptide (VIP) was examined in limb muscles of different histochemical character. The immunohistochemical demonstration of myosin heavy chain from fast-twitch muscle, and the histochemical demonstration of adenosine triphosphatase and succinic dehydrogenase, were used to determine the muscle fibre profile of 6 different limb muscles. Muscles included the oxidative type I muscle fibre-rich accessory semimembranosus muscle, the predominantly glycolytic type II muscle fibre-rich cranial gracilis and biceps brachii muscles and the plantaris, gastrocnemius medial head and triceps brachii long head of mixed muscle fibre composition. The frequency with which the VIP-immunoreactive (VIP-IR) axons innervated intramuscular arterial vessels was compared between categories of muscles defined by their muscle fibre profile. This study demonstrated that the projection of non-noradrenergic sympathetic neurons to skeletal muscle vasculature was widespread in guinea-pig limb muscles, but that it was not uniform. VIP-IR axons were more likely to innervate the arterial vasculature of muscles with a high proportion of type I and/or oxidative muscle fibres than of muscles with a large proportion of type IIb muscle fibres. This relationship between the distribution of sympathetic non-noradrenergic axons and the metabolic characteristics of muscle suggests that these presumed vasodilator neurons have an important role in matching blood flow to the particular metabolic demands of different limb muscles.
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After the Tax Reform Act of 1986 reduced the tax-deduction benefits of investing in IRAs, many healthcare employees went looking for alternative tax-shelter investments. Several options are available. One alternative for taxpayers employed by tax-exempt organizations is Section 403(b) tax-deferred annuities (TDAs). Although the Tax Reform Act left Section 403(b) TDAs largely intact, it established a comprehensive set of nondiscrimination rules for certain statutory fringe-benefit plans--including Section 403(b) plans. The new rules are designed to restrict situations that favor participation by highly paid employees to the exclusion of other employees. Perhaps one of the harshest adjustments the 1986 law mandated is the imposition of an additional 10 percent income tax on withdrawals an investor makes from Section 403(b) plans before reaching the age of 59 years and 6 months. This excise tax had already applied to early withdrawals from an IRA, but the new law extends the penalty tax to cover all qualified plans, including TDAs.
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