Narcissus and Daffodil

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Pharmacology of Narcissus compounds 337 182 ng/ml. The half-life was reported to be 8–10 hours. These values are closer to those reported by Westra et al. (1986). In a further study in eight male volunteers, Bickel et al. (1991b) observed a maximum plasma concentration of 30–60 ng/ml after oral administration of 10 mg galanthamine and 50–100 ng/ml after the same dose given by constant rate IV infusion over 30 minutes. Galanthamine showed linear, first order pharmacokinetics. The mean values for t1/2α and t1/2β were 0.16 hours and 5.68 hours, respectively. The mean total clearance was 340 ml/h/kg and renal clearance was 84 ml/h/kg. A steady state volume of distribution of 2.64 litre/kg (95% CI: 2.41–2.90 litre/kg) was calculated. Twenty-five percent of the dose was excreted unchanged in the urine. Little evidence of metabolism was found: negligible amounts of epigalanthamine and galanthaminone were detected in blood and urine. Most recently, Kewitz (1997) reported data from a 15-week clinical trial of galanthamine in 34 patients with Alzheimer’s disease, whose mean age was 75 years. A mean volume of distribution of 2.9 litre/kg, a half-life of 8.1 hours and a plasma clearance of 250 ml/h/kg were calculated. As might be expected and certainly should be remembered, clearance was 30% less in this elderly population than in healthy young volunteers. There is no direct in vivo evidence that galanthamine itself enters the human brain. However, examination of its structure (see Figure 13.1) reveals a tertiary nitrogen atom in common with many molecules that can penetrate the bloodbrain barrier. Indirectly, there is biochemical evidence from experiments in rats (Mihailova and Yomboliev, 1986). One and 3 mg/kg intravenous doses produced peak levels of 5 and 6.3 µg/g of brain tissue, respectively, 10–15 minutes after injection, declining to about 10% between 1 and 3 hours. In mice, parenteral administration of galanthamine resulted in accumulation in brain, liver and kidney tissue (Bickel et al., 1991a). Correlation of galanthamine pharmacokinetics with erythrocyte cholinesterase inhibition The inhibition of acetylcholinesterase in human erythrocytes correlates closely with the pharmacokinetics of galanthamine. A median maximal value of 53% inhibition was reported after a single, intravenous dose of 10 mg (Bickel et al., 1991b). The in vitro and ex vivo concentration responses were essentially identical, indicating that galanthamine alone, and not its metabolites, was responsible for inhibition of cholinesterase. In a previous study (Thomsen et al., 1990a), erythrocyte acetylcholinesterase activity returned to normal some 30 hours after both single dose and chronic administration at therapeutic doses (10–40 mg daily), illustrating the reversible nature of the inhibition of the enzyme by galanthamine. Kewitz (1997) recently presented data to show the relationship between the serum level of galanthamine, enzyme inhibition in erythrocytes and central nervous system (CNS) effects. Simultaneous EEG recordings were made in a healthy young male volunteer, during an IV infusion of 15 mg galanthamine. The power density of the alpha-one frequency band of the EEG at the occipital region began 7 minutes after starting the infusion, when 40% of the enzyme activity had been blocked. Power density fluctuated in synchrony with enzyme activity as the galanthamine levels fell after the infusion was stopped.
338 D. Brown Metabolism and excretion Clearly, the metabolism of any drug that is used in an elderly population needs to be characterised, given the potential effects of age on liver function. In the study by Westra et al. (1986), approximately 30% of the intravenous galanthamine dose was excreted in the urine unchanged. Biliary excretion was negligible and there was no evidence of conjugation with glucuronide or sulphation. Mihailova et al. (1989) detected the metabolites epigalanthamine (the stereo isomer of galanthamine – see Figure 13.2) and galanthaminone in plasma and urine; these metabolites possess only very weak anticholinesterase activity (
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Narcissus and Daffodil
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Narcissus and Daffodil The genus Na
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Contents Preface to the series vii
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Preface to the series There is incr
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Preface My interest in flower-bulb
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Acknowledgements I would like to th
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Gordon R. Hanks Crop and Weed Scien
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Figures 1.1 The effect of bulb stor
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Figures/Plates xvii 7.8 Accumulatio
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Figures/Plates of different segment
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2 G.R. Hanks Information about the
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4 G.R. Hanks (1999), and the polysa
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3 2 4 1 1 3 2 4 5 Flowering in 1976
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8 G.R. Hanks Figure 1.6 Diagrammati
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10 G.R. Hanks (Rees, 1969). When fl
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12 G.R. Hanks Figure 1.8 The relati
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14 G.R. Hanks root system of commer
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16 G.R. Hanks Cremer, M.C., Beijer,
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18 G.R. Hanks Roh, S.M. and Lee, J.
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20 A.C. Dweck Figure 2.1 The narcis
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22 A.C. Dweck Julians Hertfordshire
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24 A.C. Dweck Herefordshire, if daf
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26 A.C. Dweck the basis of an ancie
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28 A.C. Dweck Britten, J. and Holla
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3 Classification of the genus Narci
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(1) (2) (3)
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34 B. Mathew d. Section Jonquillae
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36 B. Mathew N. cyclamineus DC. Flo
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38 B. Mathew 1c. Section Ganymedes
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40 B. Mathew umbel, fragrant; peria
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42 B. Mathew recognition whatsoever
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44 B. Mathew Note: N. elegans shows
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46 B. Mathew ssp. praecox Gatt. and
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(1) (2) (3) (4)
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50 B. Mathew Table 3.1 Horticultura
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52 B. Mathew RHS (1958) The Classif
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54 G.R. Hanks grown for galanthamin
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56 G.R. Hanks such as drying stores
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Table 4.4 Areas of Narcissus cultiv
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60 G.R. Hanks Following planting in
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62 G.R. Hanks lost, resulting in th
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64 G.R. Hanks pathogen-tested nucle
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Figure 4.1 Mean monthly weather dat
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68 G.R. Hanks (as well as natural e
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70 G.R. Hanks compaction and its ef
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72 G.R. Hanks bulbs with base rot)
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74 G.R. Hanks Figure 4.3 Modern fro
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76 G.R. Hanks caution. Higher rates
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78 G.R. Hanks can also be prevented
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80 G.R. Hanks Figure 4.4 A typical
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82 G.R. Hanks Planting date The pra
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84 G.R. Hanks Hanks and Jones, 1986
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86 G.R. Hanks On sloping sites, gro
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88 G.R. Hanks Insecticide and nemat
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90 G.R. Hanks bulb growth, especial
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92 G.R. Hanks Figure 4.7 Changes in
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94 G.R. Hanks methods have been tes
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96 G.R. Hanks the boxes, exiting at
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98 G.R. Hanks usually collected in
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100 G.R. Hanks respond to ethylene
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102 G.R. Hanks using thiabendazole
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104 G.R. Hanks required for the eff
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106 G.R. Hanks and cross-cutting, s
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108 G.R. Hanks In practice, moulds
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110 G.R. Hanks that, with enterpris
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112 G.R. Hanks Balatková, V., Tupy
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114 G.R. Hanks (Narcissus pseudonar
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116 G.R. Hanks Flint, G.J. (1983) E
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118 G.R. Hanks Hanks, G.R. and Rees
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120 G.R. Hanks Khatib, K. al (1996)
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122 G.R. Hanks Luyten, I. (1935) Ve
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124 G.R. Hanks O’Neill, T.M., Man
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126 G.R. Hanks Ruamrungsri, S., Rua
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128 G.R. Hanks Thompson, P.A. (1977
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130 G.R. Hanks Williams, M. (1996)
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132 J.B. Briggs Table 5.1 Typical g
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134 J.B. Briggs Table 5.3 Actual gr
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136 J.B. Briggs Table 5.4 Actual co
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138 J.B. Briggs Table 5.5 Capital c
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140 J.B. Briggs ADAS (1987a) Narcis
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142 J. Bastida and F. Viladomat Fig
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Table 6.1 Narcissus alkaloid struct
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Table 6.1b Continued Alkaloid name
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Table 6.1d Tazettine type O O R1 R2
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Table 6.1f Continued MeO Alkaloid n
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Table 6.2 Continued Species* Alkalo
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162 J. Bastida and F. Viladomat Tab
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Table 6.3 Continued Alkaloid* Formu
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Table 6.3 Continued Alkaloid* Formu
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176 J. Bastida and F. Viladomat Tab
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178 J. Bastida and F. Viladomat Cri
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180 J. Bastida and F. Viladomat It
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184 J. Bastida and F. Viladomat is
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186 J. Bastida and F. Viladomat and
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Table 6.4 Continued Alkaloid Activi
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196 J. Bastida and F. Viladomat tac
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198 J. Bastida and F. Viladomat Ang
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200 J. Bastida and F. Viladomat Boi
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202 J. Bastida and F. Viladomat lyc
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204 J. Bastida and F. Viladomat Fug
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206 J. Bastida and F. Viladomat Han
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208 J. Bastida and F. Viladomat Kin
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210 J. Bastida and F. Viladomat of
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212 J. Bastida and F. Viladomat Sp
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214 J. Bastida and F. Viladomat Wil
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216 C. Codina and, consequently, hi
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218 C. Codina easily lost on transf
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220 C. Codina they might be more su
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222 C. Codina µ g/g FW µ g/g FW 3
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224 C. Codina Kinetin As observed i
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226 C. Codina Table 7.3 Total produ
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228 C. Codina Accumulation of alkal
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230 C. Codina Accumulation of alkal
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232 C. Codina Effect on growth and
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234 C. Codina mg/g DW mg/g DW 0.90
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236 C. Codina mg/g DW mg/g DW 1.4 1
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238 C. Codina mg/g DW mg/g DW 1.5 1
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240 C. Codina Hanks, G.R. and Jones
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8 Narcissus and other Amaryllidacea
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244 O.A. Cherkasov and O.N. Tolkach
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9 Studies on galanthamine extractio
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258 M. Kreh Table 9.1 Results of ga
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260 M. Kreh relation to the qualita
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262 M. Kreh Figure 9.3 Galanthamine
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264 M. Kreh 2.0 flower 2 1 3 4 0 10
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266 M. Kreh • High purity of the
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268 M. Kreh fraction of Narcissus
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H O MeO O MeO H H HO H (1) (3) + 2
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272 M. Kreh Gorinova, N.I., Atanass
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274 R.M. Moraes (Katz and Taneck, 1
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276 R.M. Moraes bulbs of many Narci
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278 R.M. Moraes Galanthamine conten
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280 R.M. Moraes Table 10.2 The effe
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282 R.M. Moraes years, a yield of 1
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284 R.M. Moraes Kosley, R.W., Jr.,
Page 307 and 308: 11 Extraction and quantitative anal
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Page 377 and 378: 356 D. Brown examination of a brain
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Page 383 and 384: 362 D. Brown statistically signific
Page 385 and 386: 364 D. Brown ( Jann, 1998); see Tab
Page 387 and 388: 366 D. Brown REFERENCES Bartus, B.T
Page 389 and 390: 368 D. Brown Wilcock, G.K., Scott,
Page 391 and 392: 370 K. Ingkaninan, H. Irth and R. V
Page 401 and 402: 16 Narcissus lectins Els J.M. Van D
Page 403 and 404: 382 E.J.M. Van Damme and W.J. Peuma
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388 E.J.M. Van Damme and W.J. Peuma
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390 E.J.M. Van Damme and W.J. Peuma
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17 Narcissus in perfumery HISTORY C
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394 C. Remy Figure 17.2 Flower coll
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Figure 17.3 Narcissus flowers sprea
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398 C. Remy CONCLUSION The use of n
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400 C.G. Julian and P.W. Bowers Fig
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406 C.G. Julian and P.W. Bowers sym
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19 Review of pharmaceutical patents
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410 J.R. Murray to certain RNA viru
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412 J.R. Murray occurs in a two-pha
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414 J.R. Murray cognitive function
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416 J.R. Murray given at a time bet
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418 J.R. Murray Hofmannor, D., Mosc
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420 Index Backache, 403 Bacterial d
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422 Index Divisions (classification
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424 Index Leaf numbers, 11 Leaf sco
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426 Index Poet’s cultivars, 34 Po
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428 Index Subgenus (taxonomy); Ajax
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