.O2 - Significant biochemical intermediate

Produced by oxidative phosphorylation

Accords with other evidence that laser acts by increasing ATP production in mitochondria

.O2 in small amounts :

Modulates biochemical processes & Triggers immune regulation

.O2 in large amounts

Damages DNA

causes cell destruction

LILT is only capable of producing tiny amounts of .02. Research shows that large doses of Laser Therapy causes no changes in cell temperature, no histological or structural changes.

Sasaki et al (1992) & Calderhead & Inomata (1992)

Physiological Changes
Low Intensity Laser Therapy has been seen to affect the following

Bradykinin , Serotonin , Macrophages , Sodium-Potassium-ATPase , Fibroblasts , Nerve Conduction , Mast cells , S.O.D. Levels , Endothelial cells , Activity in C Fibres , Keratinocytes Neutrophils

a) Super Oxide Dismutase
Acute inflammation -> superoxide free radicals

S.O.D. + arachidonic acid -> prostaglandin E

PGE - changes in nociceptor membrane potentials (increase in firing rate, increased vasodilation)

SOD amounts increase significantly after LILT.

- pain relief

- resolve inflammation

(Lombard et al, 1990; Urcuoli et al, 1991)

b) Serotonin
Serotonin is associated with pain relief and the resolution of inflammation.

LILT -> increased 5-HIAA (a breakdown product of Serotonin)

Walker (1983)

No LILT -mediated 5-HIAA production observed !

Vadi et al (1990)

The role of serotonin mediated analgesia with LILT is still unclear

c) Mast Cells
Mast cells are important mediators of inflammation, especially in connective tissue.

LILT -> mast cell degranulation -> release of Heparin, SOD, Histamine -> resolution of inflammation.

Mast cell degranulation only occurred in injured skin, not in intact skin; thus LILT did not generate an inflammatory response, it promoted an already occurring response.

Trelles et al (1989) and El Sayed & Dyson (1990)

d) Bradykinin
Bradykinin is associated with the acute inflammatory response: it produces the sensation of long duration, dull, burning pain. Bradykinin also increases the number of impulses and mitochondral volume in Bradykinin-sensitive free nerve endings.

Bradykinin was injected into Wistar rats, causing increased neural impulses. reduced the neural impulses caused by the presence of Bradykinin. pain attenuation

(Maeda, 1989)

e) Sodium-Potassium-ATP-ase
Sodium-Potassium-ATP-ase (Na-K-ATPase) reduces nociceptive impulse transmission. Increased Na-K-ATPase activity seen after LILT -> pain attenuation.

Kudoh et al (1989)

f) Nerve Conduction and Laser Mediated Analgesia
LILT to the median nerve at the wrist increases pain threshold of subjects by 10%.

Baxter & Allen (1991)

Irradiation of Erb's point attenuated experimentally induced ischaemic pain.

Mokhtar et al, (1991)

A significant increase in mean conduction latency was observed at Erb's point and at the elbow following LILT to the median nerve at the wrist. Increased conduction latency of the superficial radial nerve was seen following LILT irradiation to the wrist

Mokhtar et al, (1991) Baxter et al, (1991)

Walsh et al, (1991).

ie: a direct neurophysiological response to LILT occurs in vivo at therapeutic doses.

g) Observation of evoked activity of large diameter fibres and small diameter fibres (C fibres):

LILT -> No effect on large diameter afferents

LILT -> reduced evoked activity in small diameter afferents.

Small diameter afferents are associated with the production of 'slow' chronic pain and are thought to inhibit the cells in the substantial gelatinosa which inhibit pain transmission.

Reduced activity of C fibres -> decreased transmission and sensation of pain.

Baxter, (1992)

Makoto Yamaya*, Chiyuki Shiroto', Hiroki Kobayashi*, Shinji Naganuma*, Jyuichi Sakamoto*,
Koh-Jun Suzuki*, Shigeyuki Nakaji*, Kazuo Sugawara* and Takashi Kumae::
*Department of' Hygiene, Hirosaki University School of Medicine. Hirosaki; .-Shiroto Clinic Coshogawara, Aomori: Department of Industrial Health. The Institute of Public Health, Tokyo. Japan

There have been many reports on the applications of low reactive level laser (LLL) therapy for pain attenuation or pain removal. Our group has reported previously on the effects of in vitro irradiation of LLL particularly on the phagocytic activity of human ncutrophils. using luminol-dependent chemiluminesccnce (LmCL) for measurement of reactive oxygen species (ROS) production from human ncutrophils. But the mechanisms of the attenuation of phagocytic activity of Neutrophils by LLL irradiation is not yet full understood, In this study. we used luminol-dependent and lucigenin-dependent chemiluminescence (LgCL) for detection of affected ROS producing process of human neutrophils by LLL irradiation. Two soluble action stimuli. N-formyl-Met-Leu-Phc (fMLP) and phorbol myristate acetate (PMA) were used to avoid the possible influence of lag-time from recognition to uptake of particles at the ROS production. In case of using fMLP as a stimulus, the maximum lumincscence intensity of LULL was increased hut LgCL luminescence was decreased by LLL irradiation. When PMA was used as a stimulus, the times to reach the maximum luminescence intensity of LmCL and LgCL were shortened by LLL irradiation but there was no effect on the maximum lumincscence intensity of both. These results suggest that LLL irradiation enhances the ROS production activity of human ncutrophils by the activation of the superoxide converting system, the active clement in which is mainly myeloperoxidase. LLL irradiation enabled a more rapid activation of the superoxide production system, NADPH -oxidase.

0898-5901/93/03011 1-06$08.00 © 1993 by John Wiley & Sons. Ltd.
LASER THERAPY 1993: 5: 111-116

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