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PubMed1996

Comparison of isolated hepatocytes and tissue slices for study of liver hypothermic preservation/reperfusion injury.

Simple models are needed that effectively test the variables that may be important in liver preservation. Two such models are isolated hepatocytes and tissue slices. In this study the effects of hypothermic preservation on the viability of hepatocytes (HC) and tissue slices (TS) from rat livers were measured by LDH leakage after cold storage and rewarming. We compared how glycine, calcium, and fasting, shown previously to affect preservation injury in hepatocytes, affected both HC and TS viability. Hepatocytes were cold-stored in University of Wisconsin organ preservation solution for up to 48 h and rewarmed in Krebs-Henseleit Bicarbonate (KHB) for 120 min. Tissue slices were studied in two ways. Either livers were cold-stored intact and then tissue slices (TS-A) prepared and rewarmed in KHB, or tissue slices were prepared from the fresh liver, cold-stored, and then rewarmed (TS-B). The latter method may be similar to cold storage of HC. Freshly prepared samples (HC, TS-A, or TS-B) showed < 15% LDH leakage during the rewarming phase. Cold storage for 24 h resulted in < 30% LDH leakage in all preparations. After 48 h cold storage there was a significant increase in LDH leakage (HC, 65.1 +/- 5.1%; TS-A, 52.9 +/- 0.8%, TS-B, 53.6 +/- 2.6%). Glycine (3 mM) or calcium (1.5 mM) included in the KHB significantly reduced LDH leakage from 48 h cold-stored HC to 20.7 +/- 1.8 and 26.3 +/- 2.4%, respectively. These agents caused a smaller decrease in LDH release from tissue slices (around 40%). Hepatocytes appear more susceptible to preservation/reperfusion damage than the more structurally intact tissue slices as suggested by the greater release of LDH. Another difference was that the agents which improved preservation quality of HC were not as effective in TS. Hepatocytes may be more vulnerable to preservation/reperfusion damage because of the harsh methods used in their preparation. The damage induced during preparation appears amenable to suppression by glycine or calcium. Tissue slices, which are intact pieces of liver tissue, may be more suitable for studies related to development of better methods for liver preservation. The intact cells in TS have not been exposed to harsh conditions and maintain a more natural cell-cell relationship.

Adenosine↗
PubMed1999

Effects of hypothermosol, an experimental acellular solution for tissue preservation and cardiopulmonary bypass, on isolated newborn lamb coronary vessels subjected to ultra profound hypothermia and anoxia.

Ultra profound hypothermia (4 to 10 degrees C) is an experimental method aiming at safely prolonging organ and total body preservation. For this purpose, Hypothermosol (HTS), an investigational acellular solution for blood substitution, was demonstrated to be beneficial in animal models undergoing cardiopulmonary bypass. We investigated the beneficial versus deleterious effects of cold preservation and the role of HTS on isolated coronary arteries (CA) during cold exposure, rewarming, and post-rewarming exposure to anoxia. Newborn lamb CA rings were studied using a tissue bath technique. CA were subjected to cold (7 degrees C for 3 h) and treated with either Krebs' buffer (Krebs/hypothermia) or HTS (HTS/hypothermia) (n = 15 each). A third group maintained at 37 degrees C (Krebs/normothermia) (n = 18) served as a time control. After rewarming (37 degrees C), precontracted CA were exposed to anoxia. In Krebs/hypothermia a substantial hypercontraction (g) occurred during rewarming (1.21+/-0.07) (mean +/- SEM) but not in HTS/hypothermia (0.79+/-0.03); P<0.05. Precontraction force generated by indomethacin/U46619 was identical in all three groups. However, Krebs/hypothermia vessels demonstrated a significantly higher relative vasoconstriction (percentage) in the early (approximately 10 min) and late (30 min) anoxia exposure than the HTS/hypothermia and time control (119.5%+/- 3.7 vs. 109.5%+/-4.4 and 101.5%+/-3, and 71%+/-7.6 vs. 38.9%+/-7 and 51.5%+/-5.9, respectively; P<0.05). In conclusion, Ultra profound hypothermia promotes coronary vasoconstriction upon rewarming, which is detrimental to relaxant response to hypoxia. Both phenomena are alleviated by performing ultra profound hypothermia under HTS protection.

Animals↗
PubMed1980

The sympathetic response to profound hypothermia and circulatory arrest in infants.

It has been suggested that the increased incidence of ventricular arrhythmias recognized below 30 degrees C might be catecholamine mediated. Elevate catecholamine concentrations have been reported in experimentally induced hypothermia in animals. Plasma concentrations of epinephrine and norepinephrine were measured during profound hypothermia and total circulatory arrest in infants under one year of age undergoing surgical correction of congenital cardiac defects. There was no significant change in either epinephrine or norepinephrine levels during surface cooling to 28 degrees C. Circulatory arrest and exsanguination at 18 degrees C were not associated with a rise in catecholamine levels. However, there was a striking rise in the levels of both epinephrine and norepinephrine with the recommencement of bypass and rewarming. The mean plasma norepinephrine concentration rose from 466 pg/ml (SE +/- 81) at circulatory arrest to 4543 pg/ml (SE +/- 2058) on rewarming bypass (p less than 0.02), while the mean plasma epinephrine concentration rose from 218 pg/ml (SE +/- 54) at circulatory arrest to 3724 pg/ml (SE +/- 1064) on rewarming bypass (p less than 0.02). The plasma catecholamine concentrations fell once cardiopulmonary bypass was discontinued, when the infant's temperature was 37 degrees C. It would, therefore, appear unlikely that the ventricular irritability recognized below 30 degrees C is due to catecholamine excess. The accumulation of catecholamines and/or metabolic products in the infants during circulatory arrest with their subsequent release into the circulation during rewarming may account for the elevation of catecholamine levels during rewarming bypass.

Body Temperature↗
PubMed2004

[Therapeutic hypothermia after traumatic brain injury or subarachnoid hemorrhage. Current practices of German anaesthesia departments in intensive care].

BACKGROUND: We aimed to explore current practices in use of therapeutic hypothermia after traumatic brain injury (TBI) or subarachnoid hemorrhage (SAH) in intensive care of adults. METHODS: Questionnaires were sent to anaesthesia department chairs in German hospitals with neurosurgical care in January 2004 with a survey focussing on cooling procedures, temperature measurement, depth and duration of hypothermia, and rewarming after therapy. RESULTS: 99 (67%) questionnaires on TBI and 95 (64%) on SAH could be analysed. Hypothermia was used in 39% after TBI and 18% after SAH. Its aims were neuroprotection in approximately 45% and control of refractory intracranial hypertension in approximately 50%. However, in most cases (69% TBI, 59% SAH) hypothermia was used in less than a quarter of patients treated. A criterion for hypothermia was severe disease in approximately 40% and refractory intracranial hypertension in approximately 50%. Temperatures were targeted to 36-34 degrees C in 77% after TBI and 88% after SAH. In more than 80%, bladder temperatures were measured. For induction of hypothermia, surface cooling was applied in approximately 90%. The duration of hypothermia was 24-48 h in 62% after TBI and 29% after SAH. Cooling was orientated at the intracranial pressure (ICP) in 31% after TBI and 47% after SAH, and was used for more than 48 h in approximately 25%. After hypothermia was stopped, a rewarming rate of 0.5 degrees C/h was applied in 38% after TBI and 53% after SAH. In approximately 35%, rewarming was orientated at the ICP, and in 33% after TBI and 24% after SAH, it was performed over 24 h. After SAH, spontaneous rewarming was used in 24%. CONCLUSION: Therapeutic hypothermia is used in 39% after TBI and 18% after SAH in the intensive care of German anaesthesia departments. There is no standard in management, and there is wide variation in practices of duration of cooling and rewarming. For patients' benefit, evidence-based recommendations on therapeutic hypothermia should be published by the appropriate medical societies in the German language.

Adult↗
PubMed2003

Effects of gender and level of surgical sympathetic block on vasoconstrictor function.

Interruption of sympathetic outflow by surgical sympathetic block has been used to treat hyperhidrosis for decades. In this study the effect of gender and the level of sympathetic block (T2 vs. T3) on the rewarming kinetics following ice water immersion were assessed in a prospective study on 60 hyperhidrosis patients before, 2 days, and 3 months postoperatively. Rewarming kinetics following endoscopic sympathetic block (ESB) was massively enhanced 2 days post-operatively, but had returned to pre-operative conditions at the 3 month follow-up for ESB at level T3. ESB at level T2 provoked significantly faster rewarming as compared to T3 at the 2 day and 3 month follow-up. Independent of the level of ESB, there was a slower rewarming in women already pre-operatively. This gender difference was clearly reduced at the 2 day follow-up, but had increased again at the 3 month follow-up. There was no correlation between the rewarming kinetics of the fingertips and palmar sweating. We conclude that for the sympathetic vasoconstriction of the fingertips the sympathetic ganglion T2 is crucial. Gender differences have to be taken into account when assessing effect of ESB by cold induced vasoconstriction. It remains to be established whether the quantification of vasoconstriction has some predictive value for the long-term prognosis of sudomotor blockade.

Adolescent↗
PubMed1991

Protection from nonfreezing cold injury by quinacrine, a phospholipase inhibitor.

A recent study from our laboratory indicated additional tissue injury during rewarming of a cooled rabbit leg. Oxygen-derived free radicals were believed to play a role in such "rewarming injury." Since free radicals may attack membrane phospholipids, we analyzed the phospholipid composition in the leg tissue during cooling and rewarming. Our results indicated significant breakdown of membrane phospholipids, particularly phosphatidylcholine and phosphatidylethanolamine, with a corresponding accumulation of lysophosphatidylcholine and nonesterified fatty acids. Quinacrine, a phospholipase inhibitor, was able to preserve membrane phospholipids during rewarming of the cooled leg. Rewarming of cooled tissue was also accompanied by additional tissue injury, as evidenced by the increased release of lactic acid dehydrogenase and creatine kinase, as well as enhanced lipid peroxidation, as evidenced by increased malonaldehyde formation. Quinacrine reduced the release of these intracellular enzymes and decreased lipid peroxidation, suggesting its efficacy as a therapeutic agent against hypothermic injury.

Animals↗
PubMed1994

Effect of bretylium tosylate on ventricular fibrillation threshold during hypothermia in dogs.

How bretylium tosylate affected the ventricular fibrillation threshold, electrophysiological parameters, and plasma catecholamine levels during hypothermia in dogs was studied. Threshold for ventricular fibrillation was determined by programmed electrical stimulation using a stimulation protocol that involved applying a maximum of five extrastimuli at body temperatures 37, 34, 31, 28, and 25 degrees C, and at the same temperatures during rewarming. Electrocardiogram, epicardial monophasic action potentials (MAP), and electrograms were recorded, and ventricular effective refractory period (VERP) was determined at each of the above temperatures. In one group (n = 7), a bolus dosage of bretylium tosylate (BT), 6 mg/kg body wt, was administered at 25 degrees C before rewarming. Another group (n = 4) was exposed to cooling and rewarming without addition of BT. Cooling to 25 degrees C reduced ventricular fibrillation threshold linearly, reduced heart rate, increased VERP and MAP, and slowed myocardial conduction velocity in both groups. There was no overall increase in plasma catecholamine levels during cooling. Addition of BT at 25 degrees C increased ventricular fibrillation threshold during rewarming compared with cooling. Addition of BT at 25 degrees C increased VERP by +/- 32 milliseconds and the corrected JT time by 0.06 +/- 0.02 seconds. VERP and JTc increased during rewarming with BT compared with cooling with no drug. BT had no effect on conduction velocity, and plasma catecholamine levels were not reduced. The antiarrhythmic effect of BT during hypothermia was attributed to an increased wavelength of refractoriness by its increase in the refractory period. This increased wavelength of refractoriness may prevent excitable gaps or increase circuit pathway in the setting of reentry arrhythmias.

Action Potentials↗
PubMed2006

A cold-response index for the assessment of Raynaud's phenomenon.

BACKGROUND: Quantification of Raynaud's phenomenon (RP) is a prerequisite in the evaluation of novel therapeutic strategies. Fingertip rewarming in response to local cold provocation has been used in many studies but not been systematically validated. We have previously described the time elapsed before 63% of pre-cooling temperature is reached as a RP activity index. OBJECTIVE: A comprehensive evaluation of fingertip rewarming in primary and scleroderma-associated RP. METHODS: We defined a cold-response index (CRI) as the log transformation of the 63% rewarming time upon cold challenge. RESULTS: The CRI shows high intra-individual reproducibility. The mean CRI values were (mean+/-S.D.): 2.4+/-0.3 in controls (n=53) versus 2.7+/-0.3 in RP (n=50, p<0.0001 versus controls), and 2.7+/-0.3 in scleroderma patients (n=46, p<0.0001). In addition, baseline fingertip temperature was also found to be significantly reduced both in primary as well as scleroderma-associated RP. Kinetic analysis of rewarming temperature curves demonstrates that the CRI is independent of individual rewarming patterns. Finally, the CRI decreases significantly upon a single low-level systemic hyperthermia treatment in scleroderma patients (2.68+/-0.28 before versus 2.45+/-0.33 after, p=0.0003), while the extent of cooling remained unchanged, thus demonstrating sensitivity to change. CONCLUSION: Our results provide a solid basis for using the cold-response assay as an endpoint in addition to clinical activity scores in RP treatment trials.

Adult↗
PubMed1997

Protective effects of adenosine on myocyte contractility during cardioplegic arrest.

BACKGROUND: Adenosine delivery to the left ventricular myocardium has been demonstrated to provide protective effects in the setting of ischemia and reperfusion. However, whether adenosine has direct protective effects on isolated myocytes in the setting of cardioplegic arrest was unclear. METHODS: Isolated porcine left ventricular myocytes were assigned to one of the following treatment groups: (1) cardioplegia: 24 mEq/L K+, 4 degrees C for 2 hours followed by rewarming (cell media, 37 degrees C; n = 29); (2) cardioplegia augmented with adenosine (1 to 200 micromol/L) followed by rewarming (n = 98); and (3) normothermic control (cell media, 37 degrees C, 2 hours; n = 175). Myocyte contractility was measured by computer-aided videomicroscopy. RESULTS: Cardioplegic arrest and rewarming reduced myocyte shortening velocity compared with normothermic control (25.3 +/- 2.5 microm/s versus 50.9 +/- 1.4 microm/s, p < 0.05). Adenosine-augmented cardioplegic arrest improved myocyte contractility with rewarming in a concentration-dependent fashion. For example, cardioplegia augmented with 10 micromol/L adenosine improved myocyte shortening velocity by 33% (33.6 +/- 3.0 microm/s versus 25.3 +/- 2.5 microm/s, p < 0.05), whereas 200 micromol/L adenosine improved shortening velocity by 97% (49.9 +/- 3.4 microm/s vs 25.3 +/- 2.5 microm/s, p < 0.05) compared with conventional cardioplegia. CONCLUSIONS: This study demonstrated concentration-dependent protective effects of adenosine-augmented cardioplegia on myocyte contractile function with subsequent reperfusion and rewarming. These results suggest that stimulation of putative myocyte adenosine receptors may provide enhanced protective effects on myocyte contractile processes during cardioplegic arrest.

Adenosine↗
PubMed1998

Selective convective brain cooling during hypothermic cardiopulmonary bypass in dogs.

BACKGROUND: Neurologic complications, primarily resulting from ischemic insults, represent the leading cause of morbidity and disability, and the second most common source of death, after cardiac operations. Previous studies have reported that increases (as occur during the rewarming phase of cardiopulmonary bypass [CPB]) or decreases in brain temperature of a mere 0.5 degrees to 2 degrees C can significantly worsen or improve, respectively, postischemic neurologic outcome. The purpose of the present study was to evaluate a novel approach of selectively cooling the brain during hypothermic CPB and subsequent rewarming. METHODS: Sixteen dogs were anesthetized with either intravenous pentobarbital or inhaled halothane (n = 8 per group). Normocapnia (alpha stat technique) and a blood pressure near 75 mm Hg were maintained. Temperatures were monitored by placing thermistors in the esophagus (i.e., core), parietal epidural space, and brain parenchyma at depths of 1 and 2 cm beneath the dura. During CPB, core temperature was actively cycled from 38 degrees C to 28 degrees C, and then returned to 38 degrees C. Forced air pericranial cooling (air temperature of approximately 13 degrees C) was initiated simultaneous with the onset of CPB, and maintained throughout the bypass period. Brain-to-core temperature gradients were calculated by subtracting the core temperature from regional brain temperatures. RESULTS: In halothane-anesthetized dogs, brain temperatures at all monitoring sites were significantly less than core during all phases of CPB, with one exception (2 cm during systemic cooling). Brain cooling was most prominent during and after systemic rewarming. For example, during systemic rewarming, average temperatures in the parietal epidural space, and 1 and 2 cm beneath the dura, were 3.3 degrees +/- 1.3 degrees C (mean +/- standard deviation), 3.2+/-1.4 degrees C, and 1.6 degrees +/-1.0 degrees C, cooler than the core, respectively. Similar trends, but of a greater magnitude, were noted in pentobarbital-anesthetized dogs. For example, during systemic rewarming, corresponding brain temperatures were 6.5 degrees +/-1.7 degrees C, 6.3 degrees +/-1.6 degrees C, and 4.2+/-1.3 degrees C cooler than the core, respectively. CONCLUSIONS: The magnitude of selective brain cooling observed in both study groups typically exceeded the 0.5 degrees to 2.0 degrees C change previously reported to modulate ischemic injury, and was most prominent during the latter phases of CPB. When compared with previous research from our laboratory, application of cold forced air to the cranial surface resulted in brain temperatures that were cooler than those observed during hypothermic CPB without pericranial cooling. On the basis of the assumption that similar beneficial brain temperature changes can be induced in humans, we speculate that selective convective brain cooling may enable clinicians to improve neurologic outcome after hypothermic CPB.

Animals↗
PubMed2003

Hypothermia causes a marked injury to rat proximal tubular cells that is aggravated by all currently used preservation solutions.

Cold preservation results in cell death via iron-dependent formation of reactive oxygen species, leading to apoptosis during rewarming. We aimed to study cold-induced damage (i.e., injury as a consequence of hypothermia itself and not cold ischemia) in proximal tubular cells (PTC) in various preservation solutions presently applied and to clarify the role of mitochondria in this injury. Primary cultures of rat PTC were incubated at 4 degrees C for 24 h in culture medium, UW, Euro-Collins or HTK solution with and without the iron chelator desferal and rewarmed at 37 degrees C in culture medium. Cell damage, morphology, and apoptosis were studied and mitochondrial membrane potential was assessed by fluorescence microscopy. Cold incubation of PTC in culture medium followed by rewarming caused marked cell damage compared to warm incubation alone (LDH release 39+/-10% vs. 1.6+/-0.3%). Cold-induced damage was aggravated in all preservation solutions (LDH release 85+/-2% for UW; similar in Euro-Collins and HTK). After rewarming, cells showed features suggestive for apoptosis. Desferal prevented cell injury in all solutions (e.g., 8+/-2% for UW). Mitochondrial membrane potential was lost during rewarming and this loss could also be inhibited by desferal. Trifluoperazine, which is known to inhibit mitochondrial permeability transition (MPT), was able to prevent cold-induced injury (LDH 85+/-5% vs. 12+/-2%). We conclude that cold-induced injury occurs in PTC and is aggravated by UW, Euro-Collins, and HTK solution. Iron-dependent MPT is suggested to play a role in this damage. Strategies to prevent cold-induced injury should aim at reducing the availability of "free" iron.

Adenosine↗
PubMed1995

Quantitative electroencephalography: a method to assess cerebral injury after hypothermic circulatory arrest.

Although hypothermic circulatory arrest and low-flow cardiopulmonary bypass are routinely used for surgical correction of congenital cardiac anomalies, use of long durations of arrest, often required for more complex repairs, raises serious concerns about cerebral safety. Searching for an intraoperative assessment that can reliably predict cerebral injury, we have found an excellent correlation between changes in quantitative electroencephalography intraoperatively and immediately postoperatively after prolonged hypothermic arrest, and neurologic and behavioral evidence of cerebral injury. After epidural placement of four recording electroencephalographic electrodes and baseline neurologic/behavioral and electroencephalographic assessment, 32 puppies were randomly assigned to one of four groups: hypothermic controls in which cooling to 18 degrees C was followed immediately by rewarming, 30 minutes of hypothermic circulatory arrest at 18 degrees C, 90 minutes of arrest at 18 degrees C, and 90 minutes of low-flow cardiopulmonary bypass at 25 ml/kg per minute at 18 degrees C. An electroencephalogram was recorded at baseline, after cooling, during rewarming, and at 2, 4, and 8 hours after the start of rewarming, as well as before the operation and 1 week after the operation. Postoperative neurologic and behavioral outcome was assessed 24 hours after cardiopulmonary bypass and daily for 1 week by means of a graded scale in which 0 is normal and 12 and 13 indicate severe neurologic injury (coma and death). Thirty animals survived the experimental protocol: two animals in the 90-minute hypothermic arrest group died before neurologic evaluation could be completed, and the remainder exhibited various degrees of neurologic and behavioral impairment, more severe on day 1 than on day 6. No animal in the remaining groups had a significant neurologic deficit. Quantitative electroencephalographic analysis shows marked differences between the 90-minute arrest group and the controls in the percent electroencephalographic silence during rewarming and at 2 hours, and in the percent recovery of baseline power at 2, 4, and 8 hours. At 2 hours after the start of rewarming, a correlation between electroencephalographic amplitude and neurologic/behavioral score on day 1 was carried out, which predicts with great certainty (p < 0.00001) that if electroencephalographic power at this time is less than 500 microV2, overt neurologic injury will subsequently become apparent. In addition, a significant shift from higher to lower frequency in the day 6 postoperative electroencephalogram compared with baseline occurs only in the 90-minute arrest group.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2000

The effect of prior hypothermia on the physiological response to norepinephrine.

OBJECTIVE: this study determines the effect of prior hypothermia on the cardiovascular responses to norepinephrine (NE) after rewarming. METHODS: the experiment was a 2x2 controlled design with four groups of feline animals. The two variables were the presence or absence of previous cooling, and the use or non-use of NE after rewarming. During the 'cooling' phase, animals were either cooled using an external arterial-venous femoral shunt to 30 degrees C or maintained at 37 degrees C. After 'rewarming' animals were stratified to receive either NE at rates to deliver 0.2, 1.0 or 5 microg/kg per h or normal saline infusions. Animals were instrumented to measure mean arterial pressure (MAP) and cardiac output (CO) and systemic vascular resistance (SVR) was calculated. RESULTS: there were no differences between groups at baseline and low dose NE (0.2 microg/kg per min). At 1.0 microg/kg per min, NE caused a significant increase in CO (P<0.01) and no effect of MAP or SVR in the rewarmed animals when compared with normothermic controls. In rewarmed animals 5.0 microg/kg per min NE caused a significant increase in CO (P<0.01) and no effect on MAP or SVR. In normothermic controls there was a significant increase in SVR (P=0.02) and MAP (P=0.05) and no effect on CO. CONCLUSION: this study shows that the effect of prior hypothermia on cardiovascular responses to moderate and high doses of NE is an improved CO with no affect on SVR and MAP. This could alter the clinical utility of NE in this situation.

Animals↗
PubMed2003

Feasibility and safety of moderate hypothermia after acute ischemic stroke.

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 (MCA) 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+/-9h after stroke onset and maintained for 24-72 h; subsequently, patients passively rewarmed over a mean duration of 17 h. Outcome was assessed at 4 weeks and at 3 months. RESULTS: Time required for cooling to <33 degrees C varied from 3.5 to 11h. 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 h) rewarming period was associated with a more pronounced rise of ICP. Elevated ICP values were significantly reduced under hypothermia. 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↗
PubMed1998

Partial inhibition of Na,K-ATPase activity in cultured rabbit non-pigmented ciliary epithelium following an episode of cytoplasmic ATP depletion.

Ouabain-sensitive ATP hydrolysis (Na,K-ATPase activity) was measured in digitonin-permeabilized monolayers of cultured cells derived from rabbit non-pigmented ciliary epithelium. Diminished Na,K-ATPase activity was observed in cells that had been pre-treated 10 min with the protein kinase C activator, PDBu, as well as in cells that had been cooled to 4 degrees C for 4 h then rewarmed to 37 degrees C for 30 min (cool-rewarm manoeuvre). In the intact cells, ouabain binding was not decreased either by PDBu treatment or the cool-rewarm manoeuvre. However, both PDBu and the cool-rewarm manoeuvre increased the rate of ouabain-sensitive potassium (86Rb) uptake measured in intact cells. Cell ATP content was diminished in PDBu-treated cells and cells subjected to the cool-rewarm manoeuvre. We suggest that an episode of ATP depletion might initiate a mechanism which causes lasting, partial inhibition of Na,K-ATPase activity. In keeping with this suggestion, diminished Na,K-ATPase activity was observed in cells that had been pre-treated 20 min with the metabolic inhibitors CCCP or rotenone and in cells pre-treated 2.5 h in dextrose-free medium. This study illustrates that Na,K-ATPase activity measured in the permeabilized cell is a complex parameter which is not necessarily a reliable indicator of sodium pump responses in the intact cell.

Adenosine Triphosphate↗
PubMed1975

Temperature regulation training in a cooling environment.

Twelve young men were given biofeedback training to enable them to increase finger temperature at will. They were dressed in warm clothing, including gloves, and placed six at a time in an environmental chamber at 7 degrees C for three hours daily for eight work days. Each was to attempt six rewarmings per session. Finger temperature was presented to the subject on a multipoint recorder. Data from 554 attempts were analyzed. A training effect was not noted, but successful rewarmings were present from the start. The 12 subjects varied considerably in ability to rewarm, from 89% to 28% successes. They were divided into the most and least consistent who, nevertheless, remained over 10 degrees C above air temperature. These performances were compared with another group wearing identical, or even much more insulative, handwear under roughly comparable conditions but without voluntary rewarming; the advantage of periodic feedback rewarming to maintain finger temperature in such conditions was obvious.

Body Temperature↗
PubMed1996

Effect of hypothermia on rectal mucosal perfusion in infants undergoing cardiopulmonary bypass.

We have examined the effect of profound hypothermia on gut mucosal perfusion in 20 infants, aged 1.4-45 weeks, requiring cardiopulmonary bypass (CPB). After induction of anaesthesia, a laser Doppler probe was inserted 8 cm into the patient's rectum to allow monitoring of rectal mucosal perfusion ("flux") throughout operation. Steady-state observation periods (5 min with no change in temperature or mean arterial pressure (MAP) were achieved after 10 min on CPB at 35 degrees C, after CPB-induced cooling to 15-25 degrees C, immediately before rewarming and after rewarming to 35 degrees C. Throughout these periods flow rate was 100 ml kg-1 min-1, packed cell volume was kept constant and Paco2 maintained at 5.3 +/- 0.5 kPa. No vasoactive drugs were used. Initial warm and rewarm MAP values (46 mm Hg) were significantly lower (P = 0.008) than during the cold CPB periods (63 and 64 mm Hg). Mean flux in the first cold period (152) was significantly lower (P = 0.001) than that in the first warm CPB period (211). Post-rewarm flux (127) was significantly lower than all other CPB flux values (P = 0.004). We conclude that although hypothermia significantly reduced mucosal blood flow, rewarming produced even greater reductions in mucosal perfusion that may prove crucial in the development of mucosal hypoxia.

Blood Pressure↗
PubMed1993

Magnesium enhances function of postischaemic human myocardial tissue.

OBJECTIVES: The effect of Mg2+ on the developed force and concentrations of high energy phosphate metabolites in isolated human atrial trabeculae has been investigated. METHODS: Human atrial trabeculae, obtained from right atrial appendages of patients undergoing cardiac surgery requiring cardiopulmonary bypass, were dissected at room temperature in modified Krebs-Henseleit buffer containing 1.2 or 16 mM Mg2+, mounted on muscle stands, and rewarmed to 34 degrees C in the same buffer. After 30 minutes, their mechanical function was assessed. At the end of the protocol, trabeculae were fast frozen for measurement of concentrations of metabolites of high energy phosphates. RESULTS: Trabeculae collected and rewarmed in 16 mM Mg2+ Krebs-Henseleit buffer showed significantly higher mean developed force (0.59(SEM 0.10) g, p < 0.01) than those rewarmed in 1.2 mM Mg2+ Krebs-Henseleit buffer (0.32(0.03) g). Trabeculae that had a developed force > or = 0.8 g, a resting force < or = 0.7 g, and a cross sectional area < or = 1 mm2 ("functional" trabeculae) were selected for further comparison. New reverse phase high performance liquid chromatography techniques developed for the analysis of small samples (0.5-5 mg dry weight) were used to measure nucleotide, nucleoside, and creatine compounds. Total adenylate (ATP+ADP+AMP) concentrations in trabeculae revived in the presence of 16 mM Mg2+ (15.4(1.1) mumol.g-1 dry weight) were significantly higher (p < 0.01) than in those revived with 1.2 mM Mg2+ (11.8(1.0) mumol.g-1), but lower (p < 0.01) than in trabeculae fast frozen immediately after removal from the patient (22.6(1.0) mumol.g-1). There were no significant differences in NAD and total creatine (phosphocreatine+creatine) concentrations between the three groups. CONCLUSIONS: The presence of high Mg2+ during the rewarming of human atrial trabecular preparations maintains a significantly higher developed force and a significantly higher total adenylate pool than does collection and rewarming with normal concentrations of Mg2+.

Aged↗