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PubMed2000

Pharmacokinetic-Pharmacodynamic Modelling of the antipyretic effect of two oral formulations of ibuprofen.

OBJECTIVE: To analyse the population pharmacokinetic-pharmacodynamic relationships of racemic ibuprofen administered in suspension or as effervescent granules with the aim of exploring the effect of formulation on the relevant pharmacodynamic parameters. DESIGN: The pharmacokinetic model was developed from a randomised, cross-over bioequivalence study of the 2 formulations in healthy adults. The pharmacodynamic model was developed from a randomised, multicentre, single dose efficacy and safety study of the 2 formulations in febrile children. PATIENTS AND PARTICIPANTS: Pharmacokinetics were studied in 18 healthy volunteers aged 18 to 45 years, and pharmacodynamics were studied in 103 febrile children aged between 4 and 16 years with bodyweight 225kg. METHODS: The pharmacokinetic study consisted of two 1-day study occasions, each separated by a 1-week washout period. On each occasion ibuprofen 400mg was administered orally as suspension or granules. The time course of the antipyretic effect was evaluated in febrile children receiving a single oral dose of 7 mg/kg in suspension or 200 or 400mg as effervescent granules. During the pharmacodynamic analysis, the predicted typical pharmacokinetic profile (based on the pharmacokinetic model previously developed) was used. RESULTS: The disposition of ibuprofen was described by a 2-compartment model. No statistical differences (p > 0.05) were found between the 2 formulations in the distribution and elimination parameters. Absorption of ibuprofen from suspension was adequately described by a first-order process; however, a model with 2 parallel first-order input sites was used for the drug given as effervescent granules, leading to time to reach maximum drug concentration (tmax) values of 0.9 and 1.9 hours for suspension and granules, respectively. The time course of the antipyretic effect was best described using an indirect response model. The estimates (with percentage coefficients of variation in parentheses) of Emax (maximum inhibition of the zero-order synthesis rate of the factor causing fever), EC50 (plasma concentration eliciting half of Emax), n (slope parameter) and k(out) (first order rate constant of degradation) were 0.055 (10), 6.16 (14) mg/L, 2.71 (18) and 1.17 (23) h(-1), respectively, where To is the estimate of the basal temperature, 38.8 (1) degrees C. No significant (p > 0.05) covariate effects (including pharmaceutical formulation) were detected in any of the pharmacodynamic parameters. CONCLUSIONS: Because of the indirect nature of the effect exerted by ibuprofen, the implications of differences found in the plasma drug concentration profiles between suspension and effervescent granules are less apparent in the therapeutic response.

Adolescent↗
PubMed1997

Metabolic changes in elderly cancer patients after glucose ingestion. The role of tumor necrosis factor-alpha.

BACKGROUND: Previous studies have demonstrated an increased basal metabolic rate in cancer patients. However, no previous study has investigated the changes in energy expenditure and substrate oxidation after administration of a glucose load. Furthermore, the role of tumor necrosis factor-alpha (TNF-alpha) on cancer-induced metabolic changes is still a neglected area. METHODS: In 25 cancer patients and 16 healthy subjects matched with regard to age, body mass index, and fat-free mass, indirect calorimetry was made before and after administration of a glucose load (75 g per subject, administered orally). RESULTS: Cancer patients had fasting plasma concentrations of insulin (74 +/- 3.3 vs. 67 +/- 4.1 pmol/L; P < 0.05), lactate (0.68 +/- 0.11 vs. 0.41 +/- 0.1 mmol/L; P < 0.05), free fatty acids (884 +/- 121 vs. 342 +/- 76 mmol/mL; P < 0.001), and TNF-alpha (1.23 +/- 0.31 vs. 0.45 +/- 0.11 ng/mL; P < 0.01) greater than controls, whereas plasma glucose concentrations (4.8 +/- 0.5 vs. 5.1 +/- 0.3 mmol/L; P = not significant) were not different from controls. Indirect calorimetry at baseline demonstrated that basal metabolic rate, fat oxidation, and protein oxidation were significantly greater in cancer patients than in controls. After administration of the glucose load, carbohydrate oxidation progressively rose in both cancer patients and controls, with no differences between the two groups, whereas glucose uptake (59.3 +/- 3.8 vs.69.1 +/- 3.6 g/kg fat-free mass [FFM] x 240 minutes; P < 0.01) and storage (49.1 +/- 4.1 vs. 60.2 +/- 3.3 g/kg FFM x 240 minutes; P < 0.05) were markedly reduced in cancer patients as compared with controls. Finally, glucose-induced thermogenesis (GIT) was lower in cancer patients than in controls. CONCLUSIONS: This study demonstrated that GIT is lower in cancer patients than in healthy subjects matched with regard to age and body mass index. An overactivity of the glucose fatty acid cycle is responsible for such results. Plasma concentrations of TNF-alpha might play a modulating role in the metabolic changes that occur after administration of a glucose load. The role of TNF-alpha on glucose and lipid metabolism in cancer patients would be a worthy subject of future investigations.

Aged↗
PubMed1995

[Thermogenesis and energy utilization of olive oil and fish oil in a model study with sows].

An animal model experiment was conducted with nine adult sows to study the effect of olive oil and fish oil (40% polyunsaturated fatty acids) on thermogenesis compared to wheat starch as control. The treatments were given to each animal according to a latin square design. The basal diet (20 g DM/kg W0.75) was mainly based on barley and soybean meal, and matched 60% of the ME requirements with all the other nutrients meeting maintenance requirements. The isoenergetic supplements amounted to 176 kJ gross energy per kg W0.75 and day. During each experimental period a complete energy balance was recorded for each animal using indirect calorimetry technique (RQ-method) as well as the carbon-nitrogen-balance technique. The treatments did not influence the digestibility of the rations. Digestibility of energy and of carbon averaged 83.4% and 83.3%, respectively. All three supplements were nearly completely digested as calculated by the difference method. Fish oil increased urine energy and decreased CH4 production, the shifts, however, were in absolute terms very small. The mean O2 consumption was 1,002 l/d showing no significant treatment effects. CO2 production was lowered with olive oil by 10%, and with fish oil by 13% compared to the starch diet. The daily heat production was 20.95, 20.72, and 20.04 MJ when starch, olive oil or fish oil was given. Corrected for equal energy retention the difference of thermogenesis between olive oil and starch was -0.4 MJ/d, and between fish oil and starch -1.2 MJ/d. These differences corresponded to a relation of starch:olive oil:fish oil = 1:0.95:0.86. The relation between starch and olive oil reflected exactly the theoretical expectation, calculated from the ATP regeneration by oxidation of both nutrients. When fish oil was added, the daily heat production was lower than theoretically calculated, which might be interpreted as an effect on the metabolic rate in general rather than especially on the efficiency of ATP formation from fish oil oxidation. In any case, there was no hint of a facultative thermogenesis induced by the oils.

Adenosine Triphosphate↗
PubMed2005

Living at the physiological limits: field and maximum metabolic rates of the common shrew (Sorex araneus).

Shrews (genus Sorex, small insectivorous mammals) are well known for their extremely high basal metabolic rates (BMRs) even when corrected for their small body size. We measured energy expenditure of the common shrew (Sorex araneus) under natural conditions (field metabolic rate [FMR]) by doubly labeled water method to test whether FMR is proportional to high BMR in this species. The study was performed in summer in northeastern Poland. In addition to the FMR, we also measured maximum metabolic rates induced by cold exposure and by intense activity (MMRCOLD and MMRRUN, respectively) to evaluate the aerobic reserve (MMR-FMR) in S. araneus. This aerobic reserve was used as an indicator of the potential for metabolic constraints. The FMR averaged 2.31+/-0.32 L CO2 d(-1) (+/-SD) or 58.1+/-8.0 kJ d(-1) in 8.2-g animals. This figure constituted 216%-258% of a value predicted for a "standard" mammal of the same body mass and was the highest mass-specific field metabolic rate in mammals. Because of the high BMR level in S. araneus, the FMR to BMR ratio (2.4) was not far off mammalian standards (median value of 3.1). The rate of water efflux determined in S. araneus (20.2 mL H2O d(-1) or 2.46 mL H2O g(-1) d(-1)) exceeded all figures reported to date in other mammals and was apparently linked to the high FMR level and relatively high water content of shrews' food. Maximal metabolic rates (MMRRUN of 18.1+/-1.6 mL O2 g(-1) h(-1) and MMRCOLD of 23.5+/-1.9 mL O2 g(-1) h(-1)) were not high in proportion to BMR or FMR that resulted in relatively narrow aerobic reserve in S. araneus: 20% when calculated against the MMRRUN and 39% when compared with the MMRCOLD. Our study reveals that S. araneus has high energy costs of living and operates close to its physiological limits.

Analysis of Variance↗
PubMed1995

Temperature changes of > or = 1 degree C alter functional neurologic outcome and histopathology in a canine model of complete cerebral ischemia.

BACKGROUND: Changes in basal temperature of > or = 1 degree C (e.g., fever-induced hyperthermia or anesthesia-related hypothermia) are a common occurrence in neurologically impaired patients. The current study tested the hypothesis that temperature changes as small as 1 degree C or 2 degrees C would significantly alter post-ischemic functional neurologic outcome and cerebral histopathology. The hypothesis was tested in a canine model of transient, complete cerebral ischemia. METHODS: After institutional approval, 21 dogs were randomly assigned to one of three temperature-specific groups: (1) a reference group maintained at 37.0 +/- 0.3 degree C (target temperature +/- range); (2) a 38.0 +/- 0.3 degree C group; or (3) a 39.0 +/- 0.3 degree C group (n = 7 per group). Complete cerebral ischemia 12.5 min in duration was produced using an established model of arterial hypotension plus intracranial hypertension. Right atrial and cranial (beneath the temporalis muscles) temperatures were maintained at the target value, beginning 20 min before ischemia and ceasing 1 h postischemia. Thereafter, temperatures were returned to 37.0 +/- 0.3 degree C in all dogs. After discharge from the intensive care environment, all dogs were placed in a temperature-controlled recovery area. Neurologic assessment was performed by a blinded observer at 24, 48, and 72 h postischemia using a 100-point scoring scale. After the 72 h examination (with the dogs anesthetized) or at the time of ischemia-related death, the brains were excised and preserved. The brains subsequently were histologically scored by a neuropathologist who was unaware of the treatment groups. All 21 dogs were included in the analysis of neurologic function; however, only dogs that survived for > or = 24 h postischemia were included in the histopathology analysis. RESULTS: Dogs were well matched for systemic physiologic variables throughout the study, with the exception of temperature. During the 72 h postischemic examination, dogs maintained at 37 degrees C were either normal or near normal. In contrast, dogs maintained at 39 degrees C were either comatose or died from ischemia-related causes. Dogs maintained at 38 degrees C were intermediate between 37 degrees C and 39 degrees C dogs. When compared with the reference group, both 38 degrees C and 39 degrees C dogs had significantly worse neurologic function scores (P < 0.01 and < 0.001, respectively) and histopathology scores (P < 0.01 for both). There also was a significant correlation between neurologic function and histopathology rank scores (rs = 0.96; P < 0.001). CONCLUSIONS: Small, clinically relevant changes in temperature (1 degree C or 2 degrees C) resulted in significant alterations in both postischemic neurologic function and cerebral histopathology. Assuming that our results are transferable to humans, the results suggest that, in patients at imminent risk for ischemic neurologic injury, body temperature should be closely monitored. Further, the clinician should aggressively treat all episodes of hyperthermia until the patient is no longer at risk for ischemic neurologic injury.

Animals↗
PubMed1998

Thermogenic effects of sibutramine in humans.

BACKGROUND: Sibutramine is an effective compound for the treatment of obesity, acting both on serotonergic and noradrenergic pathways. Animal studies have shown that sibutramine exerts its effect by enhancing satiety as well as by increasing thermogenesis. OBJECTIVE: We tried to compare the acute thermogenic effect of a single 30-mg dose of sibutramine with placebo on basal energy expenditure (EE) and diet-induced thermogenesis. DESIGN: The study was randomized, double-blind, and placebo controlled. Eleven healthy, normal-weight men underwent 4 distinct treatment regimens separated by washout periods of 6-10 d. EE was measured by indirect calorimetry before and for 5.5 h after sibutramine or placebo administration with or without a 2.1-MJ breakfast. Visual analogue scales for assessment of appetite were completed hourly. RESULTS: Sibutramine caused a significant increase in EE above that for placebo (over 5.5 h) during both the fed (34%, 0.15 kJ/min) and fasted (183%, 0.20 kJ/min) states (P < 0.02) as well as during the last 3.5 h of this 5.5-h period and in the fed (87%, 0.26 kJ/min) and fasted (152%, 0.22 kJ/min) states, respectively (P < 0.01). The sibutramine-induced increase in EE was accompanied by an increase in plasma epinephrine (P < 0.01), heart rate (P < 0.001), blood pressure (P < 0.05), and plasma glucose (P < 0.02). About 25% of the increased heart rate with sibutramine could be explained by increased thermogenesis. Sibutramine increased satiety more than did placebo (5-h area under the curve, P < 0.05). CONCLUSIONS: Sibutramine caused a significant increase in both EE and satiety, which may both contribute to its weight-reducing properties.

Adult↗
PubMed1999

The effect of sibutramine on resting energy expenditure and adrenaline-induced thermogenesis in obese females.

BACKGROUND: Sibutramine, an inhibitor of serotonin and noradrenaline uptake, reduces appetite to cause weight loss. This study tested the hypothesis that an increase in energy expenditure also contributes to this weight loss. In addition, the effects of sibutramine on adrenaline induced changes in heart rate and cardiac output were determined METHODS: Nineteen obese females randomly received either sibutramine 15 mg daily or placebo for 12 weeks along with dietary advice. Resting energy expenditure (REE) was measured and then energy expenditure was measured during a 30 min infusion of adrenaline (25 ng/min/kg IBW). Cardiac output and heart rate, measured by Duplex Colour Doppler ultrasonography, were similarly measured in the basal state and post adrenaline. All measurements were recorded at baseline and then after 12 weeks. RESULTS: Ten patients who received sibutramine reduced their weight by 8.1+/-3.8% while 9 placebo treated subjects reduced their weight by 5.1+/-4.4%, P=0.13. In absolute terms, REE decreased in placebo subjects from 1500+/-201 kcal/24 h to 1357+/-231 kcal/24 h (9.4+/-9.9%) and in sibutramine subjects from 1540+/-184 kcal/24 h to 1444+/-128 kcal/24 h (5.3+/-12.0%), P=0.77. The increased weight loss in the sibutramine group was associated with an increase in the FFM adjusted REE (2.2+/-16.1%) unlike the expected decrease (5.8+/-9.5%) in the placebo group (P=0.11). There was some suggestion (P=0.09) that the usual positive correlation between loss of weight and decline in REE was lost in the sibutramine group (r=-0.30) compared with placebo (r=0.35). There was a negative correlation between loss of FFM and decline in REE/kg FFM and (P=0.029) which was not evident in placebo (P=0.83). Adrenaline induced energy expenditure was similar in the two groups at the end of the 12 week period and there were no significant cardiovascular changes between the two groups. CONCLUSIONS: Sibutramine limits the decline in REE associated with weight loss, equivalent to about 100 kcal/d. This could allow greater numbers of people to maintain a greater degree of weight loss.

Adult↗
PubMedDate not supplied

Autorhythmometry in hypertension: some methodological aspects and clinical implications.

Autorhythmometry of blood pressure is a technique easy to be performed and well accepted by hypertensive patients. A simple inspection of data self-collected 5 times a day for many days constitute a sufficiently reliable automonitoring of blood pressure both in basal conditions and in relation to the efficacy of some dietary and/or pharmacological treatment. Several examples are reported to show that more sophisticated statistical manipulation of the data collected may give rise to a better understanding of some clinical and physiological aspects. Both analysis of variance, performed on individual subsets of data averaged at each sampling hour, and single cosinor, performed on longitudinal time series, may be used to detect and quantify a circadian rhythm as a systematic daily variation, averaging towards zero the noise superimposed to the actual time series. Serial section analysis of the data, along all the experimental span, is useful to detect a) the reproducibility of the rhythm b) the variation of its parameters induced by changes in the experimental conditions c) the long-term trend. In the first subject the influence on the circadian rhythm of the pulse rate, temperature and blood pressure, due to a 4 h advancing shift in the rest-activity synchronizer, is well documented. In the first hypertensive patient a circadian rhythm is demonstrated also in blood pressure during two non-consecutive months. No difference is detected in both mesor and amplitude of blood pressure and a full resynchronization of the acrophase is achieved when a 1 h delaying shift in the rest activity synchronizer is imposed. In the second patient a well reproducible rhythm of systolic blood pressure and a low noise/signal ratio is documented by the serial section display. In the third patient the 'lability' of hypertention seems mainly due to salt sensitivity, as documented by the significant lowering of the mesor in the second experimental span, when a lowering of only 30 mEq/day in salt intake is imposed. The serial section better documents the salt-sensitivity of this patient, during a span when loading and depressing of salt intake is imposed. In the last patient the prompt effect of therapy in lowering blood pressure within normal range is well documented by serial section with 3 day interval. A possible effect of masking the circadian rhythm of blood pressure, due to therapy, is inferred by the serial section display with an interval of the same length (33 days) as the subspan without therapy. The possibility of prevention in the hypertensive disease is discussed, with the aim of autorhythmometry and statistical methods employed in this paper.

Adult↗
PubMed1993

Brain death-induced cardiac contractile dysfunction and long-term cardiac preservation. Rat heart studies of the effects of hypophysectomy.

BACKGROUND: Ischemic brain death induces cardiac contractile dysfunction, which may exclude the heart as a donor organ for transplantation; the mechanism is unknown. Since cerebral ischemia might alter pituitary function, we investigated the influence of hypophysectomy on basal contractile function, brain death-induced contractile malfunction, and the tolerance of the heart to hypothermic ischemic storage. METHODS AND RESULTS: Rats were hypophysectomized and maintained for 5 days; during this time, left ventricular developed pressure (LVDP) fell to 70% of its control value (92 +/- 8 versus 132 +/- 6 mm Hg, P < .05). Diastolic function of isolated blood-perfused hearts 5 days after hypophysectomy was severely impaired (left ventricular volume at 12 mm Hg of end-diastolic pressure was 141 +/- 20 versus 250 +/- 30 microL in sham-operated control rats; P < .05). Brain death in nonhypophysectomized rats resulted in a transient increase in mean arterial pressure (from 112 +/- 4 to 180 +/- 7 mm Hg within the first 30 seconds) followed by a rapid decline to less than 50% of the control value (54 +/- 3 mm Hg after 5 minutes, P < .05). Changes in cardiac function were comparable (cardiac index fell from 34 +/- 2 to 17 +/- 1 mL/min per 100 g body weight, and stroke volume index fell from 82 +/- 5 to 41 +/- 4 microL per beat per 100 g body weight within 10 minutes; P < .05). Brain death in hypophysectomized rats resulted in a similar (but attenuated) biphasic response with arterial pressure (already reduced to 82 +/- 9 mm Hg as a consequence of hypophysectomy) transiently increasing to 144 +/- 9 mm Hg after 30 seconds and then falling to 52 +/- 5 mm Hg by 5 minutes. Finally, we assessed the effects of coincident hypophysectomy and brain death on the ability of the heart to recover from 6 hours of hypothermic (4 degrees C) ischemic storage. Brain death alone had no effect on the postischemic recovery of LVDP (133 +/- 14 versus 129 +/- 12 mm Hg at 8 mm Hg of end-diastolic pressure in the non-brain death group). LVDP in hearts from hypophysectomized rats with brain death recovered to only 84 +/- 13 mm Hg; however, this was virtually identical to the LVDP in hearts from hypophysectomized rats that had not been subjected to brain death (83 +/- 5 mm Hg) or had not even been exposed to hypothermic ischemia (83 +/- 10 mm Hg). CONCLUSIONS: Hypophysectomy induces a deterioration of cardiac function that becomes apparent after 2 days. However, it does not exacerbate the cardiac dysfunction induced by brain death. Hearts from hypophysectomized animals, with or without brain death, recovered less well after prolonged hypothermic storage; nevertheless, the hearts recovered to preischemic levels, indicating that, although hypophysectomy impairs cardiac contractile function, it does not adversely influence the tolerance of the heart to hypothermic ischemia. Pituitary function may be an important factor in determining cardiac function without influencing resistance to ischemia or responses to brain injury.

Animals↗
PubMed1996

Autoregulation of body composition during weight recovery in human: the Minnesota Experiment revisited.

OBJECTIVES: To gain insights into the control systems underlying human variability in the regulation of body composition during weight recovery, as well as the disproportionate recovery of fat relative to lean tissue, the classical Minnesota Experiment conducted on 32 men subjected to long-term semi-starvation and refeeding was revisited with the following objectives: (1) to determine whether the control of energy-partitioning between lean and fat tissues during weight loss and weight recovery is an individual characteristic, and if a predictor can be statistically identified, (2) to determine whether the reduction in thermogenesis during weight loss persists during weight recovery, and underlies the disproportionate recovery of fat tissue and (3) to integrate the control of energy-partitioning and that of thermogenesis in order to explain the pattern of lean and fat tissue mobilisation and deposition during weight loss and weight recovery. METHODS: Individual data on body weight, body fat, fat-free-mass (FFM), and basal metabolic rate (BMR), assessed during the control baseline period (i.e. prior to weight loss), at the end of 24 weeks of semi-starvation, and at the end of a 12 week period of restricted refeeding, were used to calculate the following parameters: (i) a quantitative index of energy-partitioning, the P-ratio, defined as the proportion of body energy mobilised as protein during weight loss, or as the proportion of body energy deposited as protein during weight recovery, (ii) a quantitative index of changes in thermogenesis, defined as the change in BMR adjusted for FFM (or for both FFM and fat mass) and (iii) the degree of replenishment of fat and FFM compartments, defined as the recovery of body fat and FFM (during refeeding) as a percentage of that lost during semi-starvation. RESULTS: This re-analysis indicates the following: (i) a large inter-individual variability in P-ratio during both weight loss and weight recovery, but for a given individual, the P-ratio during refeeding is strongly correlated with the P-ratio during semi-starvation, (ii) body composition during the control period is the most important predictor of variability in P-ratio, such that the higher the initial % body fat, the lower the proportion of energy mobilised as protein, and hence the greater the propensity to mobilise fat during semi-starvation and to subsequently deposit fat during refeeding and (iii) at week 12 of refeeding, the change in adjusted BMR is found to be reduced by a magnitude which is inversely proportional to the degree of fat recovery, but is unrelated to the degree of FFM recovery. A quantitative relationship is derived between the P-ratio during refeeding, the % fat recovery, and the P-ratio during semi-starvation. CONCLUSIONS: Evidence is presented here suggesting that (i) human variability in the pattern of lean and fat tissue deposition during weight recovery is to a large extent determined by individual variations in the control of energy-partitioning, for which the initial % body fat is the most important predictor and (ii) the disproportionate gain in fat relative to lean tissue during weight recovery is contributed by a reduction in thermogenesis (i.e. increased efficiency of food utilization) for accelerating specifically the replenishment of the fat stores. These control systems, operating via energy-partitioning and thermogenesis, have been integrated into a compartmental model for the regulation of body composition during underfeeding/refeeding, and can be used to explain the individual pattern of lean and fat tissue deposition during weight recovery in situations ranging from the rehabilitation after malnutrition to the relapse of obesity.

Adipose Tissue↗
PubMedDate not supplied

[Response of skin blood flow to several respiratory maneuvers in healthy subjects].

INTRODUCTION: In the diagnosis of autonomic disturbances, the variability of skin blood flow (SBF) and the sympathetic skin response (SSR) in response to several respiratory maneuvers are not routinely studied. OBJECTIVE: We sought to standardize the method of SBF variability and SSR in healthy subjects during four respiratory maneuvers: 1) spontaneous breathing (SB); 2) rhythmic breathing at a rate of 6 per minute (RB); 3) sudden deep inspiration (SDI); 4) Valsalva maneuver (VM). SUBJECTS, MATERIAL AND METHOD: We studied 30 healthy subjects with a mean age of 32 years, 60% were men and 40% women. We used a photopletysmograph in the finger pad to measure SBF and surface electrodes on the palms of the hand to register the SSR. We also recorded the ECG and the respiratory movements. The variables were: 1) amplitude of SBF; 2) latency and duration of SSR; 3) percentage of decrease of the SBF during the maneuvers compared with the basal flow. RESULTS: During spontaneous breathing there was no respiratory modulation of the SBF and during RB the SBF was modulated with respiration. With SDI there was a 60% decrease of the SBF. VM induced a larger SBF decrease of 72 per cent. A significant statistical difference was revealed when we compared the decrease of SBF basal breathing with SDI and VM (P < 0.001). The difference was also significant between the SDI and VM (P < 0.001). The SBF decrease recovered more slowly after the SDI (beat 7) than after the VM (veat 6). The SBF decrease was more pronounced in magnitude during the VM. The latency of the SSR appears spontaneously and at random in 57% of subjects during normal breathing but it appeared consistently during RB, SDI, and VM. The latency of SSR was longer during SB (1.7 +/- 0.7 s), RB (1.6 +/- 0.7 s) than SDI (0.7 +/- 0.5 s) and VM (0.8 +/- 0.9 s) (P > 0.050). Duration of the SSR was significantly longer in the SDI (around 7.8 +/- 2.4 s) and during the VM (8 +/- 2.5 s) as compared to normal breathing (6.3 +/- 1.0 s) and RB (6.4 +/- 1.5 s) (P < 0.009). CONCLUSIONS: SB and RB induce periodic modulation of sympathetic activity to skin blood vessels and sweat glands. SDI and VM produced a much greater activation of sympathetic skin activity than SB and RB. The increased SSR duration and the profound SBF decrease with SDI and VM as compared to SB or RB are consistent with this hypothesis. The latency of the SSR is much shorter with SDI and VM than with SB or RB. The most likely explanation is that the SSR, under these circumstances, results from a central command. The recovery to normal SBF is faster after the VM as compared to SDI. This suggests that the withdrawal of sympathetic responses is faster after the VM. The explanation for this is unknown but suggests that it might be baroreceptor mediated.

Adult↗