Pupillary dilation

Activation of the parasympathetic branch causes pupillary dilation, increases salivation, constricts lung bronchi, decelerates heart rate, increases digestion, and stimulates conversion of glycose to glycogen. Whereas the parasympathetic branch is involved in physiological sexual arousal, the sympathetic branch is involved in the physiological aspect of orgasm. 

Pupil size increased rapidly to a maximum of about 7 mm at 6 hours (Fig. 52), and tended to persist longer than changes in both cognitive performance and heart rate. The probable dominance of the central component of pupillary dilation is reinforced by this observation. 

Lowering of pupillary sphincter tonus and pupillary dilation by local administration of homatropine or tropic-amide (mydriatics) allows observation of the ocular fundus. For diagnostic uses, only short-term pupillary dilation is needed. The effect of both agents subsides quickly in comparison with that of atropine (duration of several days). 

Pharmacology Epinephrine, a direct-acting sympathomimetic agent, acts on and receptors. Topical application, therefore, causes conjunctival decongestion (vasoconstriction), transient mydriasis (pupillary dilation), and reduction in intraocular pressure (lOP). It is believed lOP reduction primarily is caused by reduced aqueous production and increased aqueous outflow. The duration of decrease in lOP is 12 to 24 hours. 

Mydriasis is induced by ai-adrenoceptor-mediated contraction of the radial pupillary dilator muscle of the iris. Furthermore, activation of this receptor subtype induces an increased outflow of humor from the eye while /i-adrenoceptor stimulation mediate an enhanced humor production which contributes to an increased intraocular pressure. /3-Adrenoceptor antagonists (/3-blocker) can be used in the treatment of glaucoma. 

Specific treatment starts with the administration of atropine sulphate, a competitive antagonist of acetylcholine at muscarinic receptors. Sufficient atropine should be given to control hypersecretion and produce tachycardia and pupillary dilation. Very large doses of atropine are required atropine sulphate 2-A mg should be given intravenously every few minutes during the first hour, and then by continuous infusion. Patients may require up to 500 mg intravenously during the first day, and treatment may be needed for days. 

Ephedrine increases systolic and diastolic blood pressure heart rate is generally not increased. Contractile force of the heart and cardiac output are both increased. Ephedrine produces bronchial smooth muscle relaxation of prolonged duration when administered orally. Aside from pupillary dilation, ephedrine has little effect on the eye. 

Dry moufh, urinary retenfion, flushing, pupillary dilation, constipation, confusion, redness of fhe skin, flushing, dry skin, allergic contact dermatitis, headache, excitement, agitation, dizziness, light-headedness, drowsiness, unsteadiness, confusion, slurred speech, sedation, hyperreflexia, convulsions, vertigo, coma, mydriasis, photophobia, blurred vision, dilation of pupils Rare... 

Overdose may produce temporary paralysis of ciliary muscle pupillary dilation tachycardia palpitations hot, dry, or flushed skin absence of bowel sounds hyperthermia increased respiratory rate EGG abnormalities nausea vomiting rash over face or upper trunk CNS stimulation and psychosis (marked by agitation, restlessness, rambling speech, visual hallucinations, paranoid behavior, and delusions, followed by depression). 

Self-administration of psychostimulants by humans produces a syndrome of intoxication, the symptoms of which can include elevated pulse and blood pressure, pupillary dilation, euphoria, and psychomotor agitation. Ingestion of excessive amounts can result in compulsive behavior, psychotic symptoms that include auditory and visual hallucinations and paranoid delusions, chest pain, arrhythmias, dyskinesias, and seizures. 

Acute administration of opioids, particularly in non-tolerant individuals, produces a syndrome of intoxication characterized by pupillary dilation and initial euphoria, followed by apathy, psychomotor retardation, slurred speech, and impaired attention and memory. Opioid overdose can produce fatal respiratory depression and thus is a medical emergency. 

Eye The radial pupillary dilator muscle of the iris contains alpha-receptors activation by drugs causes mydriasis. 

Symptomatic adverse effects Topical pilocarpine therapy produces blurred vision or myopia, poor vision in dim light or sometime painful spasm. Many patients on pilocarpine may experience ciliary or conjunctival congestion, headache, photophobia. Some patient may develop pupillary dilatation following use of pilocarpine. 

These result from over-stimulation of the sympathetic nervous system anxiety, sweating, tachycardia, arrhythmia, hypertension, myocardial ischaemia, headache, cerebral haemorrhage, pulmonary oedema. Adrenaline may cause pupillary dilatation which must be distinguished from pupillary dilatation due to other causes, e.g. severe brain injury. 

The eye is a good example of an organ with multiple autonomic nervous system (ANS) functions, controlled by several autonomic receptors. As shown in Figure 6-9, the anterior chamber is the site of several autonomic effector tissues. These tissues include three muscles (pupillary dilator and constrictor muscles in the iris and the ciliary muscle) and the secretory epithelium of the ciliary body. 

The ganglion-blocking drugs cause a predictable cycloplegia with loss of accommodation because the ciliary muscle receives innervation primarily from the parasympathetic nervous system. The effect on the pupil is not so easily predicted, since the iris receives both sympathetic innervation (mediating pupillary dilation) and parasympathetic innervation (mediating pupillary constriction). Ganglionic blockade often causes moderate dilation of the pupil because parasympathetic tone usually dominates this tissue. 

Pupillary dilator muscle Contraction (dilates pupil)... 

In the eye, the radial pupillary dilator muscle of the iris contains oo receptors activation by drugs such as phenylephrine causes mydriasis (see Figure 6-9). Alpha stimulants also have important effects on intraocular pressure. Alpha agonists increase the outflow of aqueous humor from the eye and can be used clinically to reduce intraocular pressure. In contrast, agonists have little effect, but antagonists decrease the production of aqueous humor. These effects are important in the treatment of glaucoma (see Chapter 10), a leading cause of blindness. 

HO-DMT is a minor metabolite of DMT in man, and it was studied for the same reasons. Could this compound play a role in explaining the activity of the parent dialkylamine It was explored in a series of subjects who had responded spectacularly to DMT. The five volunteers in this study were former opium addicts who were serving sentences for violation of United States narcotics laws. They were administered 6-HO-DMT at either 0.75 mg/Kg (one subject) or 1.0 mg/Kg (four subjects) and reported no differences from the inactive placebo control. The objective measures (blood pressure, respiration and heart rate, pupillary dilation) confirmed this absence of activity at this level. The active control drug was DMT itself, and it showed the expected responses in all regards. 

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