Alterations in glucose kinetics induced by pentobarbital anesthesia

1987 ◽  
Vol 253 (6) ◽  
pp. E657-E663 ◽  
Author(s):  
C. H. Lang ◽  
G. J. Bagby ◽  
D. M. Hargrove ◽  
P. M. Hyde ◽  
J. J. Spitzer
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Body Temperature ◽  
Glucose Metabolism ◽  
Carbohydrate Metabolism ◽  
Whole Body ◽  
Metabolic Clearance ◽  
Glucose Kinetics ◽  
Arterial Blood ◽  
Anesthetized Rats

Because pentobarbital is often used in investigations related to carbohydrate metabolism, the in vivo effect of this drug on glucose homeostasis was studied. Glucose kinetics, assessed by the constant intravenous infusion of [6-3H]- and [U-14C]glucose, were determined in three groups of catheterized fasted rats: conscious, anesthetized and body temperature maintained, and anesthetized but body temperature not maintained. After induction of anesthesia, marked hypothermia (5 degrees C decrease in core temperature) developed in rats not provided with external heat. Anesthetized rats that developed hypothermia showed a decrease in mean arterial blood pressure (25%) and heart rate (40%), whereas no differences were seen in blood pressure and heart rate of conscious and euthermic anesthetized rats. Likewise, the plasma lactate concentration and the rates of glucose appearance, recycling, and metabolic clearance were reduced by 30-50% in the hypothermic anesthetized rats. Changes in whole-body carbohydrate metabolism were prevented when body temperature was maintained. Because plasma pentobarbital levels were similar between the euthermic and hypothermic rats during the first 2 h of the experiment, the rapid reduction in glucose metabolism in this latter group appears related to the decrease in body temperature. The continuous infusion of epinephrine produced alterations in glucose kinetics that were not different between conscious animals and anesthetized rats with body temperature maintained. However, marked differences were seen in hypothermic rats. Thus pentobarbital-anesthetized rats became hypothermic when kept at room temperature and exhibited marked decreases in glucose metabolism. Such changes were absent when body temperature was maintained during anesthesia.

scholarly journals Heat Stress and Cardiovascular, Hormonal, and Heat Shock Proteins in Humans

2012 ◽  
Vol 47 (2) ◽  
pp. 184-190 ◽  
Author(s):  
Masaki Iguchi ◽  
Andrew E. Littmann ◽  
Shuo-Hsiu Chang ◽  
Lydia A. Wester ◽  
Jane S. Knipper ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Heat Shock ◽  
Body Temperature ◽  
Controlled Trial ◽  
Whole Body ◽  
Cord Injury ◽  
Whole Body Heat Stress ◽  
Body Heat

Context: Conditions such as osteoarthritis, obesity, and spinal cord injury limit the ability of patients to exercise, preventing them from experiencing many well-documented physiologic stressors. Recent evidence indicates that some of these stressors might derive from exercise-induced body temperature increases. Objective: To determine whether whole-body heat stress without exercise triggers cardiovascular, hormonal, and extra-cellular protein responses of exercise. Design: Randomized controlled trial. Setting: University research laboratory. Patients or Other Participants: Twenty-five young, healthy adults (13 men, 12 women; age = 22.1 ± 2.4 years, height = 175.2 ± 11.6 cm, mass = 69.4 ± 14.8 kg, body mass index = 22.6 ± 4.0) volunteered. Intervention(s): Participants sat in a heat stress chamber with heat (73°C) and without heat (26°C) stress for 30 minutes on separate days. We obtained blood samples from a subset of 13 participants (7 men, 6 women) before and after exposure to heat stress. Main Outcome Measure(s): Extracellular heat shock protein (HSP72) and catecholamine plasma concentration, heart rate, blood pressure, and heat perception. Results: After 30 minutes of heat stress, body temperature measured via rectal sensor increased by 0.8°C. Heart rate increased linearly to 131.4 ± 22.4 beats per minute (F6,24 = 186, P < .001) and systolic and diastolic blood pressure decreased by 16 mm Hg (F6,24 = 10.1, P < .001) and 5 mm Hg (F6,24 = 5.4, P < .001), respectively. Norepinephrine (F1,12 = 12.1, P = .004) and prolactin (F1,12 = 30.2, P < .001) increased in the plasma (58% and 285%, respectively) (P < .05). The HSP72 (F1,12 = 44.7, P < .001) level increased with heat stress by 48.7% ± 53.9%. No cardiovascular or blood variables showed changes during the control trials (quiet sitting in the heat chamber with no heat stress), resulting in differences between heat and control trials. Conclusions: We found that whole-body heat stress triggers some of the physiologic responses observed with exercise. Future studies are necessary to investigate whether carefully prescribed heat stress constitutes a method to augment or supplement exercise.

scholarly journals Heat stress alters hemodynamic responses during the Valsalva maneuver

2010 ◽  
Vol 108 (6) ◽  
pp. 1591-1594 ◽  
Author(s):  
Scott L. Davis ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Phase Ii ◽  
Valsalva Maneuver ◽  
Late Phase ◽  
Thermal Conditions ◽  
Whole Body ◽  
Hemodynamic Responses ◽  
Arterial Blood

The Valsalva maneuver can be used as a noninvasive index of autonomic control of blood pressure and heart rate. The purpose of this investigation was to test the hypothesis that sympathetic mediated vasoconstriction, as referenced by hemodynamic responses during late phase II (phase IIb) of the Valsalva maneuver, is inhibited during whole body heating. Seven individuals (5 men, 2 women) performed three Valsalva maneuvers (each at a 30-mmHg expiratory pressure for 15 s) during normothermia and again during whole body heating (increase sublingual temperature ∼0.8°C via water-perfused suit). Each Valsalva maneuver was separated by a minimum of 5 min. Beat-to-beat mean arterial blood pressure (MAP) and heart rate were measured during each Valsalva maneuver, and responses for each phase were averaged across the three Valsalva maneuvers for both thermal conditions. Baseline MAP was not significantly different between normothermic (88 ± 11 mmHg) and heat stress (84 ± 9 mmHg) conditions. The change in MAP (ΔMAP) relative to pre-Valsalva MAP during phases IIa and IIb was significantly lower during heat stress (IIa = −20 ± 8 mmHg; IIb = −13 ± 7 mmHg) compared with normothermia (IIa = −1 ± 15 mmHg; IIb = 3 ± 13 mmHg). ΔMAP from pre-Valsalva baseline during phase IV was significantly higher during heat stress (25 ± 10 mmHg) compared with normothermia (8 ± 9 mmHg). Counter to the proposed hypothesis, the increase in MAP from the end of phase IIa to the end of phase IIb during heat stress was not attenuated. Conversely, this increase in MAP tended to be greater during heat stress relative to normothermia ( P = 0.06), suggesting that sympathetic activation may be elevated during this phase of the Valsalva while heat stressed. These data show that heat stress does not attenuate this index of vasoconstrictor responsiveness during the Valsalva maneuver.

Measurement Of Bradykinin-Induced Venous Dilation By Ultrasound And Correlation With Heart Rate, Arterial And Venous Pressure And Endothelial Damage

1981 ◽  
Author(s):  
G J Stewart ◽  
R G Schaub ◽  
R E Cartee
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Carotid Arteries ◽  
Jugular Vein ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Endothelial Damage ◽  
Whole Body ◽  
Arterial Blood

This study was done to correlate known cardiovascular responses to bradykinin (increased heart rate, lowered arterial blood pressure) with recently demonstrated endothelial damage and proposed venous dilation. Healthy dogs of mixed breed were used. Blood pressures and heart rate were monitored and recorded on a Narco physiograph. The diameter of a jugular vein was monitored with an ADR ultrasound machine using a 10 MHz probe with linear array of crystals and recorded on polaroid prints. Jugular veins and carotid arteries were removed and prepared for scanning electron microscopy after removal of blood and partial in situ fixation by whole body perfusion. The response of arterial pressure was dose dependent with no change at 6 ug/min, variable drop at 12 ug/min and 22-40% drop at 60 ug/min and above. Venous pressure increased in 1 dog but was unchanged in 4 others. The increase of heart rate paralled the drop in arterial blood pressure. The diameter of a jugular vein increased in 3 of 3 monitored dogs by 25, 33, 50% of baseline diameter (average increase 36%) with high (300 ug/min) bradykinin. Endothelial damage (microtears) occurred around 70-80% of branches, at some valves and on the main vessel occassionally. The tears were infiltrated with leukocytes and some red cells and platelets indicating that tearing occurred while blood was still circulating, i.e. before dissection for removal of vessels. Carotid arteries showed no tears. Dilation of arteries would be limited by their elastic layers (missing in veins). These observations show that venous dilation and endothelial tearing around side branches are part of the cardiovascular response to blood born bradykinin. They also show that venous dilation can be measured by ultrasound.

scholarly journals Heart Rate and Arterial Pressure Changes during Whole-Body Deep Hypothermia

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Giacomo Cavallaro ◽  
Luca Filippi ◽  
Genny Raffaeli ◽  
Gloria Cristofori ◽  
Federico Schena ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mild Hypothermia ◽  
Clinical Signs ◽  
Deep Hypothermia ◽  
Whole Body ◽  
Arterial Blood ◽  
Significant Difference ◽  
Pressure Changes ◽  
Ischemic Encephalopathy

Whole-body deep hypothermia (DH) could be a new therapeutic strategy for asphyxiated newborn. This retrospective study describes how DH modified the heart rate and arterial blood pressure if compared to mild hypothermia (MH). Fourteen in DH and 17 in MH were cooled within the first six hours of life and for the following 72 hours. Hypothermia criteria were gestational age ≥36 weeks; birth weight ≥1800 g; clinical signs of moderate/severe hypoxic-ischemic encephalopathy. Rewarming was obtained in the following 6–12 hours (0.5°C/h) after cooling. Heart rates were the same between the two groups; there was statistically significant difference at the beginning of hypothermia and during rewarming. Three babies in the DH group and 2 in the MH group showed HR < 80 bpm and QTc > 520 ms. Infant submitted to deep hypothermia had not bradycardia or Qtc elongation before cooling and after rewarming. Blood pressure was significantly lower in DH compared to MH during the cooling, and peculiar was the hypotension during rewarming in DH group. Conclusion. The deeper hypothermia is a safe and feasible, only if it is performed by a well-trained team. DH should only be associated with a clinical trial and prospective randomized trials to validate its use.

Strength training reduces arterial blood pressure but not sympathetic neural activity in young normotensive subjects

2003 ◽  
Vol 94 (6) ◽  
pp. 2212-2216 ◽  
Author(s):  
Jason R. Carter ◽  
Chester A. Ray ◽  
Emily M. Downs ◽  
William H. Cooke
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Resistance Training ◽  
Exercise Training ◽  
Resistance Exercise ◽  
Arterial Blood Pressure ◽  
Whole Body ◽  
Arterial Blood ◽  
Blood Pressures ◽  
Body Resistance

The effects of resistance training on arterial blood pressure and muscle sympathetic nerve activity (MSNA) at rest have not been established. Although endurance training is commonly recommended to lower arterial blood pressure, it is not known whether similar adaptations occur with resistance training. Therefore, we tested the hypothesis that whole body resistance training reduces arterial blood pressure at rest, with concomitant reductions in MSNA. Twelve young [21 ± 0.3 (SE) yr] subjects underwent a program of whole body resistance training 3 days/wk for 8 wk. Resting arterial blood pressure ( n = 12; automated sphygmomanometer) and MSNA ( n = 8; peroneal nerve microneurography) were measured during a 5-min period of supine rest before and after exercise training. Thirteen additional young (21 ± 0.8 yr) subjects served as controls. Resistance training significantly increased one-repetition maximum values in all trained muscle groups ( P < 0.001), and it significantly decreased systolic (130 ± 3 to 121 ± 2 mmHg; P = 0.01), diastolic (69 ± 3 to 61 ± 2 mmHg; P = 0.04), and mean (89 ± 2 to 81 ± 2 mmHg; P = 0.01) arterial blood pressures at rest. Resistance training did not affect MSNA or heart rate. Arterial blood pressures and MSNA were unchanged, but heart rate increased after 8 wk of relative inactivity for subjects in the control group (61 ± 2 to 67 ± 3 beats/min; P = 0.01). These results indicate that whole body resistance exercise training might decrease the risk for development of cardiovascular disease by lowering arterial blood pressure but that reductions of pressure are not coupled to resistance exercise-induced decreases of sympathetic tone.

scholarly journals Seasonal changes in the cardiovascular, respiratory and metabolic responses to temperature and hypoxia in the bullfrog rana catesbeiana

1998 ◽  
Vol 201 (5) ◽  
pp. 761-768 ◽  
Author(s):  
P L Rocha ◽  
L G S Branco
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Body Temperature ◽  
Arterial Blood Pressure ◽  
Plasma Glucose ◽  
Rana Catesbeiana ◽  
Breathing Frequency ◽  
Glucose Levels ◽  
Arterial Blood ◽  
The Difference

We assessed seasonal variations in the effects of temperature on hypoxia-induced alterations in the bullfrog Rana catesbeiana by measuring the heart rate, arterial blood pressure, breathing frequency, metabolic rate, blood gas levels, acid-base status and plasma glucose concentration. Regardless of the season, decreased body temperature was accompanied by a reduction in heart and breathing frequencies. Lower temperatures caused a significant decrease in arterial blood pressure during all four seasons. Hypoxia-induced changes in breathing frequency were proportional to body temperature and were more pronounced during winter, less so during spring and autumn and even smaller during summer. Season had no effect on the relationship between hypoxia and heart rate. At any temperature tested, the rate of oxygen consumption had a tendency to be highest during summer and lowest during winter, but the difference was significant only at 35 degrees C. The PaO2 and pH values showed no significant change during the year, but PaCO2 was almost twice as high during winter than in summer and spring, indicating increased plasma bicarbonate levels. Lower temperatures were accompanied by decreased plasma glucose levels, and this effect was greater during summer and smaller during autumn. Hypoxia-induced hyperglycaemia was influenced by temperature and season. During autumn and winter, plasma glucose level remained elevated regardless of temperature, probably to avoid dehydration and/or freezing. In winter, the bullfrog may be exposed not only to low temperatures but also to hypoxia. These animals show temperature-dependent responses that may be beneficial since at low body temperatures the set-points of most physiological responses to hypoxia are reduced, regardless of the season. &lt;P&gt;

Baroreflex modulation of sympathetic nerve activity to muscle in heat-stressed humans

2002 ◽  
Vol 282 (1) ◽  
pp. R252-R258 ◽  
Author(s):  
Jian Cui ◽  
Thad E. Wilson ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Whole Body ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Arterial Blood ◽  
The Relationship

To identify whether whole body heating alters arterial baroreflex control of muscle sympathetic nerve activity (MSNA), MSNA and beat-by-beat arterial blood pressure were recorded in seven healthy subjects during acute hypotensive and hypertensive stimuli in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature ( P < 0.01), MSNA ( P < 0.01), heart rate ( P< 0.01), and skin blood flow ( P < 0.001), whereas mean arterial blood pressure did not change significantly ( P > 0.05). During both normothermic and heat stress conditions, MSNA increased and then decreased significantly when blood pressure was lowered and then raised via intravenous bolus infusions of sodium nitroprusside and phenylephrine HCl, respectively. The slope of the relationship between MSNA and diastolic blood pressure during heat stress (−128.3 ± 13.9 U · beats−1 · mmHg−1) was similar ( P = 0.31) with normothermia (−140.6 ± 21.1 U · beats−1 · mmHg−1). Moreover, no significant change in the slope of the relationship between heart rate and systolic blood pressure was observed. These data suggest that arterial baroreflex modulation of MSNA and heart rate are not altered by whole body heating, with the exception of an upward shift of these baroreflex curves to accommodate changes in these variables that occur with whole body heating.

Carotid baroreflex responsiveness in heat-stressed humans

2000 ◽  
Vol 279 (4) ◽  
pp. H1955-H1962 ◽  
Author(s):  
C. G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Orthostatic Intolerance ◽  
Whole Body ◽  
Functional Reserve ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Maximal Gain ◽  
Increased Susceptibility

The effects of whole body heating on human baroreflex function are relatively unknown. The purpose of this project was to identify whether whole body heating reduces the maximal slope of the carotid baroreflex. In 12 subjects, carotid-vasomotor and carotid-cardiac baroreflex responsiveness were assessed in normothermia and during whole body heating. Whole body heating increased sublingual temperature (from 36.4 ± 0.1 to 37.4 ± 0.1°C, P < 0.01) and increased heart rate (from 59 ± 3 to 83 ± 3 beats/min, P < 0.01), whereas mean arterial blood pressure (MAP) was slightly decreased (from 88 ± 2 to 83 ± 2 mmHg, P < 0.01). Carotid-vasomotor and carotid-cardiac responsiveness were assessed by identifying the maximal gain of MAP and heart rate to R wave-triggered changes in carotid sinus transmural pressure. Whole body heating significantly decreased the responsiveness of the carotid-vasomotor baroreflex (from −0.20 ± 0.02 to −0.13 ± 0.02 mmHg/mmHg, P < 0.01) without altering the responsiveness of the carotid-cardiac baroreflex (from −0.40 ± 0.05 to −0.36 ± 0.02 beats · min−1 · mmHg−1, P = 0.21). Carotid-vasomotor and carotid-cardiac baroreflex curves were shifted downward and upward, respectively, to accommodate the decrease in blood pressure and increase in heart rate that accompanied the heat stress. Moreover, the operating point of the carotid-cardiac baroreflex was shifted closer to threshold ( P = 0.02) by the heat stress. Reduced carotid-vasomotor baroreflex responsiveness, coupled with a reduction in the functional reserve for the carotid baroreflex to increase heart rate during a hypotensive challenge, may contribute to increased susceptibility to orthostatic intolerance during a heat stress.

Circulatory and respiratory effects of whole-body vibration in anesthetized dogs

1965 ◽  
Vol 20 (6) ◽  
pp. 1157-1162 ◽  
Author(s):  
William B. Hood ◽  
Lawrence S. Higgins
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Oxygen Consumption ◽  
Whole Body Vibration ◽  
Vibration Response ◽  
Whole Body ◽  
Sinusoidal Vibration ◽  
Body Vibration ◽  
Arterial Blood ◽  
Anesthetized Dogs

Effects of whole body x-axis sinusoidal vibration were studied in 27 anesthetized dogs. At a vibratory frequency of 10 cycles/sec and at levels of peak acceleration greater than 0.3 g, increases in the accelerative force of vibration were accompanied by increases in mean arterial blood pressure, heart rate, cardiac output, oxygen consumption, central blood volume, and minute volume of ventilation. Peripheral vascular resistance decreased under the same conditions. At 6 cycles/sec similar results were obtained, the only significant differences being in blood pressure and heart rate response. In three animals curare partially blocked the increase in oxygen consumption during vibration. Reserpine had no effect in two other animals. These studies suggest that the circulatory responses observed during whole-body vibration are due to muscular exercise. vibration physiology; acceleration physiology; biomechanics; vibration and exercise; curare and vibration response; reserpine and vibration response Submitted on February 1, 1965

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