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PubMed1990

Increased airway reactivity in the guinea-pig follows exposure to intravenous isoprenaline.

1. Intravenous infusion of (+/-) isoprenaline (1-100 micrograms kg-1 h-1) enhanced airway responses (resistance, RL; and compliance, Cdyn) to histamine (1.0-1.8 micrograms kg-1) and bombesin (100-240 ng kg-1), whereas airway responses to vagal stimulation remained unchanged. 2. Bilateral vagotomy before intravenous infusion of (+/-)isoprenaline (100 micrograms kg-1 h-1) prevented development of airway hyperreactivity to histamine or bombesin, yet vagotomy after infusion of isoprenaline was without effect. 3. Prior treatment with atropine (1 mg kg-1) did not influence the capacity of (+/-)isoprenaline (100 micrograms kg-1 h-1) to increase airway reactivity to bombesin. 4. Despite a 500-fold difference in spasmolytic potency in vivo, infusion of (+)isoprenaline (100 micrograms kg-1 h-1) or (-)isoprenaline (100 micrograms kg-1 h-1) increased reactivity of the airways to histamine or bombesin to a comparable extent. 5. Neither adrenaline (100 micrograms kg-1 h-1) nor forskolin (600 micrograms kg-1 h-1) increased reactivity of the airways to histamine or bombesin. 6. Intravenous infusion of dopamine (100 micrograms kg-1 h-1) or noradrenaline (100 micrograms kg-1 h-1) increased reactivity of the airways to histamine or bombesin. 7. Intravenous infusion of (+/-) propranolol (100 micrograms kg-1 h-1) increased reactivity of the airways to histamine or bombesin which was partially inhibited by bilateral vagal section. 8. Depletion of circulating platelets by lytic anti-platelet serum or concomitant infusion of an antagonist of platelet-activating factor (PAF), ginkgolide B (1 mg kg-1 h-1) did not diminish the capacity of (+/-)isoprenaline (100 micrograms kg-1 h-1) to induce hyperreactivity of the airways to histamine or bombesin. 9. These observations indicate that (+/-)isoprenaline can induce airway hyper-reactivity by a mechanism unrelated to beta-adrenoceptor activation, but which is dependent upon intact vagus nerves.

Airway Resistance↗

PubMed2003

Influence of propiverine on hepatic microsomal cytochrome p450 enzymes in male rats.

The bladder spasmolytics propiverine was shown to induce hepatic cytochrome P450 (P450) and aminopyrine and aniline oxidation in rats. To characterize the type of enzyme induction and its dose dependence, activities of seven hepatic microsomal P450-dependent monooxygenases were measured in 72 male LEW1A albino rats (body weight 236-295 g) after oral treatment with 0.5, 2, 6, and 60 mg/kg of propiverine hydrochloride for 5 days and compared with the effects of 40 mg/kg beta-naphthoflavone, 10 mg/kg phenobarbital, and 20 mg/kg dexamethasone (each group, n = 8). CYP2B expression was measured by Western blotting. Furthermore, the inhibitory potency of propiverine on P450 enzymes was evaluated in competition assays with three most specific monooxygenases. Results show that Propiverine induced several monooxygenases and CYP2B expression dose dependently. The effects were well comparable with a phenobarbital-type inducer with 60 mg/kg being equipotent to 10 mg/kg phenobarbital. Furthermore, propiverine in low concentrations inhibited pentylresorufin O-dealkylase (for CYP2B) in vitro. In conclusion, propiverine is a phenobarbital-type inducer on hepatic P450 enzymes in rats in doses about 100-times above the therapeutic doses in man.

Animals↗

PubMed2006

Trefoil family factor 2 is expressed in murine gastric and immune cells and controls both gastrointestinal inflammation and systemic immune responses.

Trefoil family factor 2 (TFF2), also known as spasmolytic peptide, is a low-molecular-weight protein that is upregulated in gastric tissues infected with Helicobacter or having other inflammatory conditions, but a precise function is yet to be elucidated. The role of TFF2 in the development of gastritis, colitis, and inflammatory cytokine responses was examined both in vivo and in vitro using wild-type and TFF2 knockout mice. TFF2 knockout and wild-type mice were infected with Helicobacter felis (H. felis) to induce gastritis. Colitis was induced in TFF2 knockout and wild-type mice by administering dextran sodium sulfate (DSS) in drinking water. Histopathology, clinical disease (colitis), and antibody levels (H. felis) were examined. TFF2 expression in tissues was determined by reverse transcriptase PCR, and the inflammatory and proliferative responses of TFF2-expressing macrophages and spleen cells were examined by cytokine enzyme-linked immunosorbent assay, thymidine incorporation, and gene array studies. TFF2 knockout mice have increased susceptibility to H. felis-induced gastritis, with enhanced gastric inflammation. They were also more susceptible to DSS-induced colitis, with prolonged colonic hemorrhage and persistent weight loss. Remarkably, TFF2 expression was not limited to the gastrointestinal tract, as suggested in previous studies, but was also present in macrophages and lymphocytes. The inflammatory and proliferative responses of these immune cell types were dysregulated in TFF2 knockout mice. TFF2-/- cells were hyperresponsive to interleukin 1 beta stimulation but showed normal responses to lipopolysaccharide, suggesting a specific role for TFF2 in interleukin 1 receptor but not Toll-like receptor 4 signaling via their Toll-interleukin 1 resistance domains. TFF2-/- lymphocytes also produced higher levels of interleukin 2 than wild-type cells. Thus, TFF2 was expressed in the gastrointestinal cells and in immune cells and was a negative regulator of gastrointestinal inflammation and immune cell cytokine responses. Our studies suggest that TFF2 not only controls gastrointestinal repair but also regulates mononuclear cell inflammatory responses.

Animals↗

PubMed1971

Baclofen in the treatment of spasticity.

Baclofendagger (Lioresal), a derivative of gamma-aminobutyric acid, was introduced in 1966 as a possible treatment for spasticity due to corticospinal tract lesions. Preliminary studies suggested that it may be more effective than other spasmolytic agents currently available, and a double-blind controlled trial in a group of 23 patients against placebo has shown it to be significantly more effective.

Adult↗

PubMed1981

The assessment of drug treatment of spastic gait.

The technique of polarised light goniometry was used to quantify objectively parameters of the spastic gait during a double-blind cross-over trial comparing the spasmolytic effects of DS103-282, baclofen and placebo. Only minimal objective and subjective changes in gait were found when the results of treatment with DS103-282 or baclofen were compared with those of treatment with placebo.

Aged↗

PubMed1996

The trefoil peptide family.

The unique three-loop structure of the trefoil motif, formed by intrachain disulfide bonds in a 1-5, 2-4, 3-6 configuration between six conserved cysteine residues, is the defining feature of a recently recognized family of peptides. Expression of trefoil peptides is closely related to that of mucin glycoproteins in diverse biological sources. Three distinct members of the family (pS2, intestinal trefoil factor, and spasmolytic polypeptide) are produced in the mammalian gastrointestinal tract by mucus-secreting cells and targeted primarily for luminal secretion. The compact structure of the trefoil motif may be responsible for marked resistance of trefoil peptides to proteolytic digestion, enabling them to function in the harsh environment of the gastrointestinal lumen. Trefoil peptides are ectopically expressed adjacent to areas of inflammation within the gastrointestinal tract and may play an important role in both maintaining the barrier function of mucosal surfaces and facilitating healing after injury.

Amino Acid Sequence↗

PubMed1976

Diagnosis of partial gastric diverticula.

Five partial (intramural) gastric diverticula were observed in about 10,000 routine examinations of the stomach and confirmed by endoscopy or operation. All diverticula were located on the greater curvature of the antrum. A round or oval pouch with a small neck and typical changes in shape and size represent the diagnostic radiographic features of partial diverticulum. Complete filling of the diverticulum by administration of a spasmolytic and the use of the double-contrast method proved to be important for the correct diagnosis.

Adult↗

PubMed2005

Spasmolysis at CT colonography: butyl scopolamine versus glucagon.

PURPOSE: To retrospectively determine if the use of butyl scopolamine or glucagon in the supine patient improves colonic distention and reduces the number of collapsed intestinal segments at computed tomographic (CT) colonography. MATERIALS AND METHODS: This study had institutional review board approval; subject informed consent was not required. CT colonography was performed without the administration of an intravenous spasmolytic in 80 asymptomatic subjects (group 1; 45 women, 35 men; age range, 48-77 years; mean, 61.9 years). These subjects were matched with two groups of 80 subjects who were similar in age but were premedicated with glucagon (group 2; 41 women, 39 men; age range, 43-76 years; mean, 63.1 years) or butyl scopolamine (group 3; 43 women, 37 men; age range, 34-77 years; mean, 63.4 years). All 240 subjects were examined in the supine position with multisection CT and a section thickness of 1 mm after intravenous contrast agent administration and rectal carbon dioxide insufflation. The colon was divided into seven segments, and the colon length, total volume, radial distensibility, and number of non-distended segments were calculated for each subject and compared among the three groups. Statistical analysis was performed with analysis of variance and chi2 testing. RESULTS: Mean bowel length was not significantly different among the groups. Mean colon volumes and radial distensibilities, respectively, were 1.84 L and 3.69 cm in group 1, 2.14 L and 3.98 cm in group 2, and 2.35 L and 4.23 cm in group 3; differences in colon volume and radial distensibility were significant only between group 1 and group 3 (P < .001). At CT colonography, 29 segments in 20 group 1 subjects were collapsed, 23 segments in 12 group 2 subjects were collapsed, and 11 segments in six group 3 subjects were collapsed (P = .016). CONCLUSION: Premedication with butyl scopolamine or, less effectively, glucagon improves colonic distention in the supine subject.

Aged↗

PubMed2006

Differentiation of the gastric mucosa III. Animal models of oxyntic atrophy and metaplasia.

Gastric cancer in humans arises in the setting of oxyntic atrophy (parietal cell loss) and attendant hyperplastic and metaplastic lineage changes within the gastric mucosa. Helicobacter infection in mice and humans leads to spasmolytic polypeptide-expressing metaplasia (SPEM). In a number of mouse models, SPEM arises after oxyntic atrophy. In mice treated with the parietal cell toxic protonophore DMP-777, SPEM appears to arise from the transdifferentiation of chief cells. These results support the concept that intrinsic mucosal influences regulate and modulate the appearance of gastric metaplasia even in the absence of significant inflammation, whereas chronic inflammation is required for the further neoplastic transition.

Animals↗

PubMed2005

Altered metaplastic response of waved-2 EGF receptor mutant mice to acute oxyntic atrophy.

Metaplastic cell lineages are putative precursors for the development of gastric adenocarcinoma. The loss of parietal cells (oxyntic atrophy) is the initiating step in the evolution of gastric fundic mucosal lineage changes including metaplasia and hyperplasia. However, the intrinsic mucosal factors that promote and modulate the emergence of metaplastic phenotypes remain obscure. Over the past several years, we have studied pharmacologically induced, reversible oxyntic atrophy in rodents treated with DMP-777, a drug that acts as a parietal cell secretory membrane protonophore. DMP-777 elicits a rapid loss of parietal cells followed by the emergence of foveolar hyperplasia and spasmolytic polypeptide (SP)-expressing metaplasia (SPEM). The objective of the present study was to provide further insights into the intrinsic mucosal factors regulating the emergence of SPEM in the setting of oxyntic atrophy. We therefore studied the effects of DMP-777 administration on both SP/trefoil factor (TFF)2-deficient mice, which lack SP/TFF2, a marker of SPEM, and waved-2 mice, which harbor a point mutation in the EGF receptor that attenuates its tyrosine kinase activity. As in wild-type mice, treatment with DMP-777 for 7 days did elicit SPEM in SP/TFF2-deficient mice. These results suggest that SP/TFF2 does not impact on the development of metaplasia after the induction of parietal cell loss. In contrast, waved-2 homozygous mice displayed accelerated SPEM development by 3 days of treatment with DMP-777. These findings indicate that attenuation of EGF receptor signaling in waved-2 mice does elicit a more rapid emergence of SPEM. The results support a role for EGF receptor ligands in the regulation of gastric metaplasia.

Animals↗

PubMed1997

Temporal expression of trefoil peptides in the TGF-alpha knockout mouse after gastric ulceration.

Trefoil peptides are gut peptides that have been implicated in the repair of the gastric mucosa after injury. Previous studies suggest that epidermal growth factor (EGF) receptor ligands may induce the expression of trefoil peptides. Because transforming growth factor-alpha (TGF-alpha) is a major EGF receptor ligand in the gut, we tested the hypothesis that mice with a TGF-alpha null mutation (knockout) would have reduced trefoil peptide expression compared with wild-type controls after gastric ulceration. The rate of macroscopic ulcer healing was the same in knockout and wild-type mice. Spasmolytic polypeptide (SP) and intestinal trefoil factor (ITF) expression were quantified in tissue and gastric lavage. SP and ITF levels in tissue fell within 48 h of ulceration (P < 0.05), but secretion into gastric juice was unchanged. ITF peptide expression was increased (as was SP expression) in wild-type but not knockout mice 42 and 72 days after injury (P < 0.05). The induction of SP and ITF expression in the latter stages of injury repair has a TGF-alpha-dependent component and suggests a role for these peptides in gastric differentiation and cell positioning.

Animals↗

PubMed1998

Localization and significance of pp55, a gastric mucosal membrane protein with tyrosine kinase activity.

In Fischer 344 rats, induction of gastric mucosal proliferative activity, whether the result of aging or injury or occurring after administration of epidermal growth factor, gastrin, or bombesin, is associated with a rise in tyrosine kinase activity and tyrosine phosphorylation of several mucosal proteins, including a protein with a molecular mass of 53-55 kDa. We hypothesized that this phosphotyrosine membrane protein (referred to as pp55) may play a role in regulating gastric mucosal cell proliferation and differentiation. Purification and subsequent immunoprecipitation studies now show that pp55 is a tyrosine kinase. In addition, the enzyme activity in the gastric mucosa is found to be fourfold higher in aged rats than in young rats. Incubation of gastric mucosal membranes with transforming growth factor-alpha (2 x 10(-8) M) stimulates tyrosine kinase activity of pp55. Immunolocalization studies reveal that pp55 immunoreactivity is predominantly present in mucous cells that are located just above the proliferative zone and spasmolytic peptide-immunoreactive mucous neck cells. Tyrosine kinase activity as well as expression of pp55 are also greatly increased in the gastric mucosa after hypertonic saline-induced injury, a condition that results in stimulation of surface mucosal cell proliferation and differentiation. Our current data suggest that pp55 is a tyrosine kinase, likely localized to pre-surface cells. The presence of pp55 in pre-surface mucous cells and the expression and tyrosine kinase activity of this protein, which can be stimulated during mucosal cell proliferation and differentiation, strongly suggest a role for pp55 in differentiation of gastric surface mucous cells.

Aging↗

PubMed1998

Effects of enantiomers of beta 2-agonists on ACh release and smooth muscle contraction in the trachea.

The beta 2-agonists currently used as bronchodilators are racemic mixtures of R- and S-enantiomers. In the present study, we examined the effects of enantiomers of the beta 2-agonists albuterol and formoterol on acetylcholine (ACh) release from equine trachealis parasympathetic nerves. ACh release was evoked by electrical field stimulation (20 V, 0.5 ms, 0.5 Hz) and measured by high-performance liquid chromatography coupled with electrochemical detection. We also tested the effects of enantiomers of albuterol and formoterol on equine tracheal smooth muscle (TSM) contraction in response to exogenous ACh. R- and RS-albuterol (10(-8) to 10(-5) M) and RR- and RR/SS-formoterol (10(-8) to 10(-5) M) augmented ACh release in a concentration-dependent manner. Beginning at 10(-6) M, SS-formoterol significantly increased ACh release, and at 10(-5) M, release increased by 71.9 +/- 8.7% over baseline. This effect was only observed, however, when the prejunctional muscarinic autoinhibitory effect of ACh was prevented with atropine. Both the RR- and SS-formoterol-induced increases in ACh release were abolished by the beta 2-antagonist ICI-118551 (3 x 10(-7) M). The effect of S-albuterol on ACh release was variable, and the mean increase induced by 10(-5) M was 30.8 +/- 16.1% in the presence of atropine. In the muscle tension study, R- and RS-albuterol and RR- and RR/SS-formoterol (10(-8) to 10(-5) M) but not the S-enantiomers inhibited TSM contraction. Even though R-enantiomers augment ACh release, they potently inhibit TSM contraction. Because racemic beta 2-agonists are bronchodilators on acute administration, the postjunctional spasmolytic effects of R-enantiomers predominate over the spasmogenic effect evoked via increased ACh release. The S-enantiomers, in contrast, do not inhibit TSM contraction and therefore would not contribute to the observed bronchodilation of the racemate. The S-enantiomers do prejunctionally facilitate ACh release when prejunctional muscarinic autoreceptors are dysfunctional, suggesting a potentially deleterious effect.

Acetylcholine↗

PubMed2005

[Antidepressant therapy in functional gastrointestinal disorders].

The available evidence from randomized clinical trials or meta-analyses on the therapeutic efficacy of psychotropic drugs and, specifically, of antidepressants, in functional gastrointestinal disorders (FGD), are recent and still fairly limited. The use of these drugs is based on the frequent association of anxiety and depression or neurosis in patients with FGD who seek medical care and on the demonstrated efficacy of these drugs in relieving chronic pain, whatever its origin or localization, for more than 30 years. Antidepressants, even in doses under the antidepressant range, are antinociceptive due to their central and peripheral neuromodulatory effect, which is completely independent of anticholinergic, spasmolytic or antidepressant effects. This has been demonstrated in both animals and humans and, as occurs with another antinociceptive drugs such as clonidine, is mediated by alpha-adrenoreceptors. The choice of antidepressant depends both on the evidence of its analgesic activity (in general greater with tricyclic antidepressants than with the more modern selective serotonin reuptake inhibitors) and on the presence of drug-related adverse effects, which include not only anticholinergic adverse effects but also the possibility of hypotension or cardiotoxicity, which should be avoided. The main selection criteria are demonstrated efficacy and safety. Antidepressants have been shown to be effective in the specific field of non-coronary chest pain probably originating in the esophagus unrelated to gastroesophageal reflux disease, especially mianserin and trazodone, and the effect is maintained in the long term in nearly three-quarters of treated patients. Tricyclic antidepressants have also been shown to be effective in the treatment of abdominal pain in patients with irritable bowel syndrome, with an OR of 4.2 and an NNT of 3.2 in comparison with placebo. In contrast, there is insufficient evidence to recommend the use of antidepressants in functional dyspepsia.

Analgesics, Non-Narcotic↗

PubMedDate not supplied

Implications of tachykinins and calcitonin gene-related peptide in inflammatory bowel disease.

Calcitonin gene-related peptide (CGRP) and the preprotachykinin A gene-derived peptides substance P (SP) and neurokinin A (NKA) are expressed in extrinsic primary afferent nerve fibres and intrinsic enteric neurons of the gut. The actions of tachykinins on the digestive effector systems are mediated by three different types of tachykinin receptor, termed NK1, NK2 and NK3 receptors, while the gastro-intestinal actions of CGRP are brought about by CGRP1 and possibly other CGRP receptors. These neuropeptide transmitters are expressed by enteric neurons, intestinal muscle, epithelium and vascular system in a cell-specific manner and enable SP, NKA and CGRP to influence motility, electrolyte and fluid secretion, vascular and immune functions in a peptide- and region-specific fashion. Inflammatory disorders of various aetiology involve changes in the peptidergic innervation of the gut, and inflammatory bowel disease is associated with NK1 receptor upregulation in intestinal blood vessels and lymphoid structures. Some of these alterations are reproduced in experimental models of gastro-intestinal disease, and there is mounting evidence that an imbalanced function of peptidergic neurons contributes to motor, secretory, vascular and immunological disturbances in intestinal anaphylaxis, infection and inflammation. In a therapeutic perspective it seems conceivable that tachykinin and CGRP receptors antagonists can be employed as spasmolytic, antidiarrhoeal, anti-inflammatory and antinociceptive drugs.

Animals↗

PubMed1999

Maternal circulating nitrite levels are decreased in both normal normotensive pregnancies and pregnancies with preeclampsia.

OBJECTIVE: To evaluate whether maternal nitric oxide synthesis in pregnancies with preeclampsia is different from that in normal normotensive pregnancies. MATERIALS: Maternal circulating combined nitrate and nitrite levels or nitrite level were compared between 10 normotensive nonpregnant women, 30 normotensive pregnant women (10 first-trimester, 10 second-trimester, and 10 third-trimester pregnancies), 20 normotensive postpartum women (10 at 1 week after delivery, and 10 at 4 weeks after delivery), and 13 preeclamptic women (32 to 40 weeks' gestation). End-products of nitric oxide synthesis were measured from maternal venous blood samples using a fluorometric assay. RESULTS: Maternal circulating nitrite levels in nonpregnant women (1.13 +/- 0.22 microM) were significantly higher than those in the first-trimester pregnant women (0.68 +/- 0.13 microM), second-trimester pregnant women (0.65 +/- 0.13 microM), third-trimester pregnant women (0.48 +/- 0.17 microM), first puerperal week women (0.36 +/- 0.16 microM), and fourth puerperal week women (0.67 +/- 0.17 microM), respectively (p < 0.05). Maternal circulating nitrite level was decreased with advancing gestation, still remained low just after delivery, and was increased 4 weeks later. There was no significant difference in maternal circulating nitrite level between preeclamptic women (0.40 +/- 0.17 microM) and third-trimester pregnant women (0.48 +/- 0.17 microM). However, there were no significant differences in maternal circulating combined nitrate and nitrite levels among the groups. CONCLUSION: These results suggest that the maternal nitric oxide synthesis is not changed in normal normotensive pregnancies and pregnancies with preeclampsia. However, plasma nitrite level, which has stronger spasmolytic activity than the activity of the nitrate, was decreased in both normal normotensive pregnancies and pregnancies with preeclampsia.

Adult↗

PubMedDate not supplied

Memantine suppresses the glutamatergic neurotransmission of mammalian inner hair cells.

The glutamatergic synapses between inner hair cells and afferent neurons seem to be involved in pathophysiological conditions of the cochlea. The excessive release of glutamate from inner hair cells during noise trauma and ischemia affects the afferent neurons. It is possible that in tinnitus outer hair cell or inner hair cell dysfunction or damage leads to an altered spontaneous release of glutamate from inner hair cells. Thus, the pharmacological modulation of glutamatergic neurotransmission could be of great value in the therapy of certain inner ear diseases. Recently, it has been discovered that the spasmolytic drug memantine has antiglutamatergic properties. As a possible drug for inner ear diseases, we were interested in the action of memantine on the neurotransmission of inner hair cells. With the aid of microiontophoretic techniques we were able to show a strong depressing effect on spontaneous activity as well as on glutamate-induced activity. This effect seems to be mediated by a blockade of N-methyl-D-aspartate (NMDA) receptors as memantine showed a strong inhibiting effect on NMDA-induced activity but not on AMPA-induced activity. These results recommend memantine for the treatment of inner ear diseases, e.g. especially tinnitus.

Animals↗

PubMed2001

[Dyspeptic pain and phytotherapy--a review of traditional and modern herbal drugs].

Gastrointestinal complaints rank among the most frequently reasons why people asking for medical advice. About 15-30% of the adult patients suffer from different various functional dyspeptic conditions. The therapy of functional gastrointestinal disorders is one of the domains of phytotherapeutic treatments. From ancient times on, bitter herbal drugs played a very important role in the therapy of patients with dyspeptic symptoms. The mechanisms of action of the bitters are not completely understood. But there are indications that they sensorially stimulate at even very small concentrations sensorially the secretion of the stomach as well as the digestive glands and strengthen the smooth musculature of the digestive tract (via the gustatory system, N. vagus and the enteric nervous system). Across the enteral nervous system the strengthened digestive tract seems to stimulate the CNS, leading to a general tonification. At higher dosages bitters probably directly affect the mucous membranes of the stomach and the bowel. Bitters often are combined with essential oils (some volatile oils as aromatic bitters, drug combinations of a volatile oil with a bitter). Essential oils act primarily as spasmolytics, carminatives and local anesthetics. In the last years several controlled studies were carried out with phytotherapeutic combinations (e.g. with Iberis amara, caraway oil, peppermint oil, curcuma extract, ginger extract) in which the herbal drugs proved to be superior compared to placebo and were as effective as prokinetics (studies according to evidence-based medicine). The traditional phytotherapeutic approach is based upon the illness- as well as the patient-related investigations referring to the effectiveness of bitter, acrid- and essential-oil drugs. Such a treatment is supported by a rich amount of various of kinds of individual empirical experience (experience-based phytotherapy). Important traditional medical systems like the Traditional Chinese Medicine, the Ayurvedic Medicine as well as the European 'Humoral Medicine' consider different aspects of the sick human being, like the constitution of the patient (holistic approach), and take qualities of herbal drugs, vegetarian food, and spices into account for therapeutic purposes.

Drugs, Chinese Herbal↗