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Biomedical subjects

B Kaada

Publications and source records attributed to B Kaada.

At least 37 records · Page 2Linked to original sources
PubMed1988

Promoted healing of leprous ulcers by transcutaneous nerve stimulation.

Low-frequency (2 Hz) transcutaneous electrical nerve stimulation (TNS) may produce widespread and prolonged increases in skin temperature in patients with peripheral vascular insufficiency due to improved microcirculation. The method has previously been used successfully to potentiate healing of chronic ulcers of various etiology. The present report describes a similar study, using TNS treatment in attempts to accelerate healing of chronic leprous ulcers that had resisted treatment for several months or years. All other treatment, local and systemic chemotherapy, and daily regime remained as far as possible unaltered. The study was limited to ulceration in the soft tissue of the foot or lower leg. Eleven TNS sessions, each of 30 min duration, were applied per week. In 19 patients (6 out- and 13 in-patients), in whom the TNS treatment was not interrupted, all ulcers healed completely within a mean of 5.2 weeks (range 3-12 weeks). The mean size of the ulcers was 5.2 cu.cm (range 0.2-48.3 cu.cm), and they had persisted for a mean of 15.8 months (range 2-60 months). The 'healing index', i.e. the mean reduction of the ulcer cavity per week, was 1.0 cu.cm/week. The study demonstrates a clear therapeutic effect for low-frequency TNS in patients with leprous ulcers. The mechanisms involved in the accelerated healing are assumed to be increased microcirculation due to sympatho-inhibition and release of endogenous corticosteroids.

Adult↗
PubMed1987

Increase in vasoactive intestinal polypeptides (VIP) by the angiotensin converting enzyme (ACE) inhibitor lisinopril in congestive heart failure. Relation to haemodynamic and hormonal changes.

1. The effects of the angiotensin-converting enzyme (ACE) inhibitor lisinopril on plasma vasoactive intestinal polypeptides (VIP) and plasma noradrenaline, adrenaline and dopamine were studied in 12 patients with congestive heart failure over two consecutive 48-hr periods. The first day in each period served as a treatment day and the second as a control day. 2. A parallel monitoring was made of various hormonal parameters related to the renin-angiotensin-aldosterone system, and a right-heart catheter was used to monitor haemodynamics at rest. 3. Potent inhibition of the renin-system (as demonstrated by decreases in angiotensin converting enzyme (ACE) activity, angiotensin II and plasma aldosterone) together with improved haemodynamics (decreases in mean right atrial pressure, mean pulmonary arterial pressure, mean pulmonary capillary wedge pressure and mean systemic arterial pressure) were recorded. 4. Plasma VIP was significantly increased by a mean of 20.3% (P less than 0.01) on the lisinopril treatment days compared with the control days, whereas circulating catecholamines showed no significant pattern of change. 5. It is postulated that the potent vasodilatory neuromodulator VIP is implicated in the ACE inhibitor effects. 6. The ACE is a non-specific peptidase that previously has been implicated in the potentiation of other vasoactive endogenous systems (kinins and enkephalins).

Adult↗
PubMed1987

Vasoactive intestinal polypeptides in connective tissue massage. With a note on VIP in heat pack treatment.

The vasoactive intestinal polypeptide (VIP) is a powerful dilatator in a number of vascular beds. Plasma VIP is increased in active physical exercise and in transcutaneous nerve stimulation. Plasma VIP has in this study been measured during other physiotherapeutic procedures causing skin vasodilatation, such as connective tissue massage and heat packs. Plasma VIP levels and skin temperature of fingers and toes were measured in 12 patients before and at various intervals following a 30 min connective tissue massage. No significant increase in the plasma VIP was found. The same was true in a pilot study using heat pack treatment. It is suggested that somehow VIP is more involved in the vascular response to active physical activity and peripheral nerve stimulation than to passive procedures like connective tissue massage and heat pack treatment.

Adult↗
PubMed1987

Neurotransmitters in "the smoke reflex" in rabbits.

An acute form of "stress-analgesia" is evoked by allowing the smoke of a cigarette to envelope the nostrils of unanaesthetized rabbits. The response consists of an immediate and generalized arrest of spontaneous movements, including respiration and expiration, reduced muscular tone, and unresponsiveness to pinching. This motor "paralysis" is accompanied by a profound bradycardia. Attempts have been made to identify the neurotransmitters involved in "the smoke reflex" by the intervention of antagonists and psychopharmaca. The bradycardia was selectively blocked by atropine, leaving the somatomotor inhibition unaltered. All components of the response were abolished by approximately 60% by clonidine and by 40% by the tricyclic antidepressant amitriptyline, both of which are known to attenuate the release of noradrenaline as agonsits of alpha 2-adrenoceptors. Yohimbine blocked the clonidine effect. Naloxone (1-2 mg/kg), p-chlorphenylalanine and dexamethasone failed to influence the reflex response, suggesting that opiate, serotonergic and ACTH-systems do not play a critical role. The same applied to the benzodiazepine chlordiapoxide. The results suggest that this acute stress-induced analgesia is mediated via a noradrenergic system. The relationship of the smoke reflex to "the fear paralysis reflex", a possible trigger mechanism for the sudden infant death syndrome, is discussed.

Amitriptyline↗
PubMed1987

The sudden infant death syndrome induced by "the fear paralysis reflex'?

The sudden infant death syndrome (SIDS) is the greatest single cause of death between one month and one year of age in industrial countries. Its etiology still remains a mystery despite extensive research during the past decades. The outstanding problem is to define the trigger mechanism leading to death. Most theories have dealt with bodily malfunctions, infections and toxic agents, and only minor attention has been paid to a possible psychical trigger mechanism. The hypothesis is advanced that the so-called 'fear paralysis reflex' (for other terms, see below), an atavistic reflex present in the entire animal kingdom, may be a major trigger mechanism for SIDS. The reflex is evoked by fear resulting from any threatening event which is perceived as a danger, and with which the organism is unable to cope, typically in a predator confrontation. Important threatening stimuli in animals, and which may be of particular importance in human infants, are restraint of movement, sudden and unfamiliar noises, separation from the mother and companions, and sudden exposure to an unfamiliar environment. The main response characteristics are an immediate motor 'paralysis' (prolonged and generalized immobility), unresponsiveness, and abrupt and profound bradycardia. The latter may proceed to asystole and fatal cardiac arrythmias. Any hypothesis attempting to explain the cause of SIDS must account for the unique age distribution of SIDS' victims with a peak age incidence at 2-4 months, its frequent occurrence in REM sleep, and the observation that most deaths are silent. Further, it must be consistent with previously established risk factors (genetic determination, opiate-addicted mothers and cigarette smoking). The fear paralysis hypothesis is in accordance with all these facts, and it suggests new and potentially hazardous triggering mechanisms which, one recognized, possibly can be avoided. As a central reflex, it does not leave any trace in the organism, which explains the negative postmortem findings. Suggestions for testing the hypothesis are given, and possible preventive measures are presented.

Age Factors↗
PubMed1987

Successful treatment of esophageal dysmotility and Raynaud's phenomenon in systemic sclerosis and achalasia by transcutaneous nerve stimulation. Increase in plasma VIP concentration.

Dysphagia has been successfully treated by low-frequency transcutaneous nerve stimulation (TNS) in two patients with achalasia and in six patients with systemic sclerosis. A 30- to 45-min stimulation session was followed by augmentation of peristalsis in the lower half of the esophagus and relaxation of the gastroesophageal sphincter, with relief of dysphagia. The sclerotic patients were also relieved of invaliding Raynaud's phenomenon. One 30-min daily stimulation session, and later one session every 2nd or 3rd day, was sufficient to prevent relapse. After months or years of TNS treatment the stimulation could in three patients be withdrawn with no recurrence. A stimulation session produced about 30% increase in plasma vasoactive intestinal polypeptides. Activation of this neuromodulator is considered to be the cause of the beneficial effects on dysphagia and Raynaud's phenomenon.

Electric Stimulation Therapy↗
PubMed1987

Successful treatment of itching and atopic eczema by transcutaneous nerve stimulation.

Low-frequency (2 Hz) transcutaneous electrical nerve stimulation (TNS) may produce prolonged and widespread sympatho-inhibition resulting in improved skin microcirculation with increased skin temperature in patients with peripheral vascular insufficiency. The method has previously been used successfully to improve peripheral circulation in such patients and to accelerate healing of chronic skin ulcers of various etiology. The present report deals with healing of atopic eczema and relief of pruritus by low-frequency TNS treatment in a patient who was followed for 2 years, the first 8 months with daily recordings of the effects, and then for an additional 16 months during which period TNS only occasionally was used. TNS also produced increased plasma levels of ACTH, cortisol and vasoactive intestinal polypeptides (VIP). The mechanisms of the favourable clinical effects are discussed.

Adolescent↗
PubMed1986

Increase in plasma vasoactive intestinal polypeptide (VIP) in muscular exercise in humans.

We have previously shown that plasma vasoactive intestinal polypeptide (VIP) is increased in normal subjects by low-frequency transcutaneous nerve stimulation. The latter may also increase short-term physical performance in athletes (running, swimming and ergometer cycling). The present study examines whether the plasma VIP level is similarly increased in short-term ergometer exercise in seven healthy volunteers. A group of four patients with angina pectoris were included, since a lowered concentration of VIP is found in diseased heart tissue. In the group of healthy subjects, ergometer exercises with progressive increases in workload until exhaustion, lasting from 16 to 32 min (mean 26 min) and with a corresponding maximum energy output of 1500 to 5100 W (mean 3560 W), resulted in an increase in plasma VIP concentration from a pre-stimulatory level of 3.3 pmol . l-1 to 5.3, 5.2 and 5.6 pmol . l-1, measured 3, 10 and 20 min respectively, following termination of the exercise, i.e. a maximal 70% increase. In the patients with angina pectoris there was no significant VIP increase (cycling time 7-15 min, work performed 400-1350 W). Possible triggering mechanisms for VIP release and its source are discussed.

Adult↗
PubMed1985

Use of transcutaneous nerve stimulation in the attacks of acute intermittent porphyria.

A 38-year-old female with acute intermittent porphyria (AIP) was having regular recurrent premenstrual severe attacks of abdominal and chest pain due to the disease. Low-frequency transcutaneous nerve stimulation (TNS) premenstrually prevented or markedly reduced the severity of clinical attacks, associated with a reduced urinary porphyrin excretion. The possible mechanisms of the TNS-induced effects are discussed. This experience suggests that TNS may be an effective and simple prophylactic method in the management of the attacks in AIP. The method can be administered easily by the patient himself as home-treatment and is free of side-effects.

Acute Disease↗
PubMed1985

Lower plasma levels of some gastrointestinal peptides in Raynaud's disease. Influence of transcutaneous nerve stimulation.

In a previous study it was shown that Raynaud patients during ischemic attacks displayed significantly lower levels of vasoactive intestinal polypeptides (VIP) in cubital vein plasma than did normal subjects in the same relatively cold environments. Low-frequency transcutaneous nerve stimulation (TNS), producing widespread cutaneous vasodilatation, was associated with a 30-35% increase in plasma VIP in both groups. In the present study parallel observations were made in some of the same subjects under the same experimental conditions with regard to six other gastrointestinal peptides: somatostatin, motilin, pancreatic polypeptide (PP), secretin, gastric inhibitory polypeptide (GIP), and cholecystokinin (CCK), determined radioimmunochemically. Except for CCK, the mean plasma levels of all these gut peptides were similarly lower in the Raynaud patients than in the normal subjects in cold environments. However, TNS did not induce significant increases in the plasma levels of any of these 6 peptides. These findings appear to place VIP in a different functional category than the other gut peptides.

Electric Stimulation Therapy↗
PubMed1984

In search of mediators of skin vasodilation induced by transcutaneous nerve stimulation: III. Increase in plasma VIP in normal subjects and in Raynaud's disease.

Previous studies have shown that the widespread and sustained cutaneous vasodilation which can be induced by low-frequency transcutaneous nerve stimulation (TNS) in humans is dependent on a central serotonergic pathway leading to peripheral sympatho-inhibition. In addition, in a bioassay study, the release of a peripheral vasodilator was suggested. However, the TNS-induced dilator response was not blocked by antagonists to a series of known endogenous vasodilators. In the present study another candidate, the vasoactive intestinal polypeptide (VIP) was monitored by means of a specific radioimmunoassay. The results showed an increase in plasma VIP from 5.6 pmol X l-1 before TNS to 7.3 pmol X l-1 after TNS (median values for 15 normal volunteers; P less than 0.05 for the 30% increase). Patients with Raynaud's disease displayed lower levels of VIP than the normal group (median 3.7 pmol X l-1 for 20 patients; P less than 0.01 for the difference from normals). TNS-induced rewarming of the extremities in Raynaud patients was paralleled by 35% increase in plasma VIP (median 5.0 pmol X l-1; P less than 0.01 for the TNS-dependent increase). The results suggest that the TNS-induced increase in plasma VIP parallels the increase in skin temperature in the extremities. However, a causal relationship between the increase in plasma VIP and cutaneous vasodilation remains to be determined. Possible origins of the TNS-dependent increase in plasma VIP are discussed.

Electric Stimulation↗
PubMed1984

In search of mediators of skin vasodilation induced by transcutaneous nerve stimulation: IV. In vitro bioassay of the vasoinhibitory activity of sera from patients suffering from peripheral ischaemia.

The widespread cutaneous vasodilation which can be induced by low-frequency transcutaneous nerve stimulation (TNS) in humans is, at least in part, due to sympatho-inhibition. Studies on the additional involvement of an active local vasodilator have demonstrated a moderate increase in plasma vasoactive intestinal polypeptide (VIP) but excluded a series of known dilators. In the present study sera from four patients with peripheral ischaemia (three with Raynaud's disease, and one with diabetic polyneuropathy) were assayed for vasoactivity on isolated vascular smooth muscle (rat portal vein) with reactivity towards a wide series of classical neurotransmitters and neuropeptides. In the presence of cholinergic and beta-adrenergic blockade sera collected after TNS-induced vasodilation revealed an inhibitory activity which could not be accounted for by changes in osmolarity, pH or K+. The inhibitory response to the plasma samples developed more rapidly than the response to synthetic VIP. The inhibitory activity of the plasma samples excluded a series of other peptides such as substance P, neurotensin, pancreatic polypeptide, bradykinin and angiotensin II, which all enhanced the contractile activity in the rat portal vein. There was a proportional increase in skin temperature and occurrence of inhibitory activity in cubital plasma samples in response to TNS. The results suggest that a peripheral vasodilator activity besides VIP may be implicated in the sustained dilation induced by TNS in these patients.

Adult↗
PubMed1984

Failure to influence the VIP level in the cerebrospinal fluid by transcutaneous nerve stimulation in humans.

Low-frequency transcutaneous nerve stimulation (TNS) is known to produce a prolonged and widespread cutaneous vasodilatation. This is associated with a moderate but significant increase of 30-35% in the concentration of the vasoactive intestinal polypeptide (VIP) in the cubital vein plasma. A possible source of this increased plasma VIP following TNS is the central nervous system. This possibility is tested in the present experiment. The concentration of VIP in the cerebrospinal fluid (CSF) was determined by radioimmunoassay in 9 patients with no organic disease of the central nervous system, before and at various intervals (15, 30 and 45 min) after the onset of TNS. No significant change in the VIP level of the cerebrospinal fluid was encountered, although the stimulation evoked rises in finger temperature indicating effectiveness of the stimulation. It is concluded that the stimulation-induced increase in plasma VIP is due to release of VIP outside the brain.

Adult↗
PubMed1984

Improvement of physical performance by transcutaneous nerve stimulation in athletes.

The present pilot study tested the exercise response to transcutaneous nerve stimulation (TNS) of 21 volunteers, who were well-trained competitive athletes. In 62 experiments (n) they received low-frequency TNS (2 Hz) for 30-45 min prior to either a road or track race, swimming race, bicycle ergometer exercise, isometric muscular endurance test, or dynamometer hand grip test. Improvement in performance compared with a corresponding number of control tests, without TNS or with placebo stimulation in the same subjects, was almost regularly observed in running, swimming and ergometer cycling, although with great individual variations. The average improvement was 4.3 sec (2.2%) in 1.000 m road racing (n = 9); 2.3 sec (1.8%) in 800 m track racing (n = 5); 0.9 sec (1.4%) in 100 m swimming (n = 12); 1.3 sec (0.8%) in 200 m swimming (n = 6); and 2.5 sec (0.9%) in 400 m swimming (n = 3). In a bicycle ergometer test with stepwise, progressive exercise to muscular fatigue, the maximal capacity was increased by 9% (n = 4). Local isometric muscle endurance of the elbow flexors (n = 7) and hand grip strengths (n = 11) were not significantly altered. Possible mechanisms involved in the response to TNS are discussed.

Adolescent↗
PubMed1984

Treatment of peritendinitis calcarea of the shoulder by transcutaneous nerve stimulation.

Low-frequency transcutaneous nerve stimulation (TNS) is known to produce pain relief as well as widespread and prolonged increases in micro-circulation in the skin and other organs. Such stimulation has further been shown to eliminate skin calcium deposits in systemic sclerosis. The present study tested the effects of TNS on clinical symptoms in peritendinitis calcarea of the shoulder and the possibility that this procedure could eliminate calcium deposits in this disease. Ten patients with 14 calcareous shoulders received TNS-treatment with a follow-up time of 3-10 months. Two of these were classified as acute, 9 as chronic, and 3 as asymptomatic. Great relief of pain and of restricted mobility was encountered in 10 of the 11 symptomatic shoulders one week or two after the onset of daily stimulation with subsequent progressive improvement of residual complaints during the following weeks. There was one relapse after 2 months' freedom of pain. Calcium deposits persisted in the 3 asymptomatic shoulders, but was completely eliminated or greatly reduced in 7 of the 11 symptomatic ones. Comparison is made with reported untreated series. Even if most shoulders with calcified peritendinitis will spontaneously improve in time, TNS-treatment shortens the period of incapacitation and discomfort, secures freedom of pain, and allows earlier mobilization. It may thus represent an alternative method to other therapeutic procedures, such as roentgen irradiation and injection of anesthetics and hydrocortisone, in this disabling disorder.

Adult↗