Effects of Algan Hemostatic Agent on bleeding time in a rat tail hemorrhage model.

BACKGROUND: Algan Hemostatic Agent (AHA) is a multi-herbal extract containing a standardized amount of Achillea millefolium, Juglans regia, Lycopodium clavatum, Rubus caesius or Rubis fruciosus, Viscum album, and Vitis vinifera, each of which is effective in hemostasis. In this study, we aimed to investigate the effects of AHA on bleeding time in a rat tail hemorrhage model. METHODS: Forty-eight Sprague Dawley rats (5-7 weeks old, 180-210 g) were randomly and equally allocated to six groups as follows: heparin plus saline (heparinized control), heparin plus AHA-soaked sponge, heparin plus liquid form of AHA, saline (non-heparinized control), AHA-soaked sponge and liquid form of AHA. Heparin (640 IU/kg) was administered intraperitoneally three times a day for three days in heparinized groups. For the bleeding model, the tail of rats was transected. According to the study group, either saline- or AHA-soaked sponge or liquid form of AHA was applied over the hemorrhage area. In AHA- or saline-soaked sponge groups, once the bleeding time had started, it was checked every 10 seconds. If the bleeding did not stop after 40 seconds, it was accepted as a failure. In liquid AHA group, the duration of bleeding was measured using a chronometer and defined as the time (seconds) from wounding until the bleeding stopped. RESULTS: Bleeding time in the heparinized and non-heparinized control groups was over 40 seconds. After applying the sponge form of AHA on the wound area, bleeding time was significantly shortened to less than 20 seconds in both heparinized and non-heparinized rats (p<0.001 for both). The liquid form of AHA stopped bleeding in 5.0±1.2 seconds and 8.0±1.3 seconds in heparinized and non-heparinized groups, respectively. CONCLUSION: AHA is a highly effective topical hemostatic agent in a rat tail hemorrhage model, thus may provide for a unique clinically effective option for control of bleeding during surgical operations or other emergencies.

NaoXinTong Capsule Inhibits Carrageenan-Induced Thrombosis in Mice.

Formation of thrombosis is mainly associated with dysfunctions of endothelial cells. NaoXinTong capsule (NXT), a traditional Chinese medicine, has been demonstrated multiple protective effects on vascular systems. However, it is unknown the effect of NXT on thrombosis. In this study, we determined whether NXT can inhibit carrageenan-induced thrombosis and the underlying mechanisms. Two days after carrageenan injection, severe thrombi were found in blood vessels of mouse tail and liver. By contrast, thrombi were substantially reduced by NXT treatment, and the reduction was associated with reduced serum tumor necrosis factor α and P-selectin levels. In vitro, NXT reduced lipopolysaccharide-activated adhesion of THP-1 monocytes to human umbilical vein endothelial cells (HUVECs) by inhibiting expression of adhesion molecules and interleukin 6, and reducing production of mitochondrial superoxide that is related to activation of antioxidant enzymes expression. NXT also reduced oxidized low-density lipoprotein-activated adhesion of platelets to HUVECs. In addition, NXT protected HUVECs against clopidogrel-induced cell death by inhibiting expression of tumor necrosis factor-like cytokine 1A and activating expression of vascular endothelial growth factor α. Taken together, our study indicates the potential application of NXT in antithrombosis by multiple antithrombotic functions.

Roasted Barley Extract Affects Blood Flow in the Rat Tail and Increases Cutaneous Blood Flow and Skin Temperature in Humans.

Roasted barley extract (RBE, "Mugicha") is a traditional Japanese beverage reported to improve blood viscosity and affect food functionality. RBE is suggested to contain 2,5-diketopiperazines, which are the functional component with neuroprotective and immunostimulatory effects that are produced in food through roasting. In this study, we investigated the effects of RBE on blood circulation, both clinically and in rats. At first, we confirmed five 2,5-diketopiperazine derivatives in RBE by LC-MS analysis. Secondarily, we revealed that RBE affects blood flow in the rat tail and compared the efficacy on rat tail blood flow among five 2,5-diketopiperazines in RBE. Especially, cyclo(d-Phe-l-Pro) was the most effective in increasing blood flow in the rat tail. We also researched the mechanism of cyclo(d-Phe-l-Pro) with rat aorta study. As a result, we confirmed that cyclo(d-Phe-l-Pro) has an effect on vasodilatation through the release of nitric oxide in the vascular endothelium. Finally, we also confirmed that RBE affects cutaneous blood flow and increases skin temperature in humans.

3-Iodothyronamine Induces Tail Vasodilation Through Central Action in Male Mice.

3-Iodothyronamine (3-T1AM) is an endogenous thyroid hormone (TH)-derived metabolite that induces severe hypothermia in mice after systemic administration; however, the underlying mechanisms have remained enigmatic. We show here that the rapid 3-T1AM-induced loss in body temperature is a consequence of peripheral vasodilation and subsequent heat loss (e.g., over the tail surface). The condition is subsequently intensified by hypomotility and a lack of brown adipose tissue activation. Although the possible 3-T1AM targets trace amine-associated receptor 1 or α2a-adrenergic receptor were detected in tail artery and aorta respectively, myograph studies did not show any direct effect of 3-T1AM on vasodilation, suggesting that its actions are likely indirect. Intracerebroventricular application of 3-T1AM, however, replicated the phenotype of tail vasodilation and body temperature decline and led to neuronal activation in the hypothalamus, suggesting that the metabolite causes tail vasodilation through a hypothalamic signaling pathway. Consequently, the 3-T1AM response constitutes anapyrexia rather than hypothermia and closely resembles the heat-stress response mediated by hypothalamic temperature-sensitive neurons. Our results thus underline the well-known role of the hypothalamus as the body's thermostat and suggest an additional molecular link between TH signaling and the central control of body temperature.

Reduced brown adipose tissue thermogenesis during environmental interactions in transgenic rats with ataxin-3-mediated ablation of hypothalamic orexin neurons.

Thermogenesis in brown adipose tissue (BAT) contributes to substantial increases in body temperature evoked by threatening or emotional stimuli. BAT thermogenesis also contributes to increases in body temperature that occur during active phases of the basic rest-activity cycle (BRAC), as part of normal daily life. Hypothalamic orexin-synthesizing neurons influence many physiological and behavioral variables, including BAT and body temperature. In conscious unrestrained animals maintained for 3 days in a quiet environment (24-26°C) with ad libitum food and water, we compared temperatures in transgenic rats with ablation of orexin neurons induced by expression of ataxin-3 (Orx_Ab) with wild-type (WT) rats. Both baseline BAT temperature and baseline body temperature, measured at the onset of BRAC episodes, were similar in Orx_Ab and WT rats. The time interval between BRAC episodes was also similar in the two groups. However, the initial slopes and amplitudes of BRAC-related increases in BAT and body temperature were reduced in Orx_Ab rats. Similarly, the initial slopes and amplitudes of the increases in BAT temperatures induced by sudden exposure to an intruder rat (freely moving or confined to a small cage) or by sudden exposure to live cockroaches were reduced in resident Orx_Ab rats. Constriction of the tail artery induced by salient alerting stimuli was also reduced in Orx_Ab rats. Our results suggest that orexin-synthesizing neurons contribute to the intensity with which rats interact with the external environment, both when the interaction is "spontaneous" and when the interaction is provoked by threatening or salient environmental events.

Modulation of body temperature and LH secretion by hypothalamic KNDy (kisspeptin, neurokinin B and dynorphin) neurons: a novel hypothesis on the mechanism of hot flushes.

Despite affecting millions of individuals, the etiology of hot flushes remains unknown. Here we review the physiology of hot flushes, CNS pathways regulating heat-dissipation effectors, and effects of estrogen on thermoregulation in animal models. Based on the marked changes in hypothalamic kisspeptin, neurokinin B and dynorphin (KNDy) neurons in postmenopausal women, we hypothesize that KNDy neurons play a role in the mechanism of flushes. In the rat, KNDy neurons project to preoptic thermoregulatory areas that express the neurokinin 3 receptor (NK3R), the primary receptor for NKB. Furthermore, activation of NK3R in the median preoptic nucleus, part of the heat-defense pathway, reduces body temperature. Finally, ablation of KNDy neurons reduces cutaneous vasodilatation and partially blocks the effects of estrogen on thermoregulation. These data suggest that arcuate KNDy neurons relay estrogen signals to preoptic structures regulating heat-dissipation effectors, supporting the hypothesis that KNDy neurons participate in the generation of flushes.

Thermoregulatory responses elicited by microinjection of L-glutamate and its interaction with thermogenic effects of GABA and prostaglandin E2 in the preoptic area.

The aim of the present study was to investigate the thermoregulatory effects of neuronal activation with sodium L-glutamate (glutamate) in the preoptic area (POA) of the hypothalamus and to examine its possible interaction with the thermogenic effects of GABA and prostaglandin E(2) (PGE(2)). Unilateral microinjection of glutamate (5 nmol) into the lateral POA or its vicinity elicited a prompt increase in tail skin temperature and simultaneous decreases in the O(2) consumption rate (VO(2)), heart rate, and colonic temperature in urethane-chloralose-anesthetized rats. A central subpopulation of these sites at around the level of bregma was also responsive to the thermogenic and tachycardic effects of GABA (30 nmol). Although the microinjection of GABA into nearby sites elicited no direct effect, it greatly attenuated the hypothermic effects of glutamate subsequently administered to the same site. These results suggest that activation of the lateral POA elicited heat-loss responses and that its central part provided a tonic inhibitory drive toward heat production and tail vasoconstriction. On the other hand, the microinjection of glutamate elicited initial small decreases and subsequent large increases in VO(2) and heart rate in the rostromedial POA. However, no thermoregulatory response was elicited by the microinjection of glutamate at sites where the microinjection of PGE(2) (35 fmol) elicited thermogenic, tachycardic and hyperthermic responses. These results may suggest that the rostromedial POA contained two glutamate-responsive cell groups that had opposite influences on thermoregulation and that the locus that was highly sensitive to the thermogenic effect of PGE(2) was unreactive to glutamate. Collectively, activation of neurons in the lateral POA and rostromedial POA evoked distinct thermoregulatory responses.

[Postcolostral immunoglobulin G (IgG) levels in newborn piglets using three different ELISA detection systems]. / Untersuchungen zur postkolostralen Immun-globulin-G-Versorgung neugeborener Saugferkel mittels unterschiedlicher ELISA-Nachweissysteme.

UNLABELLED: Objective of the study was to evaluate whether the Colostrum Quality Counter (CQC), a new test method for immunoglobulin G (IgG) levels in newborn piglets, is easy to handle and provides comparable results to established testing regimes. MATERIAL AND METHODS: Blood samples from 219 piglets from four different farms were tested for their IgG-concentrations using three different ELISA tests. Furthermore, double samples from 30 piglets were taken from both the anterior vena cava and from the tail to determine whether the collection site affects the results. The three tests used were the Colostrum Quality Counter (CQC; FarmulaONE, NL-Best), the internal IgG-ELISA from our laboratory (MUC) and a commercially-available IgG-ELISA (NAT; NatuTec, Frankfurt/Main, Germany). RESULTS: MUC and NAT showed a higher correlation to each other than to the CQC when referring to the individual results per single piglet. The results from the CQC were higher and the standard deviation was significantly greater. The sampling site had no significant effect on the IgG concentrations measured. CLINICAL RELEVANCE: The CQC is a straightforward and simple test, being very convenient for sampling a large number of piglets. CQC results were inhomogeneous with some unusually high IgG-concentrations. MUC and NAT provided comparable results to one another and the IgG-concentrations showed a good correlation.

Allergy-preventive effects of the flowers of Impatiens textori.

The allergy-preventive activity of a 35% EtOH extract (IT) of flowers of Impatiens textori MIQ. was demonstrated in a continuing search for allergy-preventive substances from natural sources. The evaluation of its activity used an in vivo assay method for monitoring the blood flow decrease in the tail vein microcirculation of mice subjected to sensitization with hen-egg white lysozyme. Among the principal compounds in IT, apigenin (1), luteolin (3), and luteolin 7-glucoside (4) showed significant allergy-preventive effects.

Allergy-preventive effects of Hibiscus mutabilis 'versicolor' and a novel allergy-preventive flavonoid glycoside.

Allergy-preventive activity was demonstrated for the MeOH extract (HM) of the petals of Hibiscus mutabilis L. 'versicolor' MAKINO in a continuing search for allergy-preventive substances from natural sources, using the in vivo assay method. This assay system uses monitoring of a decrease in the blood flow at the tail vein of mice subjected to hen egg-white lysozyme (HEL) sensitization. By bioassay-directed fractionation, a new flavonol triglycoside, quercetin 3-O-[beta-D-xylopyranosyl(1-->2)-alpha-L-rhamnopyranosyl(1-->6)]-beta-D-galactopyranoside (1: mutabiloside), was isolated, together with four known flavonols identified as quercetin 3-O-[beta-D-xylopyranosyl(1-->2)]-beta-D-galactopyranoside (2) and kaempferol 3-O-[beta-D-xylopyranosyl(1-->2)]-beta-D-galactopyranoside (3), quercetin (4) and hyperoside (5). The structure of the new flavonol 1 was elucidated by spectroscopic methods. Among these flavonol derivatives, compounds 1 and 2 showed significant allergy-preventive effects.

Acute ex vivo effects of dimethylbenz[a]anthracene and heat shock on rat tail artery.

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental contaminants that are known to increase oxidative stress, proteotoxicity, and cytotoxicity in many cell types, but the acute effects of PAHs on vascular contractility are not known. The 70-kDa heat shock protein (HSP70) is known to protect cells against proteotoxicity and cellular apoptosis. Thus, increased HSP70 may be hypothesized to prevent any negative effects of PAHs on vascular smooth muscle. Heat shock treatment is a method used to increase expression of HSPs. Therefore, the objective of this study was to examine the acute (<24-h) ex vivo effects of a PAH (dimethylbenz[a]anthracene; DMBA), heat shock, or a combination of the two treatments on arterial contractility. The results of the present study suggest that acute ex vivo exposure of rat tail arteries to DMBA caused a transient impairment (at 6 h but not 12 h) in contractile response to norepinephrine (NE), but not to depolarization with excess KCl. The DMBA-induced impairment in NE contraction was not explained by a change in 20-kDa myosin light chain (LC20) phosphorylation. Heat shock alone impaired excess KCl-induced contraction and LC20 phosphorylation. Moreover, heat treatment failed to mitigate the effects of DMBA, suggesting that cytotoxicity was not the mechanism of DMBA effect on NE-induced contractility. Therefore, both acute ex vivo PAH exposure and heat shock impaired contractility of isolated rat tail arteries in the current study but in independent, noninteracting manners.

Ouabain at nanomolar concentration promotes synthesis and release of angiotensin II from the endothelium of the tail vascular bed of spontaneously hypertensive rats.

The effects of 1 nM ouabain (OUA) on the contractile actions of phenylephrine (PHE, 0.001-100 microg) and functional activity of the sodium pump (NKA) in isolated-perfused tail vascular beds from WKY and SHR were investigated. In preparations from SHR, perfusion with OUA in the presence of endothelium (E+) increased the sensitivity (pED50) of PHE (before: 2.14 +/- 0.06 versus after: 2.47 +/- 0.07; P < 0.05) without altering the maximal response (Emax). After endothelial damage, OUA reduced the Emax of PHE in SHR (before: 350 +/- 29 versus after: 293 +/- 25 mm Hg; P < 0.05). In SHR/E+, pretreatment with losartan (10 microM) or enalaprilat (1 microM) prevented the increased sensitivity to PHE induced by OUA. OUA increased NKA activity in SHR/E+ (before: 45 +/- 6 versus after: 58 +/- 5%, P < 0.05). Losartan (10 mg/Kg, i.v.) also abolished the increment in systolic and diastolic blood pressure induced by OUA (0.18 microg/Kg, i.v.) in anesthetized SHR. OUA did not alter the actions of PHE in either anesthetized WKY rats or vascular preparations. Results suggest that 1 nM OUA increased the vascular reactivity to PHE only in SHR/E+. This effect is mediated by OUA-induced activation of endothelial angiotensin converting enzyme that promotes the local formation of angiotensin II, which sensitizes the vascular smooth muscle to the actions of PHE.

Preventive effects of Impatiens balsamina on the hen egg-white lysozyme (HEL)-induced decrease in blood flow.

Monitoring the blood flow of unanesthesized mice was found to be a reliable and effective method for studying their anaphylactic responses, in addition to the known method of monitoring blood pressure. Hen egg-white lysozyme (HEL)-specific anaphylaxis in mice was estimated by monitoring the decrease in blood flow with a Doppler blood flow meter. This method is convenient for searching for both anaphylaxis and anti-anaphylactic substances from natural products. Using this system, we estimated the anti-anaphylactic effects of the 35% ethanol extract (IB) of petals of Impatiens balsamina L., as well as those of anti-allergic agents currently used. Kaempferol 3-rutinoside and lawsone from IB significantly inhibited the decrease of blood flow. We also found that platelet-activating factor (PAF) and serotonin participate in decreasing the blood flow, but histamine does not.

Cutaneous sympathetic motor rhythms during a fever-like response induced by prostaglandin E(1).

Neuronal population discharges within the CNS and in somatic and sympathetic motor nerves often display oscillations. Peripheral oscillations may provide a window into central mechanisms, as they often show coherence with population activity of subsets of central neurones. The reduction in heat loss through the cutaneous circulation during fever may be mediated via sympathetic premotor neurones not utilised during normal temperature regulation. Consequently, here we assessed, in anaesthetised rats, whether the frequency signature of population sympathetic discharge observed in neurones innervating the tail (thermoregulatory) circulation changed during a fever-like response induced by intracerebroventricular injection of prostaglandin E(1). We found that when core temperature was raised to 38.8-40.5 degrees C sympathetic activity was abolished. Following administration of prostaglandin (400 ng or 1 microg per rat), activity was restored to levels seen prior to heating (154+/-53.5%; n=10). Injection of vehicle had no effect (n=7). Prior to heating when most animals were in central apnoea (14/18) two peaks were observed in autospectra of sympathetic activity: one at 0.68-0.93 Hz (T-peak) and another at the frequency of ventilation (2 Hz). Central respiratory drive was recruited during hyperthermia where it was 1:2 locked to the frequency of ventilation and following prostaglandin administration, an additional peak in sympathetic autospectra was seen at this frequency. Time-evolving spectra indicated that this peak resulted from the dynamic locking of the 'T-peak' to central respiratory drive. Our data show that during a fever-like response the dominant oscillations in sympathetic activity controlling a thermoregulatory circulation and their dynamic coupling to respiratory-related inputs are similar to those seen under normal conditions. Therefore, during this fever-like response, the neural substrate(s) underlying the oscillations is not reconfigured and remains capable of sculpturing the pattern of sympathetic neuronal discharge that may be regulated by several descending pathways.

Role of Ca2+-sensitive protein kinase C in phenylephrine enhancement of Ca2+ sensitivity in rat tail artery.

We investigated the role of protein kinase C (PKC) isoforms on changes in sensitivity of contractile mechanisms to intracellular Ca(2+) (force /[Ca(2+)]i) by phenylephrine (0.1-100 microM) in rat tail arterial helical strips using simultaneous measurements of force and [Ca(2+)]i. Force/[Ca(2+)]Ii induced by phenylephrine was greater than that induced by 80 mM K+. Force/[Ca(2+)]i induced by phenylephrine in physiologic saline solution or low Ca(2+) solution was dependent on the agonist concentration. Removal of Ca(2+) completely abolished the phenylephrine-induced contraction. The PKC inhibitors staurosporine and calphostin C inhibited the increase in force/[Ca(2+)]i induced by phenylephrine to a much greater extent than that induced by 80 mM K+. LY379196, a specific PKCbeta inhibitor, did not inhibit the increase of calcium sensitivity due to phenylephrine. The classic PKC isoforms, alpha, betaI, and II not gamma were demonstrated in the artery by immunohistochemistry. These results suggest that in rat tail arterial smooth muscle, PKCalpha, and not beta or gamma, mediates the increase of changes in sensitivity of contractile mechanisms to intracellular Ca(2+) to high dose of alpha1 receptor stimulation (phenylephrine 100 microM) on nonphysiologic conditions.

Respiratory rhythmicity in the activity of postganglionic neurones supplying the rat tail during hyperthermia.

It has been suggested that thermoregulatory stimulation changes respiration-related rhythmicity in the activity of postganglionic sympathetic neurones supplying the rat tail to a distinct modulation independent of respiration. To study this possibility, single and few fibre recordings were made from ten filaments split from the ventral collector nerves of the rat during whole body warming. Sympathetic activity was analysed by autocorrelation and phrenic-triggered summation. All neurones except one were gradually inhibited and lost their on-going activity above a core temperature of 39-39.5 degrees C while the frequency of the phrenic bursts increased significantly. During hyperthermia, all neurones tested exhibited a prominent respiratory modulation in their activity which, compared to normothermia, was significantly increased in strength, or even newly acquired. No other rhythm emerged. These results speak against the hypothesis that in the rat sympathetic pathways controlling the tail vasculature and thus involved in thermoregulation, during hyperthermia become controlled by central oscillators distinct from the respiratory rhythm generator. Rather, respiratory modulation appears to remain the dominant rhythm as is common for sympathetic neurones supplying other cardiovascular targets.

The effect of diclofenac on the expression of spinal cord c-fos-like immunoreactivity after ischemia-reperfusion-induced acute hyperalgesia in the rat tail.

Ischemia-reperfusion of the rat tail for 20 min induces local acute hyperalgesia of approximately 1-h duration. We studied how this stimulus affected the expression of c-fos-like immunoreactivity (c-fos-LI) labeling of neurons of the sacral spinal cord, and how diclofenac pretreatment influenced the outcome. After ischemia, the number of c-fos-LI-labeled neurons was significantly increased when assessed at 60, 90, and 120 min after reperfusion (to 183%, 283%, and 164% of control, respectively; all P < 0.01). At 90 min, the number of regional c-fos-LI-labeled neurons was increased to 585% in laminae I-II, 183% in laminae III-IV, 270% in laminae V-X, and 286% in total, compared with respective control values (all P < 0.01). After diclofenac pretreatment (subcutaneous 40 mg/Kg, 30 min before insult) the number of c-fos-LI-labeled neurons at 90 min was increased to 424% in laminae I-II, 150% in laminae III-IV, 142% in laminae V-X, and 183% in total (all P < 0.01). Thus diclofenac pretreatment partially prevented the insult-induced increase in total and regional neuronal c-fos-LI. This acute nociceptive model involves only natural algogens. However, the results were similar to acute chemically induced or chronic adjuvant induced arthritic inflammatory pain models in which increases in c-Fos were partially inhibited by nonsteroidal antiinflammatory drugs.

The hypotensive effect of docosahexaenoic acid is associated with the enhanced release of ATP from the caudal artery of aged rats.

Fish oils have been shown to lower blood pressure in hypertensive subjects. To determine the mechanism of this hypotensive effect, we examined the effects of docosahexaenoic acid (DHA), one of the (n-3) polyunsaturated fatty acids in fish oil, on blood pressure and on the release of adenyl purines, such as ATP, ADP, AMP and adenosine, from the caudal arteries of aged rats. Aged female Wistar rats (100 wk) were fed a high cholesterol diet and were administered intragastrically ethyl all-cis-4,7,10,13,16,19-docosahexaenoate [300 mg/(kg.d)] for 12 wk (DHA group) or vehicle alone (control group). Compared with the controls, rats supplemented with DHA had significantly greater (10.1%) DHA concentrations in the caudal arteries. This was associated with more total (n-3) arterial fatty acids, a greater unsaturation index of arterial fatty acids, 43.9% lower plasma noradrenaline levels and the repression of the elevation in blood pressure observed with advancing age. The amount of purines released, both spontaneously and in response to noradrenaline, from arterial segments of DHA-supplemented rats was significantly higher than that released from tissues of control rats. Regression analysis revealed significant negative relationships between the total amount of purines released from the artery and the systolic (SBP) and diastolic (DBP) blood pressures. These results suggest that in aged rats, supplementation with DHA alters the membrane fatty acid composition as well as the amount of ATP released from vascular endothelial cells and decreases plasma noradrenaline, and that these factors may ameliorate the rise in blood pressure normally associated with advancing age.

Long-term supplementation with a high cholesterol diet decreases the release of ATP from the caudal artery in aged rats.

We examined the effects of high cholesterol (HC) diet on the spontaneous and noradrenaline-induced release of ATP, ADP, AMP and adenosine from caudal arteries and on the plasma levels of these adenyl purines in aged (100-week-old) Wistar rats. Administration of this diet for 12 weeks significantly reduced spontaneous and noradrenaline (1 micromol/L)-evoked release of adenyl purines from the caudal arteries relative to rats given the control diet The unsaturation index of fatty acids (UI), which gives the average number of double bonds, of both the plasma and the caudal artery was significantly less in the HC diet-fed rats than in those fed the control diet. The HC diet for 12 weeks produced a slight but significant increase in systolic and diastolic blood pressure with advancing age. Regression analysis revealed a significant inverse relationship between the total amount of purines released from the artery and diastolic blood pressure, and also a positive relationship between the total amount of purines released and the UI of the caudal artery. These results suggest that the high cholesterol diet decreased the release of adenyl purines from the caudal arteries of aged rats, leading to an increase in blood pressure.

Efficacy of toki-shigyakuka-gosyuyu-syokyo-to (danggui-sini-jia-wuzhuyu-shengjiang-tang) on peripheral circulation in autonomic disorders.

To investigate the improvement in peripheral circulation in autonomic disorders, we monitored skin temperature in the tails of rats by thermography before and after the oral administration of boiled water extract of Toki-shigyakuka-gosyuyu-syokyo-to (TSGS-to). Oral administration of this extract elevated the temperature, calculated as the calories of radiant heat in the rat tail 5-10 min after uptake. The temperature elevation remained stable for more than 20 min. Calories were significantly reduced 60 min after uptake and almost returned to initial values 90 min later. Some of the constituent herbs, especially Angelicae radix, Cinnamomi cortex, Evodiae fructus, and Zingiberis rhizoma, appeared to be active in relieving hypothermia.