Peripheral Cold Research Articles

Computer Simulations of Neuronal Signal Transduction: The Role of Nonlinear Dynamics and Noise

Nonlinear ionic interactions at the nerve cell membrane can account for oscillating membrane potentials and the generation of periodic neuronal impulse activity. In combination with noise, external modulation of the endogenous oscillations allows for continuous transitions between a variety of impulse patterns. Such "noisy oscillators" afford, thereby, an important mechanism of neuronal encoding as is demonstrated here with experimental data from peripheral cold receptors and corresponding computer simulations.

The pathogenesis of non-freezing cold nerve injury. Observations in the rat.

Non-freezing cold nerve injury is uncommon in civilian practice, but may reach epidemic proportions in war zones. Studied since the time of Hippocrates, its aetiology has remained elusive. We sought to replicate experimentally, a peripheral nerve cold temperature gradient, since this has been emphasized in clinical descriptions. Our observations, in the rat, of the vasa nervorum show that cold-induced intravascular aggregation is followed by a 'no-reflow' phenomenon which culminates in endothelial damage and delayed thrombotic occlusion.

A.216 Peripheral nerve stimulator vs cold saline-induced paraesthesia method for axillary block

A.216 Peripheral nerve stimulator vs cold saline-induced paraesthesia method for axillary block

COLD ACCLIMATIZATION IN ACTIVE ANTARCTIC SCUBA DIVERS 1203

The purpose of this investigation was to determine whether the cold exposure associated with polar scuba diving operations could result in measurable cold acclimatization in humans. Antarctic-cold-exposed (ACE) subjects (n=4; male) lived in semi-permanent structures in an isolated field camp (77°S 163°E) during the austral spring, conducting 4.9±0.6(4.3-5.9) dives per week for biological research (water -1.9°C; air -36.7 to -5.8°C). Matched bi-weekly-tested (BWT) subjects remained in the U.S. throughout the study period (autumn). Physiological responses to standardized peripheral (30 min digit immersion, 4°C water bath) and whole body (90 min air exposure, 5°C, supine, rest) cold tests were evaluated at two week intervals for six weeks. Analysis of variance (Group × Trial × Time) indicated significant but subtle Group × Trial interactions(p<0.05) in mean digit temperature during the peripheral tests and in mean rectal and mean skin temperatures and mean heart rate during the whole body tests (accounting for 16.4, 8.0, 1.5 and 7.7% of dependent score variability[eta squared], respectively). From the first to fourth trial, the ACE group demonstrated decreased mean digit and rectal temperatures, increased mean skin temperature and decreased mean heart rate (-0.83, -0.16 and +0.36°C and-6.0 bpm, respectively). The BWT group demonstrated increased digit, rectal and mean skin temperatures and heart rate (+0.53, +0.25 and +0.64°C and+5.5 bpm). ACE group changes in digit and rectal temperature and heart rate are consistent with hypothermic adaptation. The elevated mean skin temperature may indicate a concomitant attenuation of the vasoconstrictive responses. BWT group changes are consistent with metabolic adaptation, potentially induced by a combination of the cold testing and naturally occurring seasonal acclimatization. Given the modest changes, it is unclear whether the cold adaptation demonstrated by the divers working under polar conditions has any operational importance.

Effects of peripheral cold exposure on microvascular dynamics in systemic sclerosis.

To determine the influence of cold exposure on microvascular permeability in systemic sclerosis (SSc). Thirteen patients with SSc were studied by dynamic fluorescence videomicroscopy under basal conditions and after exposure to cold. Exposure to cold caused a significant reduction in the interstitial concentration of sodium fluorescein (P < 0.05 to 0.001). Our findings show that cold exposure has a striking effect on microvascular dynamics in SSc.

Selective neuropathy and preserved vascular responses in the diabetic Charcot foot.

Charcot arthropathy is a disabling complication of diabetic neuropathy. It is however, unclear why it occurs in only a small number of neuropathic patients. We have studied 12 diabetic patients (10 insulin-dependent) with an acute Charcot arthropathy, and compared their neuropathy and vascular responsiveness with 12 diabetic patients (10 insulin-dependent) with recurrent neuropathic foot ulceration, 12 diabetic control subjects (9 insulin-dependent) and 10 normal non-diabetic subjects. The Charcot arthropathy patients demonstrated a preservation of warm perception, 6 (5.5) degrees C, but complete loss of peripheral cold perception, 10 (0) degrees C, p less than 0.001 (median (interquartile range)). This contrasted with the ulcerated neuropathy patients, who had equally severe impairement of both warm and cold sensory thresholds, 10(0.5) degrees C vs 10(1) degrees C, respectively, the diabetic control subjects who were able to detect a 2 (1.3) degrees C warm stimulus and 3 (3.5) degrees C cold stimulus and the normal subjects, whose warm threshold was 2 (1) degrees C and cold was 2 (1) degrees C. Light touch perception at the foot was preserved in the Charcot patients 4 (4) g vs 100 (50) g, p less than 0.0002, in the ulcerated neuropathy patients. Vibration perception at the great toe and cardiovascular autonomic function tests (heart rate variability, Valsalva ratio and postural systolic blood pressure fall) were abnormal in both the Charcot patients and ulcerated neuropathy group, with no differences seen between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of peripheral cold exposure on oesophageal motility in patients with autoimmune rheumatic diseases and raynaud's phenomenon

The effects of peripheral cold exposure on oesophageal motility were studied in 14 patients with autoimmune rheumatic diseases. They were divided into two groups: 9 with and 5 without Raynaud's phenomenon. The statistical comparison of these two groups did not reveal any difference in the way they manometrically reacted during and after the cold exposure. We conclude that the oesophageal dysfunction in Raynaud's phenomenon may not be of neurogenic origin.

Cold-induced vasodilatation of finger and maximal oxygen consumption of young female athletes born in Hokkaido

To determine whether there is a direct correlation between endurance capacity and cold tolerance, maximal oxygen consumption (VO2max), and cold-induced vasodilatation (CIVD), we measured these factors in 14 young female athletes born in Hokkaido, Japan's northernmost island. We determined the VO2max by a standard incremental test on a cycle ergometer and measured the oxygen consumption (VO2) by means of the Douglas-bag method. We determined the CIVD reaction by measuring the skin temperature of the left middle finger during immersion in cold water at 0 degree C for 20 min. The athletes showed significant positive correlations between VO2max, expressed as 1/min, and CIVD as well as other peripheral cold tolerance indexes (resistance index against frostbite and CIVD index). The body weight VO2max (VO2max/kg body weight) failed to correlate significantly with either the CIVD or with other cold tolerance indexes. These results suggest that CIVD in females may depend on factors other than those determined in this study, in addition to the functional spread of the vascular beds in peripheral tissues, including striated muscle; it is known that the size and the vascular bed in this tissue are affected by exercise training and that this results in the elevation of VO2max and VO2max/kg body weight.

Humoral regulation during cold-induced coronary arterial spasm

Previous attempts to define the etiology of coronary arterial spasm have been focused on mechanisms such as autonomic nervous dysfunction and/or enhanced platelet activation. In the present study, humoral regulation was investigated in patients with vasospastic angina and scintigraphically documented transient myocardial perfusion abnormalities after a peripheral cold pressor test. Serial changes in angiotensin II, epi- and norepinephrine as well as thromboxane B2 (the stable derivate of thromboxane A2), and malondialdehyde were determined at baseline (I), immediately after 5 minutes cold water hand immersion (II), and following 10 minutes recovery (III). Angiotensin II and epinephrine remained unchanged during observation (I vs II, II vs III: P = NS). Norepinephrine was elevated after cold (I vs II: P < 0.001) and normalized after 10 minutes (I vs III: P = ns). Thromboxane B2 and malondialdehyde increased continuously (I vs III: P < 0.05 and I vs III: P < 0.002, respectively). Further radiothin-layer chromatography results indicate an activation of platelet function during myocardial ischemia. Our results do not establish a cause-effect relationship but, together with other evidence, they may suggest that thromboxane A2 is unlikely to be the cause of spasm. It might, however, play an important role in the maintenance of vasoconstriction.

The Effects of Age and Sex on Peripheral Cold Tolerance Observed from the Digital Vascular Hunting Reaction to Cold Water and the Occurrence of Chilblain

The Effects of Age and Sex on Peripheral Cold Tolerance Observed from the Digital Vascular Hunting Reaction to Cold Water and the Occurrence of Chilblain

Reversible cold-induced abnormalities in myocardial perfusion and function in systemic sclerosis.

The effects of peripheral cold exposure on myocardial perfusion and function were studied in 13 patients with scleroderma without clinically evident myocardial disease. Ten patients had at least one transient, cold-induced, myocardial perfusion defect visualized by thallium-201 scintigraphy, and 12 had reversible, cold-induced, segmental left ventricular hypokinesis by two-dimensional echocardiography. The 10 patients with transient perfusion defects all had anatomically corresponding ventricular wall motion abnormalities. No one in either of two control groups (9 normal volunteers and 7 patients with chest pain and normal coronary arteriograms) had cold-induced abnormalities. This study is the first to show the simultaneous occurrence of cold-induced abnormalities in myocardial perfusion and function in patients with scleroderma. The results suggest that cold exposure in such patients may elicit transient reflex coronary vasoconstriction resulting in reversible myocardial ischemia and dysfunction. Chronic recurrent episodes of coronary spasm may lead to focal myocardial fibrosis.

Sympathetic neurogenic control of blood flow in human nasal mucosa.

Nasal mucosal blood flow was investigated in patients undergoing a stellate ganglion blockade. Elimination of the sympathetic neurogenic control did not affect the resting blood flow in the mucosa, as registered with the 133Xe washout technique. This indicates that the basal sympathetic vasoconstrictor activity is low in the mucosal vessels that regulate blood flow. With laser doppler flowmetry, the normal pattern of spontaneous oscillations in blood flow was seen to be altered following stellate ganglion blockade. This suggests that vasomotion in the mucosa is partly dependent on sympathetic neurogenic activity. Furthermore, the decrease in blood flow normally induced by a peripheral cold provocation could not be elicited after the ganglion blockade, which means that the decrease is mediated by sympathetic vasoconstrictor fibres.

Relationship of the peripheral cold tolerance to place of birth, body mass index and alcohol consumption.

Relationship of the peripheral cold tolerance to place of birth, body mass index and alcohol consumption.

Renal and cutaneous vasomotor and respiratory rate adjustments to peripheral cold and warm stimuli and to bacterial endotoxin in conscious rabbits

In conscious rabbits peripheral cold stimuli decreased respiratory rate and increased cutaneous vasomotor tone while simultaneously renal sympathetic nervous discharge decreased. Peripheral warm stimuli produced the reverse pattern of autonomic effector activity. Injection of a bacterial endotoxin at warm ambient temperature elicited a biphasic fever response. Within the first 60 min cutaneous vasomotor tone increased, simultaneously renal sympathetic activity decreased. Thereafter, ear skin vessels dilated and renal sympathetic activity increased by about 100%. Respiratory rate remained depressed during both fever phases. Renal blood flow was investigated in a second series of experiments and showed a negative correlation with the changes of renal constrictor activity during peripheral thermal stimulation but only in the first phase of fever. The results show that renal innervation is involved in the typical thermoregulatory autonomic activity pattern by which temperature homeostasis is preserved. The vasomotor patterns of cold and heat stress developing during fever are compatible with the concept of a changed set-point of the body thermostat. The depressed respiratory rate and the lack of the renal vascular response to the increased nervous activity during the second fever phase and their reversal to normal after acetylsalicylate (ASA) indicate the participation of prostaglandins modifying peripheral and central neurotransmitter mechanisms.

Extracerebral deep-body cold sensitivity in the Pekin duck.

Pekin ducks, in which cerebral cold sensitivity is negligible, were submitted to general body cooling at warm, thermoneutral, and cold ambient temperature (Ta) with an intestinal thermode. In some animals, hypothermia was enhanced by additional hypothalamic cooling that suppressed cold defense. In other animals, the spinal cord was cooled, either selectively or during intestinal cooling. From core temperature (Tc) and metabolic heat production (M) an overall cold sensitivity of about -5 to -6 W . kg-1 . degrees C-1 was determined at thermoneutrality. Maximum M amounted to four to five times the resting M of 3.8 W . kg-1 and was attained when Tc fell by 2.5 degrees C or more. In the cold, threshold Tc for the activation of M was elevated; overall cold sensitivity remained constant. In the warmth, threshold Tc was lowered; overall cold sensitivity was reduced, if mean skin temperature (Tsk) remained at aout 39 degrees C or higher. Spinal cold sensitivity amounted to about -0.25 W . kg-1 . degrees C-1 at normal Tc and thermoneutral and warm Ta; it increased to aout -0.50 W . kg-1 . degrees C-1 in the cold and during hypothermia. Peripheral cold sensitivity was estimated from Tsk and M as -0.4 to -0.8 W . kg-1 . degrees C-1. It is concluded that overall cold sensitivity in ducks mainly depends on deep-body temperature sensors outside of the central nervous system.

Generation and processing of peripheral temperature signals in mammals.

Temperature transduction in peripheral cold receptors and processing of peripheral temperature signals in the spinal cord were studied in cats and rats. The temperature dependence of the generator potential is attributed to different temperature coefficients of an electrogenic Na-efflux and the passive Na-influx. Cold receptor activity and particularly its bursting pattern is considerably modulated by the local Ca-concentration, but the effect of elevated Ca-concentration is abolished by the ATPase blocker ouabain. — The peripheral temperature signals from the scrotal skin of rats are transformed in dorsal horn neurones (DHN) into temperature reactions, which occur only above (warm reaction) or below (cold reaction) a certain temperature threshold and are limited to an operational range of 1–4°C. Convergency of different temperature inputs were observed in one and the same DHN. Supraspinal control of temperature reactive DHN appears to be complex but predominantly excitatory.

THE EFFECT OF THE RETURN TO OKINAWA FOR SUMMER VACATION ON HEAT TOLERANCE, COLD TOLERANCE AND PERIPHERAL COLD TOLERANCE OF THE SUBTROPICAL MIGRANTS TO THE TEMPERATE ZONE

Sweating test and peripheral cold tolerance test were performed on 10 young male university students born and raised in Okinawa (the subtropical zone) but moved to the Japanese Main Islands (the temperate zone) within last three years and cold tolerance test was made on five subjects. Two series of experiments were performed in Nishinomiya, using a climatic chamber. The first series of experiments was performed in July before the return of the subjects to Okinawa (the experiment 2). The second series of experiments was performed in September after a month's stay in Okinawa in August (the experiment 1). Sweating reaction was examined on the subjects dressed in shorts only 60 min by immersing both legs in stirring water of 42 C in a room of 30 C with 70% R.H. Cold tolerance test was performed on the subjects clothed with 1.8 clo by taking off a blanket after covering with a blanket in supine position for 20 min in a room of 10 C with 70% R.H. Physiological responses of the subjects to cold were observed for 60 min. Peripheral cold tolerance test was made by dipping the left middle finger with a thermocouple attached to the nail bed into ice water for 30 min and changes of the skin temperature were measured continuously. Greater sweat volume, lower sodium concentration in sweat at the given sweat rate and less rise in oral temperature in the experiment 1 than in the experiment 2 were observed.These results indicate acclimatization to heat of the subjects was induced by the return to Okinawa in summer and heat tolerance of the subjects was slightly improved when assessed by numetrical heat tolerance index after a month's stay in Okinawa in summer.In cold tolerance test, significantly greater increase in the metabolic rate, greater frequency of shivering and considerably lower drop of the mean skin temperature in the experiment 1 than in the experiment 2 were observed. These results indicate the ratio of increase in the metabolic rate to thedrop in the mean skin temperature during cold exposure was greater in the experiment 1 than in the experiment 2. Thus it might be said that cold tolerance was reduced by the return to Okinawa in summer and living in a hot and humid climate. The mean value of time for first temperature rise of the vascular reaction of finger in the cold was significantly greater in the experiment 1 than in the experiment 2. The mean value of resistance index of frost bite caluculated by the Nakamura's method was significantly smaller in the experiment 1 than in the experiment 2. It may thus be concluded that the vascular reaction of finger in the cold is depressed and peripheral cold tolerance is reduced after the returnto Okinawa in summer.

The regulation of respiratory evaporative heat loss in the rabbit.

1. Respiratory evaporative heat loss in the rabbit has a minimum value of 0-2-0-3 W/kg and a maximum value of about 1-1 W/kg in non-evaporatively limited environments. 2. Both skin temperature and hypothalamic temperature influence respiratory evaporative heat loss, and they do so in a multiplicative fashion. Thus, at low skin temperature the hypothalamic temperature threshold for the onset of panting is above normal hypothalamic temperature and hypothalamic thermosensitivity is high. On the other hand, at high skin temperatures, the hypothalamic temperature threshold for the onset of panting is well below normal hypothalamic temperature, but hypothalamic thermosensitivity is greatly reduced. 3. The influence of mean skin temperature (Tsk) and hypothalamic temperature on respiratory evaporative heat loss (Eres) in the rabbit can be described by the equation: Eres=1-1-0-08 (Tsk-39-7) (Thy-42-9) greater than or equal to 0-3 W/kg. 4. Thus, the ability of a lowered mean skin temperature to increase the thermosensitivity of the hypothalamus in response to local temperature changes applies to heat loss mechanisms as well as heat production mechanisms. It is suggested that the characteristics of this peripheral input into the C.N.S. are fulfilled by tonic cold fibre input originating from the peripheral cold receptors on the body surface.

Metabolic reactions to changes in core and skin temperature in man.

The metabolic cold response, i.e. the increase in oxygen consumption above that for the given activity in a neutral environment, was measured in 7 subjects during cooling, resting or swimming in cold water (14, 16, 18, 20degrees C) and during rewarming in air (Ta 20, 30, 40degrees C), bicycling or resting. Esophageal temperatures varied between 38 and 34degrees C. Mean skin temperature was considered as equal to water temperature during cooling, and ranged between 25-35degrees C during rewarming in the different environments. Both central and peripheral cold stimulation induced metabolic cold responses. The skin temperature was the dominating factor in determining the response, especially in transient states. During rewarding a rising skin temperature suppressed the effects of even very low core temperatures.

Plasma ADH increase and thirst suppression elicited by preoptic heating in the dog.

Plasma ADH increase and thirst suppression elicited by preoptic heating in the dog.