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PubMed1997

Is hypothermia in the victim of major trauma protective or harmful? A randomized, prospective study.

OBJECTIVE: The purpose of this randomized, prospective clinical trial was to determine whether hypothermia during resuscitation is protective or harmful to critically injured trauma patients. SUMMARY BACKGROUND DATA: Hypothermia has both protective and harmful clinical effects. Retrospective studies show higher mortality in patients with hypothermia; however, hypothermia is more common in more severely injured patients, which makes it difficult to determine whether hypothermia contributes to mortality independently of injury severity. There are no randomized, prospective treatment studies to assess hypothermia's impact as an independent variable. METHODS: Fifty-seven hypothermic (T < or = 34.5 C), critically injured patients requiring a pulmonary artery catheter were randomized to a rapid rewarming protocol using continuous arteriovenous rewarming (CAVR) or to a standard rewarming (SR) control group. The primary outcome of interest was first 24-hour blood product and fluid resuscitation requirements. Other comparative analyses included coagulation assays, hemodynamic and oxygen transport measurements, length of stay, and mortality. RESULTS: The two groups were well matched for demographic and injury severity characteristics. CAVR rewarmed significantly faster than did SR (p < 0.01), producing two groups with different amounts of hypothermia exposure. The patients who underwent CAVR required less fluid during resuscitation to the same hemodynamic goals (24,702 mL vs. 32,540 mL, p = 0.05) and were significantly more likely to rewarm (p = 0.002). Only 2 (7%) of 29 patients who underwent CAVR failed to warm to 36 C and both died, whereas 12 (43%) of 28 patients who underwent SR failed to reach 36 C, and all 12 died. Patients who underwent CAVR had significantly less early mortality (p = 0.047). CONCLUSION: Hypothermia increases fluid requirements and independently increases acute mortality after major trauma.

Cardiopulmonary Resuscitation↗
PubMed1985

Effect of phentolamine in controlling temperature and acidosis associated with cardiopulmonary bypass.

This study assessed the effects of phentolamine on rewarming patterns and metabolic acidosis in 37 patients subjected to hypothermia during cardiopulmonary bypass for the performance of aortocoronary bypass grafting. An additional 16 patients undergoing the same surgery received no phentolamine and served as a control group. In all patients, sodium bicarbonate (44.6 mEq) was administered only when the negative base excess was 3.0 mEq/L or greater. Sixty-eight percent of the patients receiving phentolamine and 56% of the control patients exhibited a uniform rewarming pattern in which the rectal, hand, and foot temperatures increased in parallel. In 32% of the patients receiving phentolamine and in 44% of the control patients, rectal and hand temperatures increased more than foot temperature during rewarming. Analysis of base excess values in the subgroups of patients with similar rewarming patterns indicated that base deficits were significantly decreased in patients receiving phentolamine. Phentolamine administration was also associated with significantly lower blood lactate levels and sodium bicarbonate requirements, as well as improvements in overall appearance and mental status. These data suggest that the routine use of phentolamine in patients undergoing cardiopulmonary bypass may be associated with more uniform body cooling and rewarming and improved tissue perfusion.

Acidosis↗
PubMed1977

Maintenance of the functional state of isolated rat liver by hypothermic perfusion with an erythrocyte-free medium.

Isolated rat liver was studied before, during, and after hypothermic perfusion at 5 C for 24, 48, or 72 hr with an acellular perfusate consisting of 7% bovine serum albumin in Kreb-Ringer buffer containing glucose, penicillin, and streptomycin. Bile production ceased at 5 C but resumed when the temperature was raised to 35 C. The rate of flow and the total amount produced was unaffected by 24 hr of hypothermia but decreased when the cooling period was extended to 48 and 72 hr. The data of other workers was used to show a correlation between bile flow and oxygen consumption by the liver. Cooling also caused the release of potassium into the perfusate but it was quickly reaccumulated after rewarming; however, the extent and rate of reaccumulation decreased as the cooling period increased, as did the ability of the livers to retain the ion. Urea synthesis did not cease after cooling and after rewarming, the rate of synthesis increased as the period of hypothermia was lengthened. The maximum concentration of urea in the perfusate was found when rewarmed livers had produced 200 mumol of urea but at this point, control livers had produced 280 mumol. The concentration of glucose in the perfusate of livers maintained at 35 C showed peaks at 2 and 9 to 10 hr after the start of perfusion. After cooling for 24 hr these peaks arose at 2 and 7 hr after rewarming, but with 48 hr of hypothermia, these peaks were higher and appeared at 2 and 4 hr. When the cooling period was extended to 72 hr, only a single peak was seen 2 hr after rewarming. These results suggest that rat liver can be cooled to 5 C for 24 hr with little effect on its functional characteristics but a marked decline becomes apparent when the cooling period is extended beyond 24 hr. None of the livers studied was transplanted after perfusion and it remains to be seen how the functional tests conducted in vitro correlate with the ability of the livers to support life.

Animals↗
PubMed1993

Effect of fasting on hepatocytes cold stored in University of Wisconsin solution for 24 hours.

Although there have been improvements in liver preservation, liver dysfunction still remains a serious consequence of liver transplantation. This may be related to cold ischemic injury since the incidence of dysfunction increases with longer preservation times. However, even some livers preserved for short periods of time (less than 15 hr) develop liver dysfunction. One possible cause may be the lack of adequate nutritional support, and the donor may be exposed to prolonged periods of hyponutrition. In this study, we have compared the effects of fasting on functions of hepatocytes isolated from the rat. Hepatocytes were cold stored in University of Wisconsin solution for 24 hr and analyzed at the end of preservation as well as at the end of rewarming in Krebs-Henseleit buffer for 120 min. The glycogen content of fed cells was 1.57 mumol/mg protein and this was reduced by 95% in cells from fasted rats. After cold storage and rewarming, hepatocytes from fasted rats lost 84.2 +/- 2.5% of the total cellular lactate dehydrogenase versus only 32.7 +/- 3.8% (P < 0.001) in cells from fed rats. Also, ATP and reduced glutathione content of fasted cells were significantly reduced, free fatty acids were higher (P = 0.0154), and protein synthesis was reduced to 41% of controls (versus only 88% in fed cells), although there were no differences in phospholipid content. When hepatocytes from fasted rats were rewarmed in Krebs-Henseleit buffer containing fructose (10 mM), lactate dehydrogenase release was reduced from 80% to 34.4 +/- 0.2% and ATP content was significantly higher with fructose than without. Hepatocytes from fasted rats, therefore, are more sensitive to cold ischemic injury than cells from fed rats. The increased sensitivity appears related to the lack of glycogen as a source of substrates for metabolism during rewarming. This is supported by the fact that addition of fructose, which is metabolized readily by hepatocytes through glycolysis, suppressed rewarming injury to cells from fasted rats. The nutritional status of the donor, therefore, may play a pivotal role in the results of liver preservation and transplantation. Effective donor nutritional management may reduce the incidence of liver dysfunction after transplantation.

Adenosine↗
PubMed2003

Cold-induced apoptosis of rat liver endothelial cells: contribution of mitochondrial alterations.

BACKGROUND: Maintenance of the integrity of the vascular endothelium is a critical issue in liver preservation, but hypothermia, applied for cellular protection, induces apoptotic cell death in liver endothelial cells. This cold-induced apoptosis is mediated by an iron-dependent formation of reactive oxygen species. Here, we study the involvement of mitochondria in this process. METHODS: Cultured rat liver endothelial cells were incubated in cold University of Wisconsin solution for 18 hr and subsequently rewarmed in cell culture medium. Mitochondrial morphology and membrane potential were evaluated using laser scanning microscopy. RESULTS: During cold incubation in University of Wisconsin solution, a marked, progressive mitochondrial shortening and a reduction in mitochondrial membrane potential occurred. Rewarming of the cells led to mitochondrial ultracondensation, complete loss of the mitochondrial membrane potential, and subsequent apoptotic cell death. The inhibitors of mitochondrial permeability transition, trifluoperazine and fructose, or iron chelation with deferoxamine did not affect mitochondrial shortening during cold incubation but inhibited ultracondensation, loss of mitochondrial membrane potential, and loss of viability during rewarming. Moreover, in these protected cells, an almost complete reestablishment of the mitochondrial membrane potential and morphology could be observed; the few mitochondria that were irreversibly damaged were incorporated into autophagosomes during cellular recovery. CONCLUSION: Two apparently independent mitochondrial alterations take place during cold incubation and subsequent rewarming of liver endothelial cells. Cold-induced mitochondrial shortening represents a reversible process, whereas iron-mediated mitochondrial permeability transition and ultracondensation during rewarming are irreversible and constitute an important mediator of cold-induced apoptosis.

Animals↗
PubMed1987

Treatment of severe accidental hypothermia using the Clinitron bed.

Two cases of severe accidental hypothermia (core temperature less than 28 degrees C) rewarmed employing the Clinitron system are described. The physiological changes during hypothermia and rewarming are discussed and the current concepts of rewarming (active external versus internal) outlined. It is suggested that severely hypothermic patients can be successfully treated by rapid external rewarming using the Clinitron heated fluidised-bead bed. This method combines the advantages of rapid rewarming, minimal physiological disturbance and is non invasive.

Aged↗
PubMed1984

A cold-labile acetyl-coenzyme-A hydrolase from the supernatant fraction of rat liver. Reactivation and reconstitution of the active species from the inactive monomer.

An acetyl-coenzyme-A hydrolase from the supernatant fraction of rat liver is known to be rapidly inactivated at low temperature. Loss of catalytic activity is accompanied by apparent dissociation of tetrameric and dimeric forms of the enzyme into monomers. It was found that rewarming under appropriate conditions almost completely reversed the cold-induced inactivation and dissociation of the enzyme: At a protein concentration of 14 micrograms/ml, simple rewarming only partially restored the enzyme activity (less than 3% of the original activity), but at a higher concentration of the enzyme or in the presence of 1 mg/ml bovine serum albumin, the reactivation by warming was greater. Warming at 37 degrees C appeared to be optimal for reactivation; warming at 25 degrees C or at 43 degrees C was less effective. Longer exposure to cold did not affect reactivation on rewarming, but on repeated inactivation and reactivation the reactivation decreased to some extent, especially at lower concentrations of enzyme protein. Among various nucleotides tested, ATP greatly enhanced the restoration of the activity, while ITP, UTP and ADP were less effective and AMP, GTP, TTP and CTP had little effect. At an enzyme-protein concentration of 14 micrograms/ml, 2 mM ATP restored the enzyme activity to about 70% of that before cold treatment, while acetyl-CoA (0.5 mM) restored the activity about 50%. High concentrations of phosphate (0.92 M) and pyrophosphate (0.45 M) restored about 80% and 95%, respectively, of the original activity. Sucrose density gradient centrifugation of the active dimer at high enzyme concentration at 4 degrees C for 20 h produced a monomeric form without catalytic activity. Gel filtration showed that simple rewarming mostly converted the monomeric enzyme obtained in this way to the dimeric form, whereas on rewarming with ATP the monomer was mostly converted to a tetrameric form. The dimeric and tetrameric forms both had catalytic activity.

Acetyl Coenzyme A↗
PubMed2004

Mitochondrial calcium uptake regulates cold preservation-induced Bax translocation and early reperfusion apoptosis.

Mitochondrial calcium (mCa + 2) overload occurs during cold preservation and is an integral part of mitochondrial-dependent apoptotic pathways. We investigated the role of mCa + 2 overload in cell death following hypothermic storage using HepG2 cells stored in normoxic-hypothermic (4 degrees C) or hypoxic (< 0.1% O2)-hypothermic Belzer storage solution. Cells were stored for 6 h, with or without 10 microM ruthenium red (mCa + 2 uniporter inhibitor) followed by rewarming in oxygenated media at 37 degrees C. Cytoplasmic cytochrome c levels were studied by Western analysis and by fluorescent microscopy after transfection of cytochrome c-GFP expression plasmid. Immunofluorescence determined the intracellular, spatio-temporal distribution of Bax, and TUNEL staining was used to evaluate cell death after 180 min of rewarming. Caspase activation was evaluated using Western analysis and a caspase 3 activity assay. Bax translocation, cytochrome c release, and early rewarming cell death occurred following hypothermic storage and were exacerbated by hypoxia. Caspase 3 activation did not occur following hypothermic storage. Blockade of mCa + 2 uptake prevented Bax translocation, cytochrome c release, and early rewarming cell death. These studies demonstrate that mCa + 2 uptake during hypothermic storage, both hypoxic and normoxic, contributes to early rewarming apoptosis by triggering Bax translocation to mitochondria and cytochrome c release.

Apoptosis↗
PubMed1972

Activation of the electrogenic sodium pump in guinea-pig auricles by internal sodium ions.

1. The effect of various intracellular Na concentrations ([Na](i)) on the membrane potential after hypothermia was studied in guinea-pig auricles.2. For varying [Na](i), the atria were cooled for 4 hr at 4-6 degrees C in a K-poor solution with different concentrations of NaCl. The auricles were rewarmed in normal Tyrode solution at 35 degrees C.3. Extracellular space (ECS), intracellular Na and K concentrations ([Na](i) and [K](i)) and membrane potential of the atria were measured before and after hypothermia.4. The ECS, measured as inulin space, amounted to 350 ml./kg wet wt. at 35 degrees C and to 300 ml./kg wet wt. at 4-6 degrees C.5. [K](i) decreased during cooling and increased during rewarming the auricles. [Na](i) increased during hypothermia in bathing fluids containing NaCl, but decreased in NaCl- and Na-free solutions. At the beginning of rewarming a net Na transport occurred from cells with high [Na](i), while a net Na uptake took place in atria with low [Na](i).6. At the same time, the membrane potential of auricles with increased [Na](i) hyperpolarized beyond the steady-state value recorded at the end of rewarming, or even beyond the calculated K(+) equilibrium potential (E(K)). Afterwards, the hyperpolarization levelled off, while the E(K) values increased further. The membrane potential of atria with decreased [Na](i) showed no transitory hyperpolarization during rewarming.7. The hyperpolarization beyond the steady-state value of membrane potential in rewarmed auricles was significantly correlated to the active Na efflux.8. From these results it is concluded that the membrane potential of guinea-pig atria after hypothermia is affected by an active, electrogenic Na pump activated by intracellular Na ions.

Animals↗
PubMed1978

Activation of the electrogenic sodium pump in guinea-pig atria by external potassium ions.

1. When cardiac preparations are rewarmed following prolonged hypothermia a transient hyperpolarization occurs in K-containing media. This hyperpolarization is correlated with the active Na efflux. It might be due to electrogenic Na pumping or to extracellular K depletion brought about by the activity of an electroneutral Na-K exchange pump. In order to distinguish between these mechanisms the effect of various extracellular K concentrations ([K](o)) on the membrane potential of guineapig atria was studied before and after hypothermia.2. The membrane potential increased with decreasing [K](o) before cooling. It reached values of -64 and -92 mV at 10.8 and 0 mM-K, respectively.3. The membrane hyperpolarized transiently after hypothermia beyong the potential observed before cooling. Maximal values of about -94 mV were obtained during rewarming in solutions containing 0.4-2.7 mM-K. The membrane potential was significantly lower (-88 mV) in K-free media. It was also diminished at [K](o) higher than 2.7 mM and was measured to be -74 mV at 10.8 mM-K.4. The hyperpolarization of the cell membrane during the first 20 min of rewarming was maximal at 2.7 mM-K and yielded 15.5 mV. The hyperpolarization amounted to 7.2 and 10 mV at 0.4 and 10.8 mM-K, respectively. No hyperpolarization occurred in K-free solutions.5. The rate of decline of the transient hyperpolarization increased with [K](o).6. Variations of membrane input resistance after changes in [K](o) were measured in rewarmed atrial trabecula. The measurements revealed an increase in membrane resistance in lower [K](o).7. It is concluded that the transient hyperpolarization of the cardiac cell membrane during rewarming is due to the activation of an electrogenic Na pump.8. The (relative) strength of the pump current at various [K](o) was derived from the observed dependence of the hyperpolarization and of the membrane input resistance on [K](o). The current is estimated to be half-maximal at about 1.5 mM-K.

Animals↗
PubMed1980

Treatment of accidental hypothermia: a prospective clinical study.

A 15-year prospective study was carried out of 44 patients with accidental hypothermia (mean age 60 years) admitted to an intensive therapy unit. The lowest core temperature recorded in each patient ranged from 20.0 to 34.3 degrees C. The precipitating factors were poisoning (by drugs, alcohol, or coal gas) in 25 cases and various illnesses in 19. Rewarming was achieved in 42 patients by applying a radiant heat cradle over the torso, and in two patients by mediastinal irrigation with warmed fluids. Twelve patients died, but only two during the period of rewarming. Thus rewarming may be consistently and safely achieved irrespective of the cause of hypothermia, and normal body temperature may be regained as rapidly as is compatible with adequate tissue perfusion and oxygenation. Surface rewarming of the torso is perhaps the simplest technique available, but internal rewarming procedures may be desirable or essential in the presence of, for example, profound hypothermia, severe hypotension, or ventricular fibrillation. Mortality was attributable to underlying factors or disease and not to hypothermia.

Adult↗
PubMed1988

Mechanism of afterdrop after cold water immersion.

It was hypothesized that if afterdrop is a purely conductive phenomenon, the afterdrop during rewarming should proceed initially at a rate equal to the rate of cooling. Eight male subjects were cooled on three occasions in 22 degrees C water and rewarmed once by each of three procedures: spontaneous shivering, inhalation of heated (45 degrees C) and humidified air, and immersion up to the neck in 40 degrees C water. Deep body temperature was recorded at three sites: esophagus, auditory canal, and rectum. During spontaneous and inhalation rewarming, there were no significant differences between the cooling (final 30 min) and afterdrop (initial 10 min) rates as calculated for each deep body temperature site, thus supporting the hypothesis. During rapid rewarming, the afterdrop rate was significantly greater than during the preceding cooling, suggesting a convective component contributing to the increased rate of fall. The rapid reversal of the afterdrop also indicates that a convective component contributes to the rewarming process as well.

Adult↗
PubMed2002

Effects of moderate and deep hypothermia on Ca2+ signaling in rat ventricular myocytes.

BACKGROUND/AIMS: We investigated whether the degree of hypothermia determines the impairment in cardiac muscle function upon rewarming and whether the sarcoplasmic reticulum Ca2+ release channel, RyR(2), contributes to hypothermia-induced changes in myoplasmic [Ca2+]. METHODS: Tension measurements using rat papillary muscle and calcium transients (Fluorescent Ca2+ indicator Fura 2-AM) in rat ventricular myocytes were compared during deep (10 degrees C-16 degrees C) and moderate hypothermic (28 degrees C) myocardial temperatures. In a second experiment, myocytes were pretreated with dantrolene, an RyR(2) antagonist; calcium transients were determined at control temperatures (32 degrees C), 16 degrees C, and upon rewarming (32 degrees C). RESULTS: Papillary muscle contractility and myocyte calcium transients were significantly reduced during and after rewarming from 16 degrees C. At 28 degrees C, papillary muscle isometric tension was potentiated and calcium transients were unaffected. After rewarming from 28 degrees C, excitation-contraction coupling was maintained as isometric tension returned to 90% of control values. After rewarming from 16 degrees C, myocytes pretreated with dantrolene had return of calcium transients to 89% of control values while myocytes not treated with dantrolene recovered to only 50% of their control values. CONCLUSION: We conclude that deep hypothermia, as opposed to moderate hypothermia of the myocardium, disrupts excitation-contraction coupling at cellular and tissue levels. Our finding of preserved calcium transients in dantrolene-pretreated myocytes exposed to deep hypothermia suggests a potential role for the RyR(2) channel in post-hypothermia reductions in cardiac function.

Animals↗
PubMed2001

Feasibility and safety of moderate hypothermia after massive hemispheric infarction.

BACKGROUND AND PURPOSE: Moderate hypothermia decreases ischemic damage in experimental stroke models. This multicenter study was performed to evaluate (1) the safety and feasibility of moderate hypothermia and (2) its potential to reduce intracranial hypertension in acute stroke patients. METHODS: Fifty prospective patients with cerebral infarction involving at least the complete middle cerebral artery territory treated with moderate hypothermia were evaluated. Hypothermia was induced with the use of cooling blankets as well as alcohol and ice bags within 22+/-9 hours after stroke onset and maintained for 24 to 72 hours; subsequently, patients passively rewarmed over a mean duration of 17 hours. Outcome was assessed at 4 weeks and at 3 months. RESULTS: Time required for cooling to <33 degrees C varied from 3.5 to 11 hours. The most frequent complications of hypothermic therapy were thrombocytopenia (70%), bradycardia (62%), and pneumonia (48%). Four patients (8%) died during hypothermia as a result of severe coagulopathy, cardiac failure, or uncontrollable intracranial hypertension. An additional 15 patients (30%) died during or after rewarming because of rebound increase in intracranial pressure (ICP) and fatal herniation. A shorter (<16 hours) rewarming period was associated with a more pronounced rise of ICP. Elevated ICP values were significantly reduced under hypothermia. Neurological outcome according to the National Institutes of Health Stroke Scale score 4 weeks after stroke was 29, and Rankin Scale score 3 months after stroke was 2.9. CONCLUSIONS: Moderate hypothermia is feasible in patients with acute stroke, although it is associated with several side effects. Most deaths occur during rewarming as a result of excessive ICP rise. Our preliminary observation that a longer duration of the rewarming period limits the ICP increase remains to be confirmed in future studies.

Acute Disease↗
PubMed1989

Plasma and urine catecholamines and cerebrospinal fluid amine metabolites as hypothermia markers in guinea-pigs.

Changes in catecholamines (CA) in the plasma and urine and metabolites of CA and serotonin (5-HT) in the cerebrospinal fluid of guinea-pigs in hypothermia (Trec 30 degrees C) and after subsequent rewarming were determined with HPLC in order to obtain data on early stress reactions and their timing. Both noradrenaline (NA) and adrenaline (A) were low in the plasma but high in the urine after the hypothermic period. These had normalized in the plasma after rewarming but were still high in the urine. Dopamine values tended to be low (not significant). Methoxyhydroxyphenylglycol and homovanilic acid were elevated in the cerebrospinal fluid both after hypothermia and following rewarming, and 5-hydroxyindoleacetic acid after rewarming. The ratio of adrenaline to noradrenaline, the catecholamine hypothermia index, in the urine had risen 24-fold after hypothermia and 40-fold after rewarming. The results support the view that elevated catecholamine concentrations in the urine and elevated values of their metabolites in the cerebrospinal fluid could be regarded as hypothermia markers. However, other stress conditions, which have lasted at least a few hours, should be excluded in the final interpretation.

Animals↗
PubMed1998

Upper airway mucosa temperature in obstructive sleep apnoea/hypopnoea syndrome, nonapnoeic snorers and nonsnorers.

Upper airway (UA) inflammation (oedema and hyperaemia) is frequently observed in snorers and patients with sleep apnoea/hypopnoea patients. The temperature of different UA regions measured in 11 male nonsnorers, 13 nonapnoeic snorers and 10 untreated sleep apnoea/hypopnoea syndrome (SAHS) patients using infra-red video recording. Measurements were taken with the mouth open during tidal volume mouth breathing, and at the beginning and end of a 10 s end-inspiratory voluntary apnoea which followed either mouth or nasal breathing. Three measurements were obtained from the uvula and from each side of the posterior pharyngeal wall and two from each side of the soft palate. The different UA regions were characterized by their inspiratory temperature, the expiratory rewarming and the changes in UA temperature during apnoea. The temperature of the uvula was significantly lower than that of the other UA regions. For each anatomical region, there were no differences in inspiratory temperature between normals, snorers and SAHS. In normals, the expiratory rewarming was significantly higher in the uvula than in the velum and the posterior pharyngeal wall, whereas these regional differences were not observed in snorers and SAHS. The velum and posterior pharyngeal rewarming was significantly less in normals than in snorers and SAHS. During apnoea, the UA rewarming was similar to that observed during expiration. In conclusion, tissue temperature varies between the different upper airway regions and during tidal breathing and the intensity of the regional expiratory rewarming differs between normals, snorers and patients with sleep apnoea/hypopnoea syndrome.

Adult↗
PubMed2003

Differential effects of surgical sympathetic block on sudomotor and vasoconstrictor function.

OBJECTIVE: To assess the effects of a surgical block of the sympathetic chain at the T2 level on vasoconstriction and palmar sweating in patients with palmar hyperhidrosis. METHODS: In a prospective study, sympathetic vasoconstriction was measured by laser-Doppler imaging and by computer-assisted infrared thermography (rewarming kinetics following immersion of both hands in ice water [4 degrees C, 30 seconds]) in 61 patients with hyperhidrosis preoperatively and 2 days and 3 months postoperatively. In addition, palmar sweating preoperatively and 3 months postoperatively was assessed by quantitative sudometry. RESULTS: Before surgery, rewarming kinetics was significantly slower in the patients (n = 61) than in the healthy control subjects (n = 28). Two days after the block, baseline skin temperature increased by about 5 degrees C, and rewarming was massively accelerated in each of the patients. Three months postoperatively, rewarming kinetics was still accelerated in 36 hands, was unchanged from the preoperative condition in 42, and had worsened in 12. These changes were accompanied by parallel alterations of laser-Doppler flux. However, palmar sweating was massively reduced in all but one patient, irrespective of the different rewarming kinetics. CONCLUSIONS: T2 sympathectomy leads to long-lasting inhibition of palmar sweating, which does not correlate to loss of vasoconstriction. Recurrent and enhanced vasoconstrictor function 3 months following endoscopic sympathetic block has major implications for its use to treat enhanced vasoconstriction.

Adolescent↗
PubMed1986

Blood anesthetic levels during surface-induced deep hypothermia under halothane-diethyl ether azeotrope anesthesia.

Blood anesthetic concentration and clinical indicators related to anesthetic management during surface-induced deep hypothermia were determined in seven adult mongrel dogs. The azeotrope of halothane and diethyl ether was assayed by gas chromatography. Blood concentration of halothane ranged from a pre-cooling control of 0.74 vol % to 0.11 vol % at 20 degrees C rewarming; ether ranged from 0.06 vol % at 20 degrees C rewarming to 0.22 vol % at 35 degrees C rewarming. Administration of anesthetic was reduced during cooling because of the spontaneous decrease in mean arterial pressure and heart rate. After elective circulatory arrest was induced, anesthetic was not required until after cardiac resuscitation at about 22 degrees C rewarming. Initial clinical signs indicating a need to increase administration of anesthetic included spontaneous respiration and an increase in mean arterial pressure. Blood azeotrope concentration was significantly lower during rewarming than at comparable temperatures during cooling. We conclude that blood concentration of halothane and ether changes as a function of body temperature and that anesthetic demand may be diminished following total circulatory arrest.

Anesthesia, Inhalation↗