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PubMed2002

Initial experience with a novel heat-exchanging catheter in neurosurgical patients.

UNLABELLED: Even mild hypothermia provides marked protection against cerebral ischemia in animal models. Hypothermia may be of therapeutic value during neurosurgical procedures. However, current cooling systems often fail to induce sufficient hypothermia before the dura is opened. Furthermore, they usually fail to restore normothermia by the end of surgery, thus delaying extubation. We evaluated a new internal heat-exchanging catheter. Eight ASA physical status II-IV patients (29-72 yr) undergoing craniotomy were enrolled. After the induction of general anesthesia, we introduced the SetPoint catheter into the inferior vena cava via a femoral vein. The target core body temperature was 34 degrees C-34.5 degrees C. After reaching the target, core temperature was maintained until the dura was closed. Target core temperature was then set to 37.0 degrees C, and the patient was rewarmed as quickly as possible. Seven patients had a tumor resection, and one had an aneurysm clipped. The core-cooling rate was 3.9 degrees C +/- 1.6 degrees C/h, and the rewarming rate was 2.0 degrees C +/- 0.5 degrees C/h; core temperature was 35.9 degrees C +/- 0.2 degrees C by the end of surgery. Patients were subsequently kept normothermic for 3 h before the catheter was removed. No thrombus or other particulate material was identified on the extracted catheters. None of the patients suffered any complications that could be attributed to the SetPoint system or thermal management. IMPLICATIONS: Because current systems for inducing therapeutic hypothermia are too slow, we tested an internal counter-current thermal management system during hypothermic neurosurgery. The SetPoint catheter cooled at 3.9 degrees C +/- 1.6 degrees C/h and rewarmed at 2.0 degrees C +/- 0.5 degrees C/h. Catheter-based internal thermal management thus seems to be rapid and effective.

Adult↗
PubMed1989

Washin and washout of isoflurane administered via bubble oxygenators during hypothermic cardiopulmonary bypass.

Washin and washout of a volatile anesthetic given through the oxygenator during hypothermic (23.4 +/- 2.1 degrees C) cardiopulmonary bypass were studied in nine patients. The authors administered isoflurane and measured its partial pressure in arterial (Pa) and venous (Pv) blood and the gas exhausted from the oxygenator (PE) at 1, 2, 4, 8, 16, 32, and 48 min during washin. These measurements were repeated during washout, which coincided with rewarming. During washin, PE, Pa, and Pv progressively rose toward inlet gas partial pressure (PI). Equilibration of Pa with PI was 41% after 16 min, 51% after 32 min, and 57% after 48 min of washin. During washout, Pa declined to 24% of its peak after 16 min and to 13% after 32 min. Washin and washout were considerably slower in mixed venous blood. Washin of isoflurane appeared to occur more slowly during cardiopulmonary bypass than during administration via the lungs in normothermic patients, presumably because hypothermia increases tissue capacity, compensating for the effect of hemodilution that otherwise would decrease the blood/gas partition coefficient. During rewarming, washout appeared to occur as rapidly as from the lungs of normothermic patients. This may have resulted from the declining blood/gas partition coefficient (due to rewarming) and relatively limited tissue stores of isoflurane. The relationship between exhaust and arterial partial pressures was reasonably consistent; for clinical purposes, measurement of PE can be used to estimate Pa.

Cardiopulmonary Bypass↗
PubMed1992

The effect of 30% nitrous oxide on thermoregulatory responses in humans during hypothermia.

Clinical studies have reported that body core temperature decreases during prolonged surgery and anesthesia. Although this finding has been attributed primarily to increased heat loss resulting from exposure of body cavities and infusion of cold solutions, it is generally recognized that anesthesia interferes with the thermoregulatory system. The present study examined the effects of mild narcosis induced by 30% N2O on shivering thermogenesis and cutaneous thermoregulatory vasoconstriction in humans, during exposure in a much more intense peripheral thermal stimulus than the ones often used in clinical studies. Nine male subjects were immersed in 15 degrees C water on two separate occasions. During one occasion subjects inspired air (control condition), and during the other occasion the inspired gas mixture contained 20% O2, 30% N2O, and 50% N2 (N2O condition). On both occasions, subjects were immersed to the neck for 60 min, or until their core temperature decreased by 2 degrees C from the preimmersion value. Following the cooling phase, subjects rewarmed via endogenous thermogenesis while lying in a well-insulated bed for 48 min. In the N2O condition, subjects continued to inspire the anesthetic gas mixture during the 48-min period of recovery. O2 uptake (VO2), esophageal temperature (Tes), mean skin temperature (Tsk), mean heat flux (Q) and forearm-fingertip temperature gradient (Tsk-gr) were recorded at 1-min intervals. Tsk and Q in both conditions stabilized within 10 and 25 min of immersion, respectively, and were not significantly different between the two conditions. The cooling rate of Tes was greater during the N2O than the control condition. VO2 increased during the immersion in both conditions and was greater in the control than in the N2O condition. In both conditions, VO2 increased linearly with decreasing Tes, but at any given Tes, VO2 was higher in the control than in the N2O condition. No significant difference was observed in cutaneous thermoregulatory vasoconstriction between the two experimental conditions, as indicated by the Tsk-gr values. The estimated Tes threshold for shivering (estimated from the O2 consumption vs. delta Tes regression) was reduced by 0.95 +/- 0.26 (SE) degrees C during the immersion phase and by 0.39 +/- 0.05 (SE) degrees C during the rewarming phase in the N2O condition compared to the control conditions. Although the thermosensitivity (gain) of shivering appeared preserved during the immersion phase, it was reduced during the N2O rewarming phase.(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Inhalation↗
PubMed1992

Kinetics of cerebral deoxygenation during deep hypothermic circulatory arrest in neonates.

Brain injury associated with neonatal congenital heart operations performed during deep hypothermia and/or total circulatory arrest is often attributed to cerebral hypoxia. We studied the kinetic changes in cerebrovascular hemoglobin O2 saturation (HbO2%) and total hemoglobin concentration (Hbtotal) in 17 neonates undergoing cardiac surgery as they were cooled to 15 degrees C, underwent total circulatory arrest, and were rewarmed. HbO2% and Hbtotal in brain vasculature were monitored noninvasively by near-infrared spectroscopy. Neonates were cooled over 12 min and rewarmed over 15 min while being perfused using cardiopulmonary bypass (CPB). Total circulatory arrest lasted from 20 to 70 min. We found that HbO2% in brain vasculature increased during the initial 8 min of CPB as nasopharyngeal temperature decreased, and then remained constant until circulatory arrest. After the onset of circulatory arrest, cerebrovascular HbO2% decreased curvilinearly for 40 min; no further hemoglobin desaturation was observed from 40 to 70 min of arrest. The changes in cerebrovascular Hbtotal were quite different from those in HbO2%, as Hbtotal decreased during the initial minute of CPB and circulatory arrest and then remained constant until recirculation. Brain intravascular HbO2% and Hbtotal increased within 3 min after the onset of recirculation to prearrest levels, and during rewarming, HbO2% decreased to normothermic baseline values. The results demonstrate that cerebral oxygenation increased during CPB cooling; O2 was consumed by the neonatal brain during the initial 40 min of deep hypothermic circulatory arrest; and cerebral oxygenation was restored on recirculation. These observations may be important in identifying the etiologies of brain injury during neonatal congenital heart surgery.

Brain↗
PubMed2000

Perioperative heat balance.

Hypothermia during general anesthesia develops with a characteristic three-phase pattern. The initial rapid reduction in core temperature after induction of anesthesia results from an internal redistribution of body heat. Redistribution results because anesthetics inhibit the tonic vasoconstriction that normally maintains a large core-to-peripheral temperature gradient. Core temperature then decreases linearly at a rate determined by the difference between heat loss and production. However, when surgical patients become sufficiently hypothermic, they again trigger thermoregulatory vasoconstriction, which restricts core-to-peripheral flow of heat. Constraint of metabolic heat, in turn, maintains a core temperature plateau (despite continued systemic heat loss) and eventually reestablishes the normal core-to-peripheral temperature gradient. Together, these mechanisms indicate that alterations in the distribution of body heat contribute more to changes in core temperature than to systemic heat imbalance in most patients. Just as with general anesthesia, redistribution of body heat is the major initial cause of hypothermia in patients administered spinal or epidural anesthesia. However, redistribution during neuraxial anesthesia is typically restricted to the legs. Consequently, redistribution decreases core temperature about half as much during major conduction anesthesia. As during general anesthesia, core temperature subsequently decreases linearly at a rate determined by the inequality between heat loss and production. The major difference, however, is that the linear hypothermia phase is not discontinued by reemergence of thermoregulatory vasoconstriction because constriction in the legs is blocked peripherally. As a result, in patients undergoing large operations with neuraxial anesthesia, there is the potential of development of serious hypothermia. Hypothermic cardiopulmonary bypass is associated with enormous changes in body heat content. Furthermore, rapid cooling and rewarming produces large core-to-peripheral, longitudinal, and radial tissue temperature gradients. Inadequate rewarming of peripheral tissues typically produces a considerable core-to-peripheral gradient at the end of bypass. Subsequently, redistribution of heat from the core to the cooler arms and legs produces an afterdrop. Afterdrop magnitude can be reduced by prolonging rewarming, pharmacologic vasodilation, or peripheral warming. Postoperative return to normothermia occurs when brain anesthetic concentration decreases sufficiently to again trigger normal thermoregulatory defenses. However, residual anesthesia and opioids given for treatment of postoperative pain decreases the effectiveness of these responses. Consequently, return to normothermia often needs 2-5 h, depending on the degree of hypothermia and the age of the patient.

Body Temperature Regulation↗
PubMed1993

Adequacy of tissue oxygenation in cardiac surgery: regional measurements.

OBJECTIVE: The aim of the study was to measure visceral and peripheral perfusion and oxygenation during and immediately after cardiac surgery. METHODS: Central hemodynamics, blood gases, core temperature, visceral and peripheral tissue perfusion, and oxygenation were studied in eight patients undergoing coronary artery bypass grafting and in the early postoperative period in another group of ten coronary artery bypass grafting patients. DESIGN: The variables were measured after induction of anesthesia, after sternotomy, during cardiopulmonary bypass, after rewarming and after closing the wounds. Postoperatively, the measurements were carried out hourly up to 8 hrs after the arrival of patients in the ICU. PATIENTS: The patients were operated on under moderate hemodilution and systemic hypothermia. The inspired oxygen concentration was maintained at 30 volumes percent during the postoperative study. MEASUREMENTS: Visceral perfusion was indirectly assessed by determining the gastric intramucosal pH. Peripheral tissue perfusion was assessed in the upper extremity by continuous recording of subcutaneous tissue PO2, laser-Doppler skin erythrocyte flux, transcutaneous PO2, and fingertip temperature. Transcutaneous PO2 index (transcutaneous PO2/PaO2) was calculated. MAIN RESULTS: Gastric intramucosal pH, PaO2, and transcutaneous PO2 reached maximum values during cardiopulmonary bypass at the deepest level of hypothermia, and gastric intramucosal pH reached its minimum at the end of the operation. During the first 3 hrs after admission of patients to the ICU, gastric intramucosal pH decreased progressively, reached its minimum value at 5 hrs, and increased slowly thereafter. Subcutaneous tissue PO2, laser-Doppler skin erythrocyte flux, and fingertip temperature decreased markedly during cardiopulmonary bypass, increased during rewarming, and decreased again at the end of surgery. The peripheral vascular bed was vasoconstricted on ICU admission, as indicated by the low values of subcutaneous tissue PO2, transcutaneous PO2, transcutaneous PO2 index, laser-Doppler skin erythrocyte flux, and fingertip temperature. These variables began to increase over the next 2 to 4 hrs and reached their maximum value by the end of the 8-hr postoperative study period, indicating complete vasodilation of the peripheral vascular bed. CONCLUSIONS: These data suggest that the visceral perfusion of patients is well maintained during cardiopulmonary bypass, while, at the same time, these patients develop hypoperfusion and hypoxia of peripheral tissues. After closing the wounds, gastric intramucosal pH, transcutaneous PO2 index (transcutaneous PO2/PaO2), and other peripheral tissue perfusion variables were at the lowest values, indicating impending residual hypothermia and tissue hypoperfusion after rewarming. During the first few hours in the ICU, both the visceral and peripheral oxygenation and perfusion variables reflected hypoperfusion of tissues coinciding in time with the period most vulnerable for hemodynamic disasters and cardiac arrhythmias.

Blood Gas Analysis↗
PubMed1990

Heparinless extracorporeal bypass for treatment of hypothermia.

In an attempt to assess the changes occurring to the coagulation profile during internal active core rewarming with partial cardiopulmonary bypass (CPB) without heparin anticoagulation, five pigs were anesthetized, and a model for severe to moderate hypothermia was created. Femoral-femoral bypass with Bio-Pump, heat exchanger, and a membrane oxygenator were used during the rewarming for 64.8 +/- 8.5 minutes. There were no statistically significant changes in platelet count, platelet index, activated clotting time (ACT), partial thromboplastin time (PTT), prothrombin time (PT), fibrinogen, fibrinogen index and fibrin split products (p greater than 0.05). There were no thromboembolic sequelae seen at autopsy. The components of the CPB circuit showed no signs of formation of aggregates or thrombi. The results of this study are attributed to the nonthrombogenic, atraumatic design of the Bio-Pump and the enhanced physiological fibrinolysis seen in the first hour of CPB. We concluded that heparinless CPB may serve as a safe alternative for active core rewarming for severe to moderate hypothermia.

Animals↗
PubMed1991

The nature and reversibility of hypothermia-induced alterations of blood viscosity.

This study evaluates the nature and reversibility of the increase in whole blood viscosity known to be induced by hypothermia. Anticoagulated samples were obtained from normal volunteers and were assayed for cellular deformability by 4.7 microns membrane filtration of whole blood (n = 12) and washed RBCs (n = 10). Results were expressed as filtration rate. Specimens were evaluated for plasma (n = 10) and whole blood (n = 12) viscosity by cone plate viscometer. All assays were sequentially performed at 30 degrees, 34 degrees, and 37 degrees C and difference analyzed by paired t test. Hypothermia resulted in significant impairment of cellular deformability, which was reversed by rewarming: [table: see text] Hypothermia also resulted in a significant increase in plasma viscosity (mean difference = 0.5426 centipoise, p less than 0.02), which was likewise reduced on rewarming. The increase in whole blood viscosity associated with hypothermia is secondary to both diminished cellular deformability and increased plasma viscosity. Both of these alterations are reversible with appropriate rewarming.

Blood Viscosity↗
PubMed1999

Membrane stabilizing effects of calcium and taxol during the cold storage of isolated rat hepatocytes.

BACKGROUND: Calcium plays an important role in liver preservation and preservation induces depletion of cellular Ca. This may affect hepatocyte cytoskeleton integrity necessary for maintaining cell shape and organ viability. We tested the effects of a microtubular stabilizer (Taxol) in liver cell preservation. METHODS: Isolated rat hepatocytes were preincubated with or without a microtubule stabilizing agent, 100 microM Taxol, at 37 degrees C for 20 min, then stored in the University of Wisconsin (UW) solution +/-1.5 mM CaC12 at 4 degrees C for up to 48 hr. After storage, the cells were rewarmed in Krebs-Henseleit buffer with air at 37 degrees C for 1 hr. Morphological changes in the plasma membrane (scanning electron microscopy) and cell viability (percentage of lactate dehydrogenase [LDH] release) before and after rewarming were studied. RESULTS: Hepatocytes showed time-dependent increase in bleb formation (cytoskeleton disruption) during cold storage. Rewarming the cells caused even greater bleb formation and increased LDH release (cell death). Pretreatment of cells with Taxol and cold storage in the UW solution with 1.5 mM Ca suppressed both bleb formation and LDH release in 48-hr coldstored cells. CONCLUSIONS: Cold storage of hepatocytes leads to reperfusion injury and cell death. This can be suppressed with Taxol and Ca. This suggests that hypothermia induces changes in cellular Ca and a disruption of the microtubules, leading to loss of cell viability. Improved liver preservation may require suppression of Ca-dependent disruption of the cytoskeleton system of liver cells.

Adenosine↗
PubMed2000

Transhepatic neutrophil and monocyte activation during clinical liver transplantation.

BACKGROUND: During experimental liver transplantation, neutrophil sequestration results in increased oxygen free radical production and correlates inversely with graft viability. Neutrophil activation in clinical liver transplantation is poorly understood. METHODS: We assessed leukocyte sequestration and transhepatic differences of neutrophil and monocyte CD11b expression, neutrophil free radical production, and plasma concentrations of interleukin 6 and interleukin 8 in nine patients during liver transplantation. RESULTS: Significant hepatic neutrophil sequestration occurred during initial graft rewarming with portal blood, after inferior vena cava declamping, and after hepatic artery declamping (all P<0.05). A positive transhepatic difference (i.e., outcoming - ingoing) in CD11b expression of neutrophils was observed after portal vein declamping (51+/-32 relative fluorescence unit [RFU]) and in CD11b expression of monocytes during initial graft rewarming (67+/-86 RFU, both P<0.05). A transcoronary increase in both unstimulated (74+/-80 RFU) and N-formyl-methionyl-leucylphenylalanine-stimulated (112+/-168 RFU) neutrophil free radical production took place after hepatic artery declamping (both P<0.05). A negative transcoronary difference of interleukin 6 occurred during initial graft rewarming (-192+/-176 pg/ml) and a positive difference of interleukin 8 occurred after hepatic artery declamping (17+/-23 pg/ml, both P<0.05). CONCLUSIONS: Hepatic sequestration and transhepatic activation of neutrophils, and hepatic production of interleukin 8 occur during clinical liver transplantation. A splanchnic influx of interleukin 6 occurs to the graft, possibly modulating neutrophil-mediated graft reperfusion injury.

Adult↗
PubMed2003

Noninvasive, near infrared spectroscopic-measured muscle pH and PO2 indicate tissue perfusion for cardiac surgical patients undergoing cardiopulmonary bypass.

OBJECTIVE: To determine whether near infrared spectroscopic measurement of tissue pH and Po2 has sufficient accuracy to assess variation in tissue perfusion resulting from changes in blood pressure and metabolic demand during cardiopulmonary bypass. DESIGN: Prospective clinical study. SETTING: Academic medical center. SUBJECTS: Eighteen elective cardiac surgical patients. INTERVENTION: Cardiac surgery under cardiopulmonary bypass. MEASUREMENTS AND MAIN RESULTS: A near infrared spectroscopic fiber optic probe was placed over the hypothenar eminence. Reference Po2 and pH sensors were inserted in the abductor digiti minimi (V). Data were collected every 30 secs during surgery and for 6 hrs following cardiopulmonary bypass. Calibration equations developed from one third of the data were used with the remaining data to investigate sensitivity of the near infrared spectroscopic measurement to physiologic changes resulting from cardiopulmonary bypass. Near infrared spectroscopic and reference pH and Po2 measurements were compared for each subject using standard error of prediction. Near infrared spectroscopic pH and Po2 at baseline were compared with values during cardiopulmonary bypass just before rewarming commenced (hypotensive, hypothermic), after rewarming (hypotensive, normothermic) just before discontinuation of cardiopulmonary bypass, and at 6 hrs following cardiopulmonary bypass (normotensive, normothermic) using mixed-model analysis of variance. Near infrared spectroscopic pH and Po2 were well correlated with the invasive measurement of pH (R2 =.84) and Po2 (R 2 =.66) with an average standard error of prediction of 0.022 +/- 0.008 pH units and 6 +/- 3 mm Hg, respectively. The average difference between the invasive and near infrared spectroscopic measurement was near zero for both the pH and Po2 measurements. Near infrared spectroscopic Po2 significantly decreased 50% on initiation of cardiopulmonary bypass and remained depressed throughout the bypass and monitored intensive care period. Near infrared spectroscopic pH decreased significantly during cardiopulmonary bypass, decreased significantly during rewarming, and remained depressed 6 hrs after cardiopulmonary bypass. Diabetic patients responded differently than nondiabetic subjects to cardiopulmonary bypass, with lower muscle pH values (p =.02). CONCLUSIONS: Near infrared spectroscopic-measured muscle pH and Po2 are sensitive to changes in tissue perfusion during cardiopulmonary bypass.

Aged↗
PubMed2000

Involvement of polyamines in the chilling tolerance of cucumber cultivars.

The possible involvement of polyamines (PAs) in the chilling tolerance of cucumber (Cucumis sativus L. cv Jinchun No. 3 and cv Suyo) was investigated. Plants with the first expanded leaves were exposed to 3 degrees C or 15 degrees C in the dark for 24 h (chilling), and then transferred to 28 degrees C/22 degrees C under a 12-h photoperiod for another 24 h (rewarming). Chilling-tolerant cv Jinchun No. 3 showed a marked increase of free spermidine (Spd) in leaves, once during chilling and again during rewarming. Putrescine increased significantly during rewarming, but the increase of spermine was slight. Any of these PAs did not increase in chilling-sensitive cv Suyo during either period. PA-biosynthetic enzyme activities appear to mediate these differences between cultivars. Pretreatment of Spd to cv Suyo prevented chill-induced increases in the contents of hydrogen peroxide in leaves and activities of NADPH oxidases and NADPH-dependent superoxide generation in microsomes and alleviated chilling injury. Pretreatment of methylglyoxal-bis-(guanylhydrazone), a PA biosynthesis inhibitor, to chilled cv Jinchun No. 3 prevented Spd increase and enhanced microsomal NADPH oxidase activity and chilling injury. The results suggest that Spd plays important roles in chilling tolerance of cucumber, probably through prevention of chill-induced activation of NADPH oxidases in microsomes.

Adaptation, Physiological↗
PubMed1988

Changes in protein synthesis induced in tomato by chilling.

Impaired chloroplast function is responsible for nearly two-thirds of the inhibition of net photosynthesis caused by dark chilling in tomato (Lycopersicon esculentum Mill.). Yet the plant can eventually recover full photosynthetic capacity if it is rewarmed in darkness at high relative humidity. As a means of identifying potential sites of chilling injury in tomato, we monitored leaf protein synthesis in chilled plants during this rewarming recovery phase, since changes in the synthesis of certain proteins might be indicative of damaged processes in need of repair. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of proteins pulse labeled with [(35)S]methionine revealed discrete changes in the pattern of protein synthesis as a result of chilling. A protein of M(r) = 27 kilodaltons (kD), abundantly synthesized by unchilled plants, declined to undetectable levels in chilled plants. Reillumination restored the synthesis of this protein in plants rewarmed for 8 hours. Peptide mapping analysis showed the 27 kD protein to be the major chlorophyll a/b binding protein of the photosystem II light-harvesting complex (LHCP-II). The identity of this protein was confirmed by its immunoprecipitation from leaf extracts by a monoclonal antibody specific for the major LHCP-II species. While chilling abolished the synthesis of the major LHCP-II species, it also induced the synthesis of an entirely new protein of M(r) = 35 kD. The protein was synthesized on cytoplasmic ribosomes, and two-dimensional polyacrylamide gel electrophroesis showed it to exist as a single isoelectric species. This chilling-induced 35 kD protein is structurally distinct from the 27 kD LHCP-II and appears to be synthesized specifically in response to low temperature. While the 35 kD protein was found not to be associated with the chloroplast thylakoid membrane, chilling did cause selective changes in thylakoid membrane protein synthesis. The synthesis of two unidentified proteins, M(r) = 14 and 41 kD, and the beta-subunit of the chloroplast coupling factor were substantially reduced after chilling. These losses may provide clues as to the causes of the overall reduction in net photosynthesis caused by chilling.

Journal Article↗
PubMed2004

The effect of bloodless pump prime on cerebral oxygenation in paediatric patients.

BACKGROUND: In paediatric patients, crystalloid prime for cardiopulmonary bypass (CPB) causes further haemodilution in comparison with blood-containing prime. Thus it may affect the cerebral oxygen supply/demand balance. The purpose of the study was to compare the effect of bloodless pump prime with that of blood-containing prime on cerebral oxygenation in children. METHODS: Thirty-six paediatric patients scheduled for elective repair of atrial or ventricular septal defect were enrolled. In Group C (n = 18), the CPB circuit was primed only with crystalloid. In Group B (n = 18), red blood cells were added to achieve a haematocrit (Hct) of 20% during CPB. The regional cerebral oxygen saturation (rSO(2)) value measured by near-infrared spectroscopy was compared between the two groups. RESULTS: In both groups, rSO(2) decreased below baseline at the start of CPB and during rewarming (P < 0.001, for both groups during each period). At the start of CPB, haemodilution was greater in Group C than in Group B (Hct 16.1 +/- 0.7% vs. 20.7 +/- 0.5%; P < 0.01), and there was a greater reduction in rSO(2) in Group C (49.0 +/- 5.4% vs. 59.2 +/- 7.0%; P < 0.01). During rewarming, rSO(2) was significantly lower in Group C than in Group B (57.8 +/- 5.3% vs. 62.8 +/- 6.2%; P < 0.01). CONCLUSIONS: In paediatric patients, the haemodilution associated with crystalloid priming causes a greater reduction in rSO(2) than with blood-containing prime at the starting period of CPB and the rewarming period.

Analysis of Variance↗
PubMed1995

Redistribution of GPIb/IX and GPIIb/IIIa during spreading of discoid platelets.

The purpose of the present study was to prelabel mobile receptors on discoid platelets with specific ligands identifiable in the electron microscope and follow their redistribution during spreading. Platelets were incubated in suspension with cytochalasin E (CE) to preserve discoid form, chilled and mounted on cold formvar grids or glass slide fragments to inhibit receptor movement, covered with cold bovine or ristocetin-activated human plasmas as sources of vWF to bind GPIb/IX, fibrinogen-coated gold particles (Fgn/Au) to couple GPIIb/IIIa, or both probes simultaneously, washed to remove CE and rewarmed to 37 degrees C for intervals up to 30 min to stimulate spreading. After brief fixation grids and glass fragments were incubated with anti-vWF antibody and, subsequently, staphylococcal protein A coupled to 5 nm and 10 nm gold particles to detect vWF multimers. Virtually all of the CE-treated chilled platelets retained their discoid shape. Half of the discs (53.3%) bound Fgn/Au, and all bound vWF. Receptors for both ligands were randomly dispersed on discoid cells from edge to edge. During rewarming discoid platelets expanded into spread forms. Fgn/Au-GPIIb/IIIa complexes moved into caps over cell centres and into residual channels of the open canalicular system (OCS). vWF bound to GPIb/IX moved with the cell membrane as the surface expanded during spreading. Discoid platelets prelabelled with both ligands demonstrated similar findings. During rewarming Fgn/Au-GPIIb/IIIa complexes moved to cell centres and into OCS channels. vWF multimers bound to GPIb/IX moved apart from each other toward peripheral margins of the spread cells. Thus, surface activation resulting in conversion of discoid platelets to spread forms does not cause clearance of GPIb/IX receptors to cell centres and channels of the OCS in the manner that GPIIb/IIIa receptors coupled to Fgn/Au are simultaneously translocated and concentrated in OCS channels.

Blood Platelets↗
PubMed1979

Myocardial performance early after aorto-coronary bypass surgery. Cardioplegic arrest versus coronary perfusion.

Haemodynamic adaptation was studied during the first 10 h after aorto-coronary bypass surgery. In a control group of 12 patients the heart was fibrillating and perfused during cardiopulmonary bypass (at 30 degrees C), and in 11 patients cold cardioplegic arrest was used. The first 4--5 h were characterized by rewarming, with increasing oesophageal temperature, cutaneous vasoconstriction and elevated systemic vascular resistance (SVR). A phase of vasodilation followed. In the control group the oxygen uptake index increased by 57% during rewarming, but the cardiac index (CI) was constant (about 2.9 l . min-1.m-2). The arterio-venous oxygen content difference (AVDo2) therefore increased (max. 3.0 mmol . l-1). The postoperative left ventricular performance was better and the serum levels of aspartate aminotransferase (ASAT) during the first 2 days postoperatively were lower in the cardioplegic patients than in the controls, indicating more efficient myocardial preservation. In the cardioplegic-hypothermic group, CI was constant at about 3.2 l . min-1.m-2 (significantly higher than in the control group) and AVDo2 remained normal during the rewarming period. The heart rate was lower initially in the cardioplegic patients than in the controls, implying a favourable influence on myocardial oxygen consumption. The better myocardial function in the cardioplegic-hypothermic group was associated with an only moderately increased SVR. This suggests that the elevated SVR in the control group could have been due to myocardial depression.

Adult↗
PubMed1986

Accidental hypothermia. Review of the literature.

The pathophysiology and treatment of accidental hypothermia are discussed. Special attention is paid to the pathophysiologic problems of rewarming. For severely hypothermic patients we would recommend peritoneal dialysis as the method of choice for rewarming in a hospital situation. In a "field situation" passive or slow active rewarming is recommended.

Humans↗
PubMed1992

Monitoring of the neuromuscular transmission by electromyography (I). Stability and temperature dependence of evoked EMG response compared to mechanical twitch recordings in the cat.

The stability over time and the effect of muscle temperature change were evaluated for the evoked compound EMG and for the mechanomyogram of the tibialis anterior muscle of 7 anaesthetized cats. Both EMG areas and amplitudes were recorded. During stimulation for 3 h with 0.1 Hz (one leg) and train-of-four (TOF) (the other leg), the EMG was stable while the mechanomyogram initially increased 35-50% in the first 7-8 min and then decreased 19-22% and 5-8% over the first and second 1.5-h period, respectively. During subsequent mean muscle temperature reduction to 28.8 degrees C (0.1 Hz) and 29.7 degrees C (TOF) and rewarming, an inverse linear relationship was found between temperature and both the EMG and the mechanomyogram. During temperature reduction EMG increased about 6% (areas) and 2% (amplitudes) per degrees C. During rewarming, parameters decreased about 4.5% and 2% per degrees C, respectively (P less than 0.05 comparing EMG areas during cooling and rewarming). TOF ratio of the EMG was not affected by temperature. A very large interindividual variation was observed for the effect of temperature on the mechanomyogram with changes ranging up to 15% per degrees C for some cats. TOF ratio of the mechanomyogram was reduced from 1.02 to 0.94 at lowest muscle temperature. It is concluded that the evoked EMG may be preferable to the mechanomyogram in cat experiments investigating the neuromuscular transmission.

Animals↗