तत्रोष्णतीक्ष्णसूक्ष्मव्यवायिविकाशीन्यौषधानि स्ववीर्येण हृदयमुपेत्य धमनीरनुसृत्य स्थूलाणुस्रोतोभ्यः केवलं शरीरगतं दोषसङ्घातमाग्नेयत्वाद् विष्यन्दयन्ति, तैक्ष्ण्याद् विच्छिन्दन्ति, स विच्छिन्नः परिप्लवन्  स्नेहभाविते काये स्नेहाक्तभाजनस्थमिव क्षौद्रमसज्जन्नणुप्रवणभावादामाशयमागम्योदानप्रणुन्नोऽग्निवाय्वात्मकत्वादूर्ध्वभागप्रभावादौषधस्योर्ध्वमुत्क्षिप्यते, सलिलपृथिव्यात्मकत्वादधोभागप्रभावाच्चौषधस्याधः प्रवर्तते, उभयतश्चोभयगुणत्वात्| इति लक्षणोद्देशः||                                                                                 (Cha. Ka.1/5)

Vāmaka Dravyās are Uṣṇa, Tīkṣṇa, Sukṣma, Vyavāyi, Vikāṣi in nature. By the Vīrya/ potency of the drug, it reaches Hṛdayaand later circulates through the blood vessels. Due to the predominance of Agni Mahābhūta, the drug possesses Āgneyanature. Because of their TīkṣṇaGuṇa, they liquefy the adhered Doṣas in the gross and subtle  channels (Srotas) of the body. After separation these morbid materials floats in the body channels without adhesion like how honey kept in a pot smeared with fat, the morbid materials finally reach the stomach. By the predominance of Agni and Vāyu Mahābhūta and their Vāmaka Prabhāva(specific action to move upward), the morbid materials get propelled by udānavāyu through the upward tract.

According to Ācārya Caraka, Vamana Auṣadhī possess Guṇas such as Uṣṇa, Tīkṣṇa, Sūkṣma, Vyavāyi and Vikāṣi to reach at the site of the Doṣās and cause Samprāpti Vighaṭṭana. Apart from these Guṇas, Suśruta mentioned Saratva Guṇa instead of Vyavāyi. The role of each Guṇain the Samprāpti Vighaṭṭana of Vyādhi by inducing therapeutic emesis is being discussed below:

सूक्ष्मस्य भावः सौक्ष्म्यं सूक्ष्मस्रोतोऽनुसारित्वं; तीक्ष्णस्य भावस्तैक्ष्ण्यं शीघ्रतरदोषस्रावणकरत्वम्; उष्णस्य भाव औष्ण्यं, सौम्यद्रव्योपमर्दनकरणसामार्थ्यं; विकाशिनो भावः विकाशित्वं, विकाशिभावेन धातोः शैथिल्यकरणसामर्थ्यम्| अत्र प्रकृतिः, स्वभावः, शक्तिविशेषः, प्रभावो, वीर्यमित्यनर्थान्तरम्| तेन प्रकृत्या वीर्येणान्यथागतमूर्ध्वगतं, सत्यपि सरत्वादिविरेचनगुणसाम्ये वमनस्योर्ध्वगामित्वं

1. Uṣṇa

Uṣṇa is Āgneya, which produces Dahana, Pācana and plays an important role in theprocess of Viṣyandana of the DoṣaSanghāta responsible for the disease. ĀcāryaCakṛapāṇicommentthatVisṣyandayatimeans”VilīnamKurvanti”,Viiinammeanstodissolveortoliquefy.

1. Tīkṣṇa

Dāha,Pāka and Srāva are produced by Tīkṣṇa. Tīkṣṇa acts for Vicchindana. Cakṛapāṇi mentions that Vicchindanti is nothing but the breaking down of the morbid matter into the small possible Particles. Ḍalhaṇa explains that because of Tīkṣṇa property waste Products (Doṣā)oozes out immediately. Tīkṣṇa is also Āgneya. It Produces Śodhana, Pācana, Chedana andSrāvanaof Doṣā.

1. Sūkṣma

The drugs can pass through minute Srotas due to SūkṣmaGuṇa. Vayu, Ākāśa and AgniMahābhūta are dominant in its Bhautika constitution. Due to Sūkṣma Guṇa, Vamana drugs enter Sthula and Aṇu Srotas. Both Ācārya Śāraṅgadhara and Ḍalhaṇa has mentioned the same. Vamana drugs after breaking the Doṣa Sanghāta by its Uṣṇa and Tīkṣṇa properties, due to their Aṇu-Pravaṇabhāva brings, the Doṣa into the Kostha.

• Vyavāyi

Vyavāyi drugs are acts directly on the body. As soon as these types of drugs are ingested, their action starts before digestion. Due to this property, the Vamana drugs get absorbed and then act quickly. Ḍalhaṇa mentions that due to Vyavāyiguna, Vamana drugs spread into the body without changing its form. Charaka attributes VyavāyiGuṇa to Viṣa and Madya. Cakṛapāṇi comments, Vyavāyi means spread out in whole body in the Viṣa Cikitsā Adhyaya. In Madātyaya Cikitsā, Sarva Vyāpakatva is mentioned for Vyavāyi Guṇa. So, on the basis of the above references, it can be said that, due to Vyavāyi property Vamana drugs spread out in whole body and starts the action of Uṣṇa, Tīkṣṇa and Sūkṣmagunas before its Pācana, like ViṣaandMadya.

1. Vikāṣi

The drugs, which are having VikāṣiGuṇa, produce Śaithilyain Sandhi and especially in Ojas. It has been mentioned in Suśruta Saṃhita that Vikāṣi are those which loosen (Vimokṣayet) the Dhātu Bandhana. Ḍalhaṇa explains that Vamana drugs due to Vikāṣi property also pervade through whole body without digestion like that of Vyavāyi. Further he mentions that loosening of Dhātu Bandhana means Dhātu Śaithilya.

• Saratva

Saratva Guna for Vamana is mentioned by Suśruta. Ḍalhaṇa opines that due to Saratva Guṇa Anulomana is possible. Gaya another expounder isof.the opinion that Saratva is Visarana i.e.sliding, spreading. It is possible that due to Saratva Guṇa, Malas which are brought towards the Koṣṭha from Śākhā may be evacuated. Thus removal of Doṣā may been enhanced.

• Prabhāva

Caraka clearly mentions that the main action of Vamana is due to its Prabhāva. Charaka said “Ūrdhvva Bhāga Prabhāvat Auṣadhasya Ūrdhvvam Utkṣipyate”. Elaborating Prabhāva of Vamana drugs,Cakṛapāṇi mentions that due to dominance of Agni and Vāyu Mahābhūta in their Panchabhautika constitution, there is a tendency of ŪrdhvvaGati of Vamana drugs. It is initiated by UdānaVāyu. However Chakṛapani emphatically mentions that it is the Prabhāva of Vamana drugs,which have important role in Ūrdhva Gati.

Modern view: Emesis

Vomiting is the forceful evacuation of gastric contents due to the irritation of upper gastro intestinal tract due to some special type of irritative impulses and excessive distension of stomach. The contraction of musculature of the gut and thoracic – abdominal wall plays vital role in the oral expulsion of gastrointestinal contents during vomiting. Vomiting is coordinated by the brain stem and is affected by responses in the gut, pharynx and thoracic abdominal wall.

Pathophysiology of Vomiting Reflex:

Vomiting is a reflex act that is mediated neurologically by the activation of the bilateral nucleus tractus solitarii, or emetic centre, which is expressed in the parvicellular reticular formation in the lateral region of the medulla oblongata. This is the area that initiates, controls, regulates, and organizes the vomiting reflex. Vomiting can be triggered by both neural and humoral pathways. The neural pathway comprises six fundamental components. The emetic centre receives input from the gastrointestinal tract (afferent neurons), the higher centres of the brain, and the vestibular apparatus. Finally, to coordinate the vomiting reflex, the vomiting centre sends signals through the efferent motor neurons. The vagal and sympathetic afferent neurons originate from the gastrointestinal tract, particularly the duodenum, as well as other areas, including the urinary and reproductive system, liver, pancreas, peritoneum, and cardiac vessels. Stimulation of these neurons initiates the impulse that travels directly to the emetic centre. The higher centres of the brain, including the cerebral cortex and the limbic system, can trigger emesis through three mechanisms: direct stimulation of the vomiting centre by inflammatory diseases, hydrocephalus, or neoplasia; psychogenic stimulation caused by fear, stress, excitement, or pain; and traumatic stimulation related to head injuries and increased intracranial pressure. The CRTZ is a bilateral set of centres in the brainstem, located on the floor of the fourth ventricle. It possesses free nerve endings that maintain direct contact with the cerebrospinal fluid via ependymal pores or the sheath surrounding fenestrated capillaries. These free nerve endings are activated by the vestibular system or through the humoral pathway by conditions affecting the blood or cerebrospinal fluid (e.g., drug administration, infection, osmolar and acid–base disorders, electrolyte derangements, metabolic diseases). Finally, to initiate the vomiting reflex, efferent motor signals must be transmitted to the upper gastrointestinal tract through the sensory aspect of cranial nerves V, VII, IX, X, and XII and to the diaphragm and abdominal muscles via the spinal nerves. The act of vomiting is composed of three phases: nausea, retching, and expulsion of proximal duodenal and gastric contents.

Nausea:

The mechanisms underlying nausea are poorly understood, but electroencephalographic studies supported that cerebral cortex is involved in this process because nausea requires conscious perception. Nausea is the conscious recognition of subconscious excitation in an area of the medulla that is closely associated with the vomiting centre. This excitation is caused by irritative impulses coming from the gastrointestinal tract, lower brain, or cerebral cortex. Ptyalism, tachycardia, nervousness, hiding or seeking attention, shivering, and yawning are all characteristic signs of nausea triggered by general activation of the sympathetic and parasympathetic branches of the autonomic nervous system. Hypersalivation stimulates swallowing, which stimulates relaxation of the gastroesophageal sphincter. The bicarbonate-rich saliva secreted by the salivary glands in the mouth lubricates the oesophagus and helps to neutralize the stomach’s acidic environment before vomiting.

Before retching, aboral gastric and oesophageal motility diminishes and the lower oesophageal and pyloric sphincters relax.

Retching:

Retching is the second phase of vomiting and begins with the onset of a retrograde giant contraction. This contraction is a single-phase, retrograde, peristaltic motion that empties the proximal duodenal contents into the stomach. It is followed by deep inspiratory movements, forceful contractions of the muscles of abdomen, diaphragm, and closure of the glottis. These actions produce negative intra-thoracic pressure and positive intraabdominal pressure, facilitating the movement of gastric contents into the oesophagus.

Before expulsion, the respiratory centre is inhibited and the nasopharynx and glottis close to prevent pulmonary aspiration and nasal regurgitation of the gastric contents. The third and last phase of vomiting is the expulsion of stomach contents through the mouth.

Cytotoxic drugs and emetic pathway:

The drugs like Apomorphine, morphine, chemotherapy, cytotoxic drugs and digitalis are directly acting on the (CTZ) chemoreceptor trigger zone in the area posterma (AP) and via the CTZ the vomiting centre got stimulated and causes emesis. The region AP is devoid of blood brain barrier (BBB) therefore it is quickly detect the toxins which are absorbed in the blood eventually causes emesis. The area postrema mainly contain receptors like 5- hydroxytrypamine-3  (5HT3),  Dopamine  (D2),   Histamine   (H1), Muscarinic acetylcholine receptors (MI), Cannabinoid (CB1). Compared to other co-receptors the receptor 5HT3 have major role in the activationof Vomiting Centre (VC). Any lesion in AP will not sense the stimulation generated by these emetogens and emesis will not occur.

Motion sickness and emeticpathway:

In the case of motion sickness the vestibular nerve in the labyrinth carries the impulses to the CTZ it later stimulate the VC and causes emesis here mainly the H1, M1 receptors are plays the major role in generating emesis.

Pain like Sensations and emetic pathway:

Some of the sensations like pain, smell, sight, taste, memories are having direct effect over the higher centers and causes emesis.

Gag reflux and emeticpathway:

In the case of gag reflux the glossopharyngeal nerve carries the impulse to the nucleus tractus solitaries (NTS) and its sensory nuclei stimulates the vomiting centre for causing emesis. The NTS contains receptors like NK1, 5HT3, D2, H1, M1.

Gastric obstruction like pathology related emetic pathway:

In the clinical conditions like gastric outlet obstruction, ingestion of toxins, small and large bowel obstruction, ingestion of ipecac syrup and viral gastritis causes emesis by the stimulation of vagal nerve. In these intra peritoneal causes the emetic pathway can occur in two ways. Impulses from vagus nerve directly stimulate the receptors in AP then later from CTZ it sensitize the VC or through the receptors in NTS receives stimulation from vagus nerve the sensory nuclei of NTS stimulate VC results emesis. In the latter pathway receptor NK1 plays major role, while in the former pathway the emetogens causes release of 5HT(serotonin) from the intestinal enterochromaffin cells (EC cells) and it may stimulate the abdominal afferent vagal nerves via 5-HT3 receptors .The vomiting centre receives input from the afferent discharge of vagal fibres which finally evokes the emeticreflux.