Nasalotherapy for treatment asthma and – Breathing chronic inflammatory diseases (página 2)

Partes: 1, 2

TREATMENT

The present document will omit the description of the
multiple existing treatments, with their degree of effectiveness,
faults and collateral effects, sufficiently known by medical
personnel, in order to go on with the new proposal of
treatment.

The proposed medication must combine and improve the
favorable attributes of: oral bronchodilators, inhalators, and
intranasal corticoids (5).

Such medication must have anti-inflammatory qualities
on the airways and diminish the collateral effects of
bronchodilators, corticosteroid and antiallergenic drugs
(5).

It should also diminish the excessive dosage and use
of inhalators, as well as the high costs and the limited action
of the antileukotrienes.

In the search of a new treatment we must consider its
effectiveness, diminution or elimination of collateral effects,
long nonsynthomatic periods and diminution of costs.

Development of an oral medication would be the ideal,
but it has been demonstrated that the most effective
antiasthmatic therapies are those administered by nasal
route.

The patients and they are the only approved therapy to
reduce the inflammation of the airways of the asthmatic
patient.

Inhaled corticosteroid can inhibit the eosinophils
activation in the bronchial epithelium (6).

LOCAL
ANESTHETICS

Local anesthetics have long been used as topical
application on the nasal mucosa for a great number of
otorrinolaringologic procedures (14).

Chemistry of the local anesthetics

Cocaine is the classic local anesthetic, and it is
obtained from a plant, the other anesthetic agents are synthetic
products.

Group 1. Ester type

Group 2. Amide type

Conformation of the molecule:

An aromatic lipophylic chain
An intermediate chain
An amino hydrophilic group

In ester type compounds as procaine, the aromatic
lipophylic chain provides the P-amino benzoic acid.

In the agents amide type as lidocaine, the xylidine
constitutes the aromatic lipophylic chain.

The aromatic lipophylic group makes the molecule
easily soluble in lipids of cell membranes.

Procaine

Procaine, (P-aminobenzoil-dietil-amino-ethanol
chlorhidrate), was the first synthetic local
anesthetic.

It is probably the least toxic of all local anesthetics,
with the fastest beginning of action and with the shortest
duration. The liver destroys it quickly when it reaches the blood
stream.

Great amounts of procaine may be given to animals of
laboratory by intravenous injection without causing the
death.

In usual doses that are used in general and special
surgery, just like in odontolgy, procaine is almost free of
disagreeable effects on respiratory and circulatory
systems.

There have been injected up to 360 cc of the solution
concentrated to 1% and up to 570 cc of the solution to the 0, 5%
without annoying symptoms.

Infiltrating 0, 5 cc of the solution concentrated to 2%
does not produce vasoconstriction or vasodilatation and it does
not leave later effects on tissues.

Minimum lethal dose in milligrams by kilogram
of corporal weight

750 milligrams/kg in rats, subcutaneous

425 mgs/kg in cobay, subcutaneous

53 mgs/Kg in rabbits, by intravenous route
(p)

Lidocaine

Lidocaine is the local anesthetic of amide type, it is
the local anesthetic with more use at present, and it has quite
fast beginning of action, long lasting duration of action, with a
power and toxicity 2 or 3 times greater than procaine.

There are solutions to 4% for topical use on
tracheobronchial tree, nose, and orofarynx. Lidocaine has a great
number of nonanesthesic uses, as antiarrhythmic in patients with
ventricular arrhythmia, antiepileptic, and analgesic intravenous
(o).

Absorption and metabolism of the local
anesthetic

Local anesthetics do not penetrate the intact skin in
important degree. Absorption of local anesthetic after its
topical application on mucous membranes may be fast, and in some
cases the concentration in blood may be similar to the
concentration obtained by intravenous route.

Local anesthetics spread not only towards the inner of
the epithelial cells but also towards the neighboring blood
vessels. The sanguineous mass of local anesthetics is diluted
mainly in its passage through the lung, which provides a
cushioning base against the elevated concentration of the local
anesthetic. It is excreted in small amounts by renal route
without modification.

Most of it is metabolized in the blood or the liver to
conjugated metabolites that are pharmacologically inactive and
are excreted easily. These processes are made with relative speed
of such way that half of the medication in the blood disappears
generally in a lapse of 15 to 20 minutes (14).

Toxicity of the local anesthetics

Local anesthetics have the advantage that they are
administered by the same health personnel, who are present, if
any toxic phenomenon occurs.

The toxicity of the local anesthetic depends on the
dose, the nature of the drug, the individual idiosyncrasy, the
speed of absorption, and its elimination.

Respiratory depression is the most important toxic
effect, and constitutes the habitual cause of death in procanic
poisoning, also circulatory depression, effects on the central
nervous system and on the cerebral cortex, cutaneous reactions of
edematous or urticarial type and anaphylactic shock
(15).

MECHANISM OF ACTION
OF LOCAL ANESTHETICS

Within the mechanisms of action of local anesthetics,
the properties mentioned will be only those that might have to do
with their possible effect in the treatment of the bronchial
asthma and inflammatory diseases of the respiratory system, which
is the goal of the present document.

Local anesthetics have lipophylic properties because of
their lipophylic aromatic chain.

Local anesthetic substitutes calcium ions (Ca++) not
only in nervous membrane but also in any cell membrane
(15)

THEORY ON THE
MECHANISM OF ACTION OF THE LOCAL ANESTHETICS IN THE RELIEF OF
BRONCHIAL ASTHMA AND CHRONIC DISEASES OF THE RESPIRATORY
TRACT

Anti-inflammatory action

The antinflammatory action of the local anesthetics is
made at level of the epithelium of the air way by the following
mechanisms:

The stabilization of the cell membrane produced by the
anesthetic’s aromatic lipophylic chain which adheres to
membranes lipid portion.

This stabilization of the cell membranes of the
epithelium blocks the citoquines and neuropeptides
releasing.

The stabilization of the cell membranes of mast cells
and eosinophyls by the same process blocking the histamine and
leukotrienes releasing.

The occupation of the lipidic portion of the cell
membrane blocks the action of the CAM (complex of attack of
membrane of the complement), also blocking y the releasing of
inflammatory mediators.

The stabilization of the membrane blocks the action of
the IgE.

It also blocks the activation of the system of the
complement by the displacement of the ions of Ca++,

Bronchodilatation

The local anesthetic's action is due to the autonomous
system blockade producing a simpaticolitic and parasimpaticolitic
effect.

The autonomous blockade produces relaxation of the
bronchial smooth muscle.

The relaxation of the bronchial smooth muscle is also
obtained by the displacement of the ions of Ca++ blocking the
interaction of the actina and miosina which is necessary for
muscular contraction.

Blocking glands secretion

Autonomic blockade caused by local anesthetic also
blocks the cholinergic action on gland of the respiratory tract,
and so it results in diminution of gland secretion

SCHEME OF TREATMENT AND
PROCEDURES

USING PROCAINE

5.0 (five) milliliters of procaine 1% diluted in 50
(fifty) milliliters of distilled water

USING LIDOCAINE

3.0 (three) milliliters of lidocaine 1% without
epinephrine diluted in 50(fifty) milliliters of distilled
water.

Procedures

Instillation of 5 milliliters of the solution in each
nasal window, till completing 50 milliliters.

You must use a disposable 10cc syringe without
needle.

The solution must be allowed to leave normally but the
patient is asked not to shake the nose.

So we can obtain a suitable perfusion and absorption of
the medication by the nasal mucosa.

Respiratory exercises for clearing

Ask the patient to make long and deep inspirations and
prolonged expirations

The therapist must press the patient thorax at the
moment of the expiration, placing each hand on the costal grate
side to side of the breastbone. This maneuver can be made by a
patient relative at home two or three times per day.

This maneuver may cause intense cough in patients with
abundant secretion, which contributes to a faster cleaning of the
bronchial tree.

3 sessions of nasalotherapy with intervals of 3
days are performed to obtain an improvement of about 90%, but the
patient improves his breathing since the first
session.

When procaine is used, the total dose of procaine
chlorhidrate provided to the patient is of 50 milligrams, most of
which do not reach the blood stream because it remains in
epithelium of the nasal mucosa or is expelled by the patient
during the procedure.

When lidocaine is used, the total dose of lidocaine
chlorhidrate is about 30 milligrams, with which occurs just like
with procaine.

These doses are below the doses used in other procedures
and very below the minimum lethal dose mentioned in the present
document.

This treatment provides an improvement over 90 % in the
great majority of the patients, with asymptomatic periods until
by six months and more.

Materiales y métodos

Estudio no comparativo en 30 pacientes asmáticos
manejados previamente con tratamiento convencional en el hospital
san Rafael de Andes y en el hospital Gabriel Peláez M. del
municipio de Jardín (Ant.Col)

Se administro 35 miligramos de lidocaína
disuelta en 30 c.c. De agua destilada
en forma tópica sobre la mucosa nasal, en tres sesiones,
con intervalos entre sesión y sesión de 5 a 7
días, para un total de 105 miligramos de lidocaína
por paciente

Signos-síntomas y patologías
asociados

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