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P Safar

Publications and source records attributed to P Safar.

At least 37 records · Page 2Linked to original sources
PubMed2000

Mild or moderate hypothermia, but not increased oxygen breathing, increases long-term survival after uncontrolled hemorrhagic shock in rats.

OBJECTIVE: To test the hypotheses that, for uncontrolled hemorrhagic shock (UHS) in rats, mild hypothermia, compared with normothermia, would increase long-term survival as well as moderate hypothermia, oxygen breathing would increase survival further, and hypothermia and oxygen would mitigate visceral ischemia (dysoxia) during UHS. DESIGN: Prospective, randomized study. SETTING: Animal research laboratory. SUBJECTS: A total of 54 male Sprague-Dawley rats. INTERVENTIONS: Under light anesthesia and spontaneous breathing, rats underwent UHS phase I of 75 mins, with initial withdrawal of 3 mL/100 g of blood over 15 mins, followed by UHS via tail amputation and limited fluid resuscitation to maintain mean arterial pressure at > or =40 mm Hg; resuscitation phase II of 60 mins (from 75 mins to 135 mins) with hemostasis and aggressive fluid resuscitation to normalize hemodynamics; and observation phase III to 72 hrs. Rats were randomly divided into nine groups (n = 6 each) with three rectal temperature levels (38 degrees C [normothermia] vs. 34 degrees C [mild hypothermia] vs. 30 degrees C [moderate hypothermia]) by surface cooling; each with 3 FIO2 levels (0.25 vs. 0.5 vs. 1.0). MEASUREMENTS AND MAIN RESULTS: Hypothermia increased blood pressure compared with normothermia. Increased FIO2 had no effect on blood pressure. Additional blood loss from the tail cut was small, with no differences among groups. Hypothermia and FIO2 of 0.5 decreased visceral hypoxia, as measured by the difference between visceral (liver and jejunum) surface Pco2 and PaCO2 during UHS. Compared with normothermia, mild hypothermia increased the survival time and rate as well as moderate hypothermia (p < .01 by life table), without a significant difference between mild and moderate hypothermia. Increased FIO2 had no effect on survival time or rate. CONCLUSIONS: After severe UHS and resuscitation in rats, mild hypothermia during UHS, compared with normothermia, increases blood pressure, survival time and 72-hr survival rate as well as moderate hypothermia. Mild hypothermia is clinically more feasible and safer than moderate hypothermia. Increased FIO2 seems to have no significant effect on outcome.

Animals↗
PubMed2000

Delayed, spontaneous hypothermia reduces neuronal damage after asphyxial cardiac arrest in rats.

OBJECTIVE: Core temperature is reduced spontaneously after asphyxial cardiac arrest in rats. To determine whether spontaneous hypothermia influences neurologic damage after asphyxial arrest, we compared neurologic outcome in rats permitted to develop spontaneous hypothermia vs. rats managed with controlled normothermia. INTERVENTIONS: Male Sprague-Dawley rats were asphyxiated for 8 mins and resuscitated. After extubation, a cohort of rats was managed with controlled normothermia (CN) by placement in a servo-controlled incubator set to maintain rectal temperature at 37.4 degrees C for 48 hrs. CN rats were compared with permissive hypothermia (PH) rats that were returned to an ambient temperature environment after extubation. Rats were killed at either 72 hrs (PH72hr, n = 14; CN72hr, n = 9) or 6 wks (PH6wk, n = 6, CN6wk, n = 6) after resuscitation. PH72 rats were historic controls for the CN72 rats, whereas PH6 and CN6 rats were randomized and studied contemporaneously. MEASUREMENTS: A clinical neurodeficit score (NDS) was determined daily. A pathologist blinded to group scored 40 hematoxylin and eosin -stained brain regions for damage by using a 5-point scale (0 = none, 5 = severe). Quantitative analysis of CA1 hippocampus injury was performed by counting normal-appearing neurons in a defined subsection of CA1. MAIN RESULTS: Mean rectal temperatures measured in the PH6wk rats (n = 6) were 36.9, 34.8, 35.5, 36.7, and 37.4 degrees C at 2, 8, 12, 24, and 36 hrs, respectively. Mortality rate (before termination) was lower in PH compared with CN (0/20 vs. 7/15; p < .005). PH demonstrated a more favorable progression of NDS (p = .04) and less weight loss (p < .005) compared with CN. Median histopathology scores were lower (less damage) in PH72hr vs. CN72hr for temporal cortex (0 vs. 2.5), parietal cortex (0 vs. 2), thalamus (0 vs. 3), CA1 hippocampus (1.5 vs. 4.5), CA2 hippocampus (0 vs. 3.5), subiculum (0 vs. 4), and cerebellar Purkinje cell layer (2 vs. 4) (all p < .05). There was almost complete loss of normal-appearing CA1 neurons in CN72hr rats (6 +/- 2 [mean +/- SD] normal neurons compared with 109 +/- 12 in naïve controls). In contrast, PH72hr rats demonstrated marked protection (97 +/- 23 normal-appearing neurons) that was still evident, although attenuated, at 6 wks (42 +/- 24 normal-appearing neurons, PH6wk). CONCLUSION: Rats resuscitated from asphyxial cardiac arrest develop delayed, mild to moderate, prolonged hypothermia that is neuroprotective.

Animals↗
PubMed2000

Suspended animation for delayed resuscitation from prolonged cardiac arrest that is unresuscitable by standard cardiopulmonary-cerebral resuscitation.

Standard cardiopulmonary-cerebral resuscitation fails to achieve restoration of spontaneous circulation in approximately 50% of normovolemic sudden cardiac arrests outside hospitals and in essentially all victims of penetrating truncal trauma who exsanguinate rapidly to cardiac arrest. Among cardiopulmonary-cerebral resuscitation innovations since the 1960s, automatic external defibrillation, mild hypothermia, emergency (portable) cardiopulmonary bypass, and suspended animation have potentials for clinical breakthrough effects. Suspended animation has been suggested for presently unresuscitable conditions and consists of the rapid induction of preservation (using hypothermia with or without drugs) of viability of the brain, heart, and organism (within 5 mins of normothermic cardiac arrest no-flow), which increases the time available for transport and resuscitative surgery, followed by delayed resuscitation. Since 1988, we have developed and used novel dog models of exsanguination cardiac arrest to explore suspended animation potentials with hypothermic and pharmacologic strategies using aortic cold flush and emergency portable cardiopulmonary bypass. Outcome evaluation was at 72 or 96 hrs after cardiac arrest. Cardiopulmonary bypass cannot be initiated rapidly. A single aortic flush of cold saline (4 degrees C) at the start of cardiac arrest rapidly induced (depending on flush volume) mild-to-deep cerebral hypothermia (35 degrees to 10 degrees C), without cardiopulmonary bypass, and preserved viability during a cardiac arrest no-flow period of up to 120 mins. In contrast, except for one antioxidant (Tempol), explorations of 14 different drugs added to the aortic flush at room temperature (24 degrees C) have thus far had disappointing outcome results. Profound hypothermia (10 degrees C) during 60-min cardiac arrest induced and reversed with cardiopulmonary bypass achieved survival without functional or histologic brain damage. Further plans for the systematic development of suspended animation include the following: a) aortic flush, combining hypothermia with mechanism-specific drugs and novel fluids; b) extension of suspended animation by ultraprofound hypothermic preservation (0 degrees to 5 degrees C) with cardiopulmonary bypass; c) development of the most effective suspended animation protocol for clinical trials in trauma patients with cardiac arrest; and d) modification of suspended animation protocols for possible use in normovolemic ventricular fibrillation cardiac arrest, in which attempts to achieve restoration of spontaneous circulation by standard external cardiopulmonary resuscitation-advanced life support have failed.

Advanced Cardiac Life Support↗
PubMed2000

Peritoneal ventilation with oxygen improves outcome after hemorrhagic shock in rats.

OBJECTIVE: In experimental pulmonary consolidation with hypoxemia in rabbits, peritoneal ventilation (PV) with 100% oxygen (PV-O2) improved PaO2. We hypothesized that PV-O2 could improve outcome after hemorrhagic shock (HS) with normal lungs, by mitigating dysoxia of the abdominal viscera. DESIGN: Randomized, controlled, laboratory animal study. SETTING: University animal research facility. SUBJECTIVE: Male Sprague-Dawley rats. INTERVENTIONS: Thirty rats under light anesthesia (N2O/oxygen plus halothane) and spontaneous breathing underwent blood withdrawal of 3 mL/100 g over 15 mins. After volume-controlled HS phase 1 of 60 mins, resuscitation phase 2 of 60 mins included infusion of shed blood and, if necessary, additional lactated Ringer's solution intravenously to control normotension from 60 to 120 mins. This was followed by observation phase 3 for 7 days. We randomized three groups of ten rats each: group I received PV-O2, starting at 15 mins of HS at a rate of 40 inflations/min, and a peritoneal "tidal volume" of 6 mL, until the end of phase 2. Group II received the same PV with room air (PV-Air). Control group III was treated without PV. MEASUREMENTS AND MAIN RESULTS: During the second half of HS phase 1, mean arterial pressures were higher in the PV-O2 group I compared with the PV-Air group II and control group III (p < .05). All 30 rats survived the 120 mins of phases 1 and 2. Survival to 7 days was achieved by ten of ten rats in PV-O2 group I; by nine of ten in PV-Air group II; and by five of ten in control group III (p < .05 vs. group I; NS vs. group II). Survival times of <7 days were 5 days in the one death of group II and ranged between 6 hrs and 4 days in the five deaths of group III. In 7-day survivors, neurologic deficit scores (0% to 10% = normal, 100% = death) were normal, ranging between zero and 8%. Necropsies of rats that died during phase 3 showed multiple areas of necrosis of the gut, some with perforations. Necropsies in the five survivors to 7 days of group III showed marked macroscopic and microscopic changes (scattered areas of necrosis of stomach and intestine, adhesions, and pale areas in the liver). These changes were absent or less severe in the nine survivors of group II. Viscera appeared normal in all ten rats of PV-O2 group I. CONCLUSIONS: Peritoneal ventilation with oxygen during and after severe hemorrhagic shock in rats seems to decrease morbidity and mortality by helping preserve viability of abdominal viscera.

Animals↗
PubMed2000

Rapid induction of mild cerebral hypothermia by cold aortic flush achieves normal recovery in a dog outcome model with 20-minute exsanguination cardiac arrest.

OBJECTIVES: Resuscitation attempts in trauma victims who suffer cardiac arrest (CA) from exsanguination almost always fail. The authors hypothesized that an aortic arch flush with cold normal saline solution (NSS) at the start of exsanguination CA can preserve cerebral viability during 20-minute no-flow. METHODS: Twelve dogs were exsanguinated over 5 minutes to CA of 20-minute no-flow, resuscitated by cardiopulmonary bypass, followed by post-CA mild hypothermia (34 degrees C) continued to 12 hours, controlled ventilation to 20 hours, and intensive care to 72 hours. At CA 2 minutes, the dogs received a 500-mL flush of NSS at either 24 degrees C (group 1, n = 6) or 4 degrees C (group 2, n = 6), using a balloon-tipped catheter inserted via the femoral artery into the descending thoracic aorta. RESULTS: The flush at 24 degrees C (group 1) decreased tympanic membrane temperature [mean (+/-SD)] from 37.5 degrees C (+/-0.1) to 35.7 degrees C (+/-0.2); the flush at 4 degrees C (group 2) to 34.0 degrees C (+/-1.1) (p = 0.005). In group 1, one dog achieved overall performance category (OPC) 2 (moderate disability), one OPC 3 (severe disability), and four OPC 4 (coma). In group 2, four dogs achieved OPC 1 (normal), one OPC 2, and one OPC 3 (p = 0.008). Neurologic deficit scores (0-10% normal, 100% brain death) [median (25th-75th percentile)] were 62% (40-66) in group 1 and 5% (0-19) in group 2 (p = 0.01). Total brain histologic damage scores were 130 (62-137) in group 1 and 24 (10-55) in group 2 (p = 0.008). CONCLUSIONS: Aortic arch flush of 4 degrees C at the start of CA of 20 minutes rapidly induces mild cerebral hypothermia and can lead to normal functional recovery with minimal histologic brain damage. The same model with aortic arch flush of 24 degrees C results in survival with brain damage in all dogs, which makes it suitable for testing other (e.g., pharmacologic) preservation potentials.

Animals↗
PubMed2000

On the future of reanimatology.

This article is adapted from a presentation given at the 1999 SAEM annual meeting by Dr. Peter Safar. Dr. Safar has been involved in resuscitation research for 44 years, and is a distinguished professor and past initiating chairman of the Department of Anesthesiology and Critical Care Medicine at the University of Pittsburgh. He is the founder and director of the Safar Center for Resuscitation Research at the University of Pittsburgh, and has been the research mentor of many critical care and emergency medicine research fellows. Here he presents a brief history of past accomplishments, recent findings, and future potentials for resuscitation research. Additional advances in resuscitation, from acute terminal states and clinical death, will build upon the lessons learned from the history of reanimatology, including optimal delivery by emergency medical services of already documented cardiopulmonary cerebral resuscitation, basic-advanced-prolonged life support, and future scientific breakthroughs. Current controversies, such as how to best educate the public in life-supporting first aid, how to restore normotensive spontaneous circulation after cardiac arrest, how to rapidly induce mild hypothermia for cerebral protection, and how to minimize secondary insult after cerebral ischemia, are discussed, and must be resolved if advances are to be made. Dr. Safar also summarizes future technologies already under preliminary investigation, such as ultra-advanced life support for reversing prolonged cardiac arrest, extending the "golden hour" of shock tolerance, and suspended animation for delayed resuscitation.

Advanced Cardiac Life Support↗
PubMed2000

Hypothermia and hyperthermia in children after resuscitation from cardiac arrest.

OBJECTIVE: In experimental models of ischemic-anoxic brain injury, changes in body temperature after the insult have a profound influence on neurologic outcome. Specifically, hypothermia ameliorates whereas hyperthermia exacerbates neurologic injury. Accordingly, we sought to determine the temperature changes occurring in children after resuscitation from cardiac arrest. STUDY DESIGN: The clinical records of 13 children resuscitated from cardiac arrest were analyzed. Patients were identified through the emergency department and pediatric intensive care unit arrest logs. Only patients surviving for > or =12 hours after resuscitation were considered for analysis. Charts were reviewed for body temperatures, warming or cooling interventions, antipyretic and antimicrobial administration, and evidence of infection. RESULTS: Seven patients had a minimum temperature (T min) of < or =35 degrees C and 11 had a maximum temperature (T max) of > or =38.1 degrees C. Hypothermia often preceded hyperthermia. All 7 patients with T min < or =35 degrees C were actively warmed with heating lamps and 5 of 7 responded to warming with a rebound of body temperatures > or =38.1 degrees C. None of the 6 patients with T min >35 degrees C were actively warmed but all developed T max > or =38.1 degrees C. Six patients received antipyretics and 11 received antibiotics. Fever was not associated with a positive culture in any case. Conclusion. Spontaneous hypothermia followed by hyperthermia is common after resuscitation from cardiac arrest. Temperature should be closely monitored after cardiac arrest and fever should be managed expectantly.

Body Temperature↗
PubMed1999

Therapeutic hypothermia in traumatology.

Despite its proven clinical application for protection-preservation of the brain and heart during cardiac surgery, hypothermia research has fallen in and out of favor many times since its inception. Since the 1980s, there has been renewed research and clinical interest in therapeutic hypothermia for resuscitation of the brain after cardiac arrest or TBI and for preservation-resuscitation of extracerebral organs, particularly the abdominal viscera in low-flow states such as HS. Although some of the fears regarding the side effects of hypothermia are warranted, others are not. Without further laboratory and clinical studies, the significance of these effects cannot be determined and ways to overcome these problems cannot be developed. Currently, at the turn of the century, there are significant data demonstrating the benefit of mild-to-moderate hypothermia in animals and humans after cardiac arrest or TBI and in animals during and after HS. The clinical implications of uncontrolled versus controlled hypothermia in trauma patients and the best way to assure poikilothermia for cooling without shivering are still unclear. It is time to consider a prospective trial of therapeutic, controlled hypothermia for patients during traumatic HS and resuscitation. The authors believe that the new millennium will witness remarkable advantages of the use of controlled hypothermia in trauma. Starting in the prehospital phase, mild hypothermia will be induced in hypovolemic patients, which will not only decrease the immediate mortality rate but perhaps also will protect cells and reduce the likelihood of secondary inflammatory response syndrome, multiple organ failure, and late deaths. The most futuristic applications will be hypothermic strategies to achieve prolonged suspended animation for delayed resuscitation in traumatic exsanguination cardiac arrest.

Animals↗
PubMed1999

Life supporting first aid training of the public--review and recommendations.

Since the introduction around 1960 of external cardiopulmonary resuscitation (CPR) basic life support (BLS) without equipment, i.e. steps A (airway control)-B (mouth-to-mouth breathing)-C (chest (cardiac) compressions), training courses by instructors have been provided, first to medical personnel and later to some but not all lay persons. At present, fewer than 30% of out-of-hospital resuscitation attempts are initiated by lay bystanders. The numbers of lives saved have remained suboptimal, in part because of a weak or absent first link in the life support chain. This review concerns education research aimed at helping more lay persons to acquire high life supporting first aid (LSFA) skill levels and to use these skills. In the 1960s, Safar and Laerdal studied and promoted self-training in LSFA, which includes: call for the ambulance (without abandoning the patient) (now also call for an automatic external defibrillator); CPR-BLS steps A-B-C; external hemorrhage control; and positioning for shock and unconsciousness (coma). LSFA steps are psychomotor skills. Organizations like the American Red Cross and the American Heart Association have produced instructor-courses of many more first aid skills, or for cardiac arrest only-not of LSFA skills needed by all suddenly comatose victims. Self-training methods might help all people acquire LSFA skills. Implementation is still lacking. Variable proportions of lay trainees evaluated, ranging from school children to elderly persons, were found capable of performing LSFA skills on manikins. Audio-tape or video-tape coached self-practice on manikins was more effective than instructor-courses. Mere viewing of demonstrations (e.g. televised films) without practice has enabled more persons to perform some skills effectively compared to untrained control groups. The quality of LSFA performance in the field and its impact on outcome of patients remain to be evaluated. Psychological factors have been associated with skill acquisition and retention, and motivational factors with application. Manikin practice proved necessary for best skill acquisition of steps B and C. Simplicity and repetition proved important. Repetitive television spots and brief internet movies for motivating and demonstrating would reach all people. LSFA should be part of basic health education. LSFA self-learning laboratories should be set up and maintained in schools and drivers' license stations. The trauma-focused steps of LSFA are important for 'buddy help' in military combat casualty care, and natural mass disasters.

Cardiopulmonary Resuscitation↗
PubMed1999

Ventilation and cardiopulmonary resuscitation.

Ventilation is essential for oxygenation of the alveoli and arterial blood. Comatose humans have upper airway soft tissue obstruction unless the head is tilted backwards and sometimes, in addition, the jaw thrust forward. In 1960, measurements on comatose humans with or without cardiac arrest, with or without a tracheal tube, showed essentially no ventilation by sternal compressions alone. This led to combining step A (airway control), step B (mouth-to-mouth ventilation), and step C (sternal (cardiac) compressions) into basic life support. In animal models, sternal compressions alone can produce some ventilation with or without a tracheal tube, because the straight upper airways of animals do not obstruct in coma. In witnessed sudden cardiac death, the C-A-B sequence makes physiological sense, but other causes of sudden coma need the A-B-C sequence. Lay persons should continue to be taught cardiopulmonary resuscitation steps A-B-C.

Journal Article↗
PubMed1999

Mild or moderate hypothermia but not increased oxygen breathing prolongs survival during lethal uncontrolled hemorrhagic shock in rats, with monitoring of visceral dysoxia.

OBJECTIVE: To test the hypotheses that during lethal uncontrolled hemorrhagic shock (UHS) in rats compared with normothermia and room air breathing: a) mild hypothermia would prolong survival time as well as moderate hypothermia; b) oxygen breathing would prolong survival further; and c) hypothermia and oxygen would mitigate visceral ischemia (dysoxia) during UHS. DESIGN: Prospective, randomized, controlled laboratory animal study. SETTING: Animal research facility. SUBJECTS: Male Sprague-Dawley rats. INTERVENTION: Fifty-four rats were lightly anesthetized with halothane during spontaneous breathing. UHS was induced by blood withdrawal of 3 mL/100 g over 15 mins, followed by 75% tail amputation with topical application of heparin. Five minutes after tail cut, rats were randomly divided into nine groups (6 rats each) with three rectal temperature levels (38 degrees C [100.4 degrees F; normothermia] vs. 34 degrees C [93.2 degrees F; mild hypothermia] vs. 30 degrees C [86 degrees F; moderate hypothermia]) by surface cooling; each with 3 FIO2 levels (0.25 vs. 0.5 vs. 1.0). Rats were observed without fluid resuscitation until death (apnea and pulselessness). Visceral ischemia was monitored by observing liver and gut surface PCO2. MEASUREMENTS AND MAIN RESULTS: Mean survival time, which was 51 mins in the control group with normothermia and FIO2 of 0.25, was more than doubled with hypothermia, to 119 mins in the combined mild hypothermia groups (p < .05) and to 132 mins in the combined moderate hypothermia groups (p < .05; NS for moderate vs. mild hypothermia). FIO2 had no statistically significant effect on survival time. Increases in visceral surface PCO2 correlated with hypotension (r2 = .22 for intestine and .40 for liver). Transiently, increased FIO2, not hypothermia, mitigated visceral ischemia. CONCLUSIONS: Both mild and moderate hypothermia prolonged survival time during untreated, lethal UHS in rats. Increased FIO2 had no effect on survival. The effects of hypothermia and increased FIO2 during UHS on viscera, the ability to be resuscitated, and outcome should be explored further.

Animals↗
PubMed1999

Hypothermic aortic arch flush for preservation during exsanguination cardiac arrest of 15 minutes in dogs.

BACKGROUND: Trauma victims rarely survive cardiac arrest from exsanguination. Survivors may suffer neurologic damage. Our hypothesis was that a hypothermic aortic arch flush of 500 mL of isotonic saline solution at 4 degrees C, compared with 24 degrees C (room temperature), administered at the start of prolonged exsanguination cardiac arrest (CA) would improve functional neurologic outcome in dogs. METHODS: Seventeen male hunting dogs were prepared under light N2O-halothane anesthesia. The animals were randomized into two groups: group I (n = 9) received 4 degrees C isotonic saline flush and group II (n = 6) received 24 degrees C flush. Two additional dogs received no flush. While spontaneously breathing, the dogs underwent normothermic (tympanic membrane temperature [Ttm] = 37.5 degrees C) exsanguination over 5 minutes to cardiac arrest, assured by electric induction of ventricular fibrillation. After 2 minutes of arrest, the flush was administered over 1 minute into the aortic arch by means of a 13 French balloon-tipped catheter inserted by means of the femoral artery. After 15 minutes of CA, resuscitation was with closed-chest cardiopulmonary bypass, return of shed blood, and defibrillation. For the first 12 hours after CA, core temperature was maintained at 34 degrees C. Mechanical ventilation was continued to 20 hours and intensive care to 72 hours, when final evaluation and perfusion-fixation killing for brain histologic damage scoring were performed. RESULTS: Three dogs in group I were excluded because of extracerebral complications. All 14 dogs that followed protocol survived. During CA, the Ttm decreased to 33.6 +/- 1.2 degrees C in group I and 35.9 +/- 0.4 degrees C in group II (p = 0.002). At 72 hours, in group I, all dogs achieved an overall performance category (OPC) of 1 (normal). In group II, 1 dog was OPC 2 (moderate disability), 3 dogs were OPC 3 (severe disability), and 2 dogs were OPC 4 (coma). Both dogs without flush were OPC 4. Neurologic deficit scores (NDS 0% = normal, 100% = brain death) were 1 +/- 1% in group I and 41 +/- 12% in group II (p < 0.05). The two dogs without flush achieved an NDS of 47% and 59%. Total brain histologic damage scores were 35 +/- 28 in group I and 82 +/- 17 in group II (p < 0.01); and 124 and 200 in the nonflushed dogs. CONCLUSION: At the start of 15 minutes of exsanguination cardiac arrest in dogs, hypothermic aortic arch flush allows resuscitation to survival with normal neurologic function and histologically almost clean brains.

Animals↗
PubMed1999

Do standard monitoring sites affect true brain temperature when hyperthermia is rapidly induced and reversed.

BACKGROUND: Accurate measurements of brain and core temperatures during warming and cooling of the whole organism, accidentally or therapeutically, are important for studies of thermoregulation and cerebral insults and resuscitation. HYPOTHESIS: During steady states and normal circulation, temperatures in the brain, nasopharynx, esophagus and rectum (the latter are core temperatures) equilibrate quickly; and that during rapid cooling or warming, slight temperature gradients occur, with esophageal core temperature reflecting brain temperature better than rectal temperature. METHODS: We evaluated 5 mongrel dogs and 12 pigtail monkeys. The animals were exposed to total body hyperthermia by immersion into water at 45 degrees C to achieve cerebral temperature 42 degrees C which was maintained until cardiac arrest. In monkeys, at cardiac arrest, surface cooling and cardiopulmonary resuscitation were attempted for up to 30 min to determine resuscitability at 38.5 degrees C. Continuously monitored were brain (epidural) (Tep), esophageal (Tes), rectal (Tre) and nasopharyngeal temperatures (Tnp). Also monitored were mean arterial pressure and intracranial pressure. RESULTS: At normothermia, in dogs and monkeys, Tep, Tre, Tes and Tnp correlated well. In the dogs, during heating, Tes, Tnp and Tre at first correlated well. Vigorous panting started as Tep reached 41 degrees C, which immediately lowered Tnp and Tep to increase less steeply than Tes and Tre. After about 40 min of panting, with cerebral perfusion pressure still normal, Tep decreased sharply and reached the levels of Tnp, while Tre remained high. In the monkeys during heating, Tep, Tes and Tre correlated well. When cerebral perfusion pressure decreased below 50 mmHg, Tep declined significantly as compared with Tre, which continued to be high in severe arterial hypotension. Tes at that time achieved levels between Tep and Tre. During cooling in monkeys, the decline in Tre was slower as compared with the decline in Tes and Tep. CONCLUSIONS: In normal dogs and monkeys, rectal, esophageal and nasopharyngeal temperatures are almost identical with brain temperatures; but during rapid external warming or cooling, brain temperature is reflected in nasopharyngeal temperature, somewhat in higher esophageal temperature, but not in even higher rectal temperature. For clinical monitoring during temperature changes, one should use primarily esophageal temperature and, if feasible, brain (epidural) temperature as well.

Animals↗
PubMed1998

Glucose plus insulin infusion improves cerebral outcome after asphyxial cardiac arrest.

Hyperglycemia before ischemia worsens cerebral outcome. The aim of this study was to determine the cerebral effects of giving glucose with or without insulin after asphyxial cardiac arrest. Rats underwent 8 min of asphyxial cardiac arrest. After arrest, Group 1 received NaCl; Group 2, insulin; Group 3, glucose; and Group 4, glucose plus insulin, all intravenously. Neurological deficit (ND) scores were 14+/-10%, 22+/-12%, 12+/-10% and 2+/-2% in Groups 1-4, respectively, 72 h after reperfusion. Overall histological damage (HD) scores were 4, 2, 3 and 1, respectively. Group 4 fared significantly better than group 1 on both scores. Glucose after asphyxial cardiac arrest in rats produces no increased brain damage while glucose plus insulin improves cerebral outcome.

Animals↗