• 沒有找到結果。

Braum A., Trigatti BL., Post MJ., Sato K., Simons M., Edelberg JM., Rosenberg RD., Schrenzel M., Krieger M. Loss of SR-BI expression leads to the early onset of occlususive atherosclerotic coronary artery diaease, spontanneous myocardial infarcyions,severe cardiac dysfunction and premature death in apolipopretein. Circ Res.

2002;90:270-276.

Bribbin B., Honour AJ, Pickering GW, Sleight P, Smyth HS. Diminished baroreflex sensitivity in high blood pressure. Circulation.

1969;34:48-54.

Berne RM, Levry MN, Koeppn BM, Stanton BA. Physiology. 4th ed.

Mosby Inc., St. Louis, Missouri, U.S.A. PP.450-453, 508-509,1998.

Chen HI. Stinnett HO .Peterson DF. Bishop VS. Enhancement of vagal restraint on systemic blood pressure during hemorrhage.Am J Physiol.

1978;234:H192-H198.

Chen CC, Chen HY, Shiao MS, Lin YL, Kuo YH, Ou JC. Inhibition of low density lipoprotein oxidation by tetrahydrofurofuran lignans from

Forsythia suspensa and Magnolia coco..Planta Med., 1999; 65,

709-711.

Collin RG. P-selection or intercellular adhesion molecule deficiency substantially protects against atherosclerosis in apolipoprotein E–deficient mice. J Exp Med. 2000;191:189-194.

Fujisana Y, Mori N, Yube K, Miyanaka H, Miyatake A, Abe Y. Role of nitric oxide in regulation of renal sympathetic nerve activity during hemorrhage in conscious rats. Am J Physiol. 1999;277:H8-14.

Garg UC, Hassid A. Nitric oxide-generating vasodilator and 8-bromo-cyclic guanosine monophosphate inhibit mitogenesis and proliferation of cultured rat vascular smooth muscle cells. J Clin Invest.

1989; 83:1774-1777.

Gianaros PJ, J Jennings Richard, Benedikt OG, Andrew S, Sutton TK, Muldoon MF, Manuck SB. Greater intima media thickness in the carotid bulb is associated with reduced baroreflex sensitivity.

Am J Hypert. 2002;15:486-491.

Gianfranco P, Rienzo MarcoDi, Mancia Giuseppe. How to measure baroreflex sensit ivity: from the cardiovascular laboratory to daily life.

J Hypert. 2000;18:7-19.

Grassi G, Seravalle G, Cattaneo BM, Lanfranchi A, Vailati S, Giannattasio C. Sympathetic activation and loss of reflex sympathetic control in mild congestive heart failure. Circulation 1995;92:3206-3211.

Gonzalez GJ, Valeriano JJC, Rodriguez MF. Autonomic mediation of short-term cardiovascular oscillations after acute hemorrhage in conscious rats. Journal of the Autonomic Nervous System.

1995;55:123-130.

Hong CY, Huang SS, Tsai SK. Magnolol reduces infarct size and suppresses ventricular arrhythmia in rats subjected to coronary ligation.

Clin Exp Pharmacol Physiol. 1996;23:660-664.

Huang CH, Hong CY, Tsai SK, Lai ST. Effect of magnolol on coronary vascular resistance in rabbit: measurement with pulsed Doppler velocimetry. J Formos Med Assoc. 2000;99:554-558.

Jimenez A, Arriero MM, Almudena L-B, Fernando G-F,Garcia R, Fortes J, Millas I, Velasco S, Miguel LSD, Rico L, Farre J, Casado S, Antonio LF. Regulation of endothelial nitric oxide synthase expression in the vascular wall and in mononuclear cells form hypercholesterolemic rabbits. Circulation. 2001;104:1822-1830.

Kalinowski L, Malinski T. Endothelial NADH/NADPH-Dependent enzymatic Sources of Superoxide Production : Relationship to Endothelial Dysfunction. Acta Biochimica Polonica. 2004;51:459-469 Kirchheim HR. Systemic arterial baroreceptor reflexes. Physiol Rev.

1976;56:100-176.

Lang RE, Bruckner UB, Hermann K, Kempf B, Rascher W, Sturm V, Unger TDG. Effect of hemorrhagic shock on the concomitant release of endorphin and enkephalin like peptides from the pituitary and adrenal gland in the dog. Adv Biochem Psychopharmacol. 1982; 33:363-368.

Libby P. Changing concepts of atherogenesis. J Intern Med. 1999;

247:349-358.

Li Z, Hui Z, Abboud FM, Chapleau MW. Oxygen-derived free radicals contribute to baroreceptor dysfunction in atherosclerotic rabbits. Circ

Res. 1996;79:802-811.

Lo WC, Hsiao M, Tung CS, Tseng CJ. The Cardiovascular Effects of Nitric Oxide and Carbon Monoxide in The Nucleus Tractus Solitarii of Rats. J Hyperyens. 2004;22:1182-1190.

Lusis AJ. Atherosclerosis . Nature. 2000;407:233-241.

Matsumura K, Tsuchihashi T, Kagiyama S, Abe I, Fujishima M. Role of nitric oxide in thenuleus of the solitary tract of rats. Brain Res.

1998;789:232-238.

Miyawaki T, Goodchild AK, Pilowsky PM. Activation of mu-opioid receptors in rat ventrolateral medulia selectively locks baroreceptor reflexes while activation of delta opioid receptors blocks somato-sympathetic reflexes. Neuroscience. 2002;109:133-144.

Morita H, Vatner S. Effects of hemorrhage on renal nerve activity in conscious .Circ.Res. 1985;57:788-793.

Moncada S, Higgs EA. The L-arginine -nitric oxide pathway. N Engl J

Med. 1993;329:2002-2012.

Murad F, Ishii K, Forstermann U, Gorsky L, Kerwin JF, Pollock J, Hiller M. EDRF is an intracellular second messenger and autacoid for

regulate cyclic GMP synthesis in many cells. Adv Sec Messeng

Phosphoprot Res. 1990;24:441-448.

Oemar BS. Tschudi MR. Godoy Nelson. Brovkovich V. Malinski T.

Luscher TF. Reduced Endothelial Nitric Oxide Synthase Expression and Production in Human Atherosclerosis. Circulation. 1998;97:2494- 2498.

Palmer RMJ, Rees DD, Ashton DS. L-arginine is the physiological precursor for the formation of nitric oxide in endothelium dependent relaxation. Biochem Biophys Res Commun. 1988;153:1251-1256.

Patterson D, Dick JBC, Struthers AD. Intensive Statin Treatment Improves Baroreflex Sensitivity:Another Cardioprotective Mechanism for Statins? Heart. 2002;88:415-416.

Peotta VA, Vasquez EC, Meyrelles SS. Cardiovascular Neural Reflexes in L-NAME-Induced Hypertension in Mice. Hypertension. 2001;38:555.

Podrez EA. Macrophage scavenger receptor CD36 is the major receptor for LDL modified by monocyte-generated reactive nitrogen species. J

Clin Invest. 2000;105:1095-1108.

Ross R. Atherosclerosis - an inflammatory disease. N Engl J Med.

1999;340: 115-123.

Rubin PC, Mclean K, Reid JL. Endogenous opioid and baroreflex control in humans. Hypertension. 1983;5:535-538.

Schwartz CJ, Valente AJ, Sprage EA. A modern view of atherogenesis.

Am J Cardiol. 1993;71:9B-14B.

Shih PT. Blocking very late antigen-4 integrin decreases leukocyte entry and fatty streak formation in mice fed an atherogenic diet. Circ Res.

1998;84:345-351.

Smith JD. Decreased atherosclerosis in mice deficient in both macrophage colony-stimulating factor and apolipoprotein E. Proc Natl

Acad Sci. 1995;92:8264-8268.

Song K, Shiota N, Takai S, Takashima H, Iwasaki H, Kim S, Miyazaki M.

Induction of angiotensin converting enzyme and angiotensin II receptors in the atherosclerotic aorta of high-cholesterol fed cynomolgus monkeys. Atherosclerosis. 1998;138:171-182.

Souza HCD, Ballejo G, Salgado MCO, Diasdasilva VJ., Salgado HC. Cardiac sympathetic overactivity and decreased baroreflex sensitivity in L-NAME hypertensive rats. Am J Physiol. 2001; 280:

H844-H850.

Tabrizchi R. Cardiovascular effects of noradrenaline in hypovolemic haemorrhage: role of inducible nitric oxide synthase. Eur J Pharmacol.

1998;361:227-234.

Timmers HJLM, Wieling W, Karemaker J, Lenders JW. Cardiovascular Responses to Stress after Carotid Baroreceptor Denervation in Humans. Ann N Y Acad Sci.2004;1018:515-519.

Thiemermann C, Szab C, Mitchell JA, Vane JR. Vascular hyporeactivity to vasoconstrictor agents and hemodynamic decompensation in hemorrhagic shock is mediated by nitric oxide. Proc Natl Acad Sci.

1993;90:267-271.

Thiemermann C. The role of the L-arginine:nitric oxide pathway in circulatory shock. Adv Pharmacol. 1994;28:45-79.

Thompson MA, Henderson KK, Woodman CR, Turk JR, Rush JW, Price E, Laughlin MH. Exercise preserves endothelium-dependent relaxation in coronary arteries of hypercholesterolemic male pigs. J Appl Physiol.

2004;96:1114-1126.

Tao L, Liu HR, Gao E, Teng ZP, Lopez BL, Christopher TA, Ma XL, Ines BH, Willette RN, Ohlstein EH, Yue TL. Antioxidative, Antinitrative, and vasculoprotective effects of a peroxisome proliferator–activated receptor- agonist in hypercholesterolemia. Circulation. 2003; 108:

2805-2810.

Wilfert K, Drischel K, Unbehaun A, Guski H, Persson PB, Stauss HM.

Vascular response to angiotensin II in atherosclerosis role of the baroreflex. Hypertension. 2000;35:685

Yang BC, Phillips MI, Mohuczy D, Meng H , Shen L, Mehta P, Mehta JL.

Increased angiotensin II type 1 receptor expression in hypercholesterolemic atherosclerosis in rabbits. Arterioscler Thromb

Vasc Biol. 1998;18:1433-1439.

Zollei E, Paprika D, Makra P, Gingl Z, Vezendi K, Rudas L.Human Autonomic Responses to Blood Donation. Autonomic Neuroscience :

Basic and Clinical. 2004;110:114-120.

Zucker IH, Schultz HD, Li YF, Wang Y, Wang W, Patel KP. The Origin of Sympathetic Outflow in Heart Failure:the Roles of Angiotensin II and Nitric oxide. Progress in Biophysics & Molecular Biology.

2004;84:217-232.

蔡勝國. 厚朴的抗氧化成分對大白鼠心肌保護作用的研究. 行政院衛

生中醫藥年報. 1997;15:334-346

吳介信. 厚朴及澤瀉抗動脈粥狀硬化之研究. 行政院衛生中醫藥年

報.2000;18:673-686

賴榮祥, 陳美睦. 厚朴的種種問題及其相關生藥製劑之應用.生藥資

訊. 2000;8:1-18.

黃瑞東. 厚朴的成分與藥理. 生藥資訊. 2000;8:19-21.

Table 1.

Plasma levels of cholesterol (CHO) and triglycerides (TG) of rabbits fed with various diets at the 8th week.

Group Control(7) Cholesterol(3) Magnolia(9)

CHO (mg/dL) 70±5 781±60* 514±139*

TG (mg/dL) 138±5 164±3 191±27

All values are expressed as means ± SE (standard error of means). The sample sizes are indicated in parentheses. The Control group were fed with normal rabbit chow. The Cholesterol group were fed with normal rabbit chow plus 10﹪(w/w) corn oil and 0.5﹪(w/w) cholesterol. The Magnolia group were fed with the same diet as the Cholesterol group, but plus l﹪

(w/w) Magnolia officinalis methanol extract (see text for detail).

*

: P<

0.05, compared with the Control group.

Table 2. Baseline systemic blood pressure (BP), heart rate (HR) and BRS of rabbits fed with various diets at the 4th and 8th week.

Group Control Cholesterol Magnolia

Week 4(14) 8(21) 4(9) 8(18) 4(8) 8(12)

BP (mmHg) 95±1 96±2 94±2 109±2* 101±4 109±2*

HR (bpm) 248±8 255±5 233±10 257±5 246±5 274±11 B R S(bpm/mmHg) - 2.22±0.29 - 2 . 2 6±0.21 -1 . 7 1±0. 3 5 - 1.28±0 . 0 5 * - 1 . 9 4±0.22 -1 . 6 5±0 . 1 1 * #

All values are expressed as means ± SE (standard error of means). The sample sizes are indicated in parentheses. The Control group were fed with normal rabbit chow. The Cholesterol group were fed with normal rabbit chow plus 10﹪(w/w) corn oil and 0.5﹪(w/w) cholesterol. The Magnolia group were fed with the same diet as the Cholesterol group, but plus l﹪

(w/w) Magnolia officinalis methanol extract (see text for detail).

*

: P<

0.05, compared with the Control group of the same week. # P<0.05, compared with the Cholesterol group of the same week.

Table 3. Effects of NO synthase blockade with L-NAME on the systemic blood pressure (BP) and heart rate (HR) of rabbits fed with various diets at the 8th week.

BP(mmHg) HR(bpm)

Group Control (9) Cholesterol(7) Magnolia (4) Control Cholesterol Magnoli a Before 88 ±4 98±3* 108 ±4* 247 ±9 252±9 277±32

After 99±5# 114 ±4**# 121 ±5**# 222 ±15 201 ±12# 197 ±30

%Change 12 ± 3 16 ± 2 12 ± 2 -10± 6 -21± 3 -28±6

All values are expressed as means ± SE (standard error of means). The sample sizes are indicated in parentheses. The Control group were fed with normal rabbit chow. The Cholesterol group were fed with normal rabbit chow plus 10﹪(w/w) corn oil and 0.5﹪(w/w) cholesterol. The Magnolia group were fed with the same diet as the Cholesterol group, but plus l﹪(w/w) Magnolia officinalis methanol extract (see text for detail).

*

: P<0.05, compared with the Control group before L-NAME was added .

**

: P<0.05, compared with the Control group after L-NAME was added . # : P<0.05, compared with the same group before L-NAME was added.

Table 4. Systemic blood pressure (BP) and heart rate (HR) profile during induction of hemorrhage in rabbits fed with various diets at the 8th week.

BP (mmH) HR (bpm)

Group Control(8) Cholesterol(9) Magnolia(6) Control Cholesterol Magnoli a Baseline 94±4 112±3 108±3 288 ±13 271 ±12 260 ±20 PeakHR 71±3 78±3 76±6 310 ±17 296±12 335±20 Lowest HR 5 8 ± 3 5 6 ± 3 58 ± 3 2 7 4 ± 1 5 2 4 7 ± 1 0 2 3 6 ± 15 Lower plateau 76±8 74±4 66± 3 296±10 278±13 293±23

All values are expressed as means ± SE (standard error of means). The sample sizes are indicated in parentheses. The diet treatment of each group was the same as described in Table 1. Baseline: baseline BP and HR before induction of hemorrhage. Peak HR: phase of hemorrhage when HR reached the highest level.

Lowest HR: phase of hemorrhage after HR was decreased from peak HR to a lowest point before developed to a steady plateau. Lower plateau: phase of hemorrhage when criteria of hemorrhage were reached, and both BP and HR reached a plateau (also see text and Fig. 4 for more detail).

BRS (bpm/mmHg)

-3 -2 -1

4 week 8 week

Cntrol Cholesterol Magnolia

*

*

#

Fig 1. BRS of rabbits fed with different diets at the 4th and 8th week.

All values are expressed as means ± SE (standard error of means). The sample sizes are indicated in parentheses. The Control group were fed with normal rabbit chow. The Cholesterol group were fed with normal rabbit chow plus 10

﹪(w/w) corn oil and 0.5﹪(w/w) cholesterol. The Magnolia group were fed with the same diet as the Cholesterol group, but plus l﹪(w/w) Magnolia officinalis methanol extract (see text for detail).

*

: P<0.05, compared with the Control group of the same week. #: P<0.05, compared with the Cholesterol group of the same week.

Fig. 2. Effects of NO synthase blockade with L-NAME on the systemic blood pressure and heart rate in rabbits fed with different diets.

The Control group were fed with normal rabbit chow. The Cholesterol group were fed with normal rabbit chow plus 10 ﹪ (w/w) corn oil and 0.5 ﹪ (w/w) cholesterol. The Magnolia group were fed with the same diet as the Cholesterol group, but plus l﹪(w/w) Magnolia officinalis methanol extract (see text for detail).

BRS (bpm/mmHg)

-3 -2 -1

baseline +L-NAME Control Cholesterol Magnolia

*

*

#

#

Fig 3. Effects of NO synthase blockade with L-NAME on BRS in rabbits fed with different diets.

The Control group were fed with normal rabbit chow. The Cholesterol group were fed with normal rabbit chow plus 10﹪(w/w) corn oil and 0.5﹪(w/w) cholesterol. The Magnolia group were fed with the same diet as the Cholesterol group, but plus l﹪(w/w) Magnolia officinalis methanol extract (see text for detail).

*

: P<0.05, compared with the baseline values (before L-NAME) of the Control group. # : P < 0.05, compared with the baseline values of the Cholesterol group.

Fig. 4. Changes of systemic blood pressure and heart rate during the induction of hemorrhage.

After the Baseline was recorded, procedure of hemorrhage was initiated (arrow).

Note that the hemorrhage started with a non hypotensive phase with a gradual increase in heart rate. Then the hemorrhage developed into a hypotensive phase with a further increase of heart rate (Peak HR). However, as hemorrhage progressed into a more severe phase, the heart rate was paradoxically decreased. The hemorrhage was continued until the mean arterial blood pressure dropped below 70 mmHg (Lowest HR), and then the procedure of hemorrhage was terminated. The blood pressure and heart rate would then level off (Lower plateau).

BRS (bpm/mmHg)

Fig.5. Effects of NO synthase blockade with L-NAME on BRS during hemorrhage in rabbits fed with different diets.

P < 0.05 was considered statistically significant. Statistical notations are defined as follows. *: compared with the baseline of the Control group. #:

compared with the baseline of the Cholesterol group.**: compared with the hemorrhagic state (Hemo) of the Control group. ##: compared with the hemorrhagic state (Hemo) of the Cholesterol group.***: compared with the hemorrhagic state with NO synthase blockade (H+L-NAME) of the Control group. ###: compared with the hemorrhagic state with NO synthase blockade (H+L-NAME) of the Cholesterol group. The Control group were fed with normal rabbit chow. The Cholesterol group were fed with normal rabbit chow plus 10﹪(w/w) corn oil and 0.5﹪(w/w) cholesterol. The Magnolia group were fed with the same diet as the Cholesterol group, but plus l﹪(w/w) Magnolia officinalis methanol extract (see text for detail).

相關文件