MSc., Faculty of Science, University of the Witwatersrand, 2011 / Wild animals are captured for management, health, translocation and research purposes. Capture is an unnaturally stressful event, which may result in morbidity or mortality. An attributing cause of the morbidity and mortality is capture-induced hyperthermia; the larger the magnitude and the longer the duration of this captured-induced hyperthermia, the greater the likely risk to the animal. The most common practice currently used in the field to lower body temperature is to douse hyperthermic animals with water. However, the water used is often at ambient temperatures and its efficacy is not known. We investigated whether this method and alternative methods are effective at lowering the body temperature of hyperthermic animals. To achieve these aims we implanted 19 blesbok with miniature temperature-sensitive data loggers in their abdomens and into their subcutaneous layers (at the sites of the flank, groin, lower neck and upper neck). The loggers continuously recorded core body temperatures of the blesbok throughout the study period at an interval of six minutes. We successfully retrieved complete data sets from 12 blesbok. The animals were captured on six separate occasions using a technique which elicited hyperthermia. Five animals were cooled by dousing with water of different temperatures (4°C, 17°C, 28°C) and fanning after dousing with 28°C water, in random order. Seven animals were cooled by ice packs, spraying a fine mist spray, intravenous (IV) infusion of one litre of 4°C water and 28°C water-dousing. Through the use of our continuous logging of body temperature we established the normal body temperature of the blesbok, which displayed a regular 24 hour body temperature pattern. The average daily body temperature of the blesbok was 38.8°C ± 0.4°C, with a minimum body temperature of 37.9°C ± 0.1°C and a maximum body temperature of 39.4°C ± 0.1°C. The body temperature after capture was as high as 41°C-42°C, which was significantly higher than the normal body temperature (Student’s t-test, P < 0.05). The animals were cooled once they were immobilised and the start of cooling was denoted as time zero. In the control (no active cooling) intervention the body temperature decreased to only about 40°C. Dousing animals with water, irrespective of its temperature, resulted in significant cooling (P < 0.05) of the animals, as indicated by their minimum body temperature reached, change in body temperature and rate of cooling. The water-dousing interventions decreased the body temperature to about 38°C after an hour, which was significantly lower than the control (RM-ANOVA, P < 0.05) but there was no significant difference in the minimum body temperature reached between the different water temperatures or by the addition of fanning (RM-ANOVA, P > 0.05). The water-dousing interventions cooled the animals more quickly than did the control (RM-ANOVA, P < 0.05), and the coldest water (4°) cooled the animals quicker than did the 28°C water-dousing (RM-ANOVA, P < 0.05). The core body temperature minus the subcutaneous temperature was calculated, and revealed a peak difference of about 3.5°C after the 4°C water-dousing. Ice-packs also resulted in significant cooling (P < 0.05) of the animals, as depicted by their minimum body temperature reached, change in body temperature and rate of cooling. The ice-packs lowered the body temperature to a minimum of about 38°C, which was significantly lower than the control (RM-ANOVA, P < 0.05). The ice-packs also cooled the animals significantly faster than did the control, intravenous infusion and mist spray (RM-ANOVA, P < 0.05) but cooled as quickly as the 28°C water-dousing (RM-ANOVA, P > 0.05). The core body temperature minus the subcutaneous temperature for the ice-packs peaked at a difference of about 3°C. The IV infusion and mist spray were ineffective cooling methods and did not significantly (P > 0.05) alter the minimum body temperature or rate of cooling. Even though the IV infusion caused a significant reduction in body temperature by 1°C, the cooling effect from the IV infusion was short-lived because the minimum body temperature reached after the intravenous infusion and mist spray was ultimately similar to the body temperature seen in animals receiving the control (RM-ANOVA P > 0.05). Also, the intravenous infusion and mist-spray cooled as slowly as did the control (RM-ANOVA P > 0.05). Therefore, water-dousing in this study was the most effective and practical method to cool hyperthermic blesbok. Although all the water temperatures (4°C, 17°C and 28°C) that we tested were effective, the coldest water (4°C) cooled the animals quickest. The addition of fanning to the 28°C water-dousing did not increase cooling. Ice-packs were also effective but may be not as easy to use as the water-dousing method as ice-packs are large and need to be kept frozen, and therefore are cumbersome for use in the field.

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INTRODUÇÃO: Evidências relevantes acerca dos benefícios da hipotermia terapêutica provieram da utilização de técnicas de resfriamento sistêmico. Essas técnicas, no entanto, podem causar complicações graves que poderiam ser evitadas com métodos de hipotermia encefálica seletiva. O presente estudo objetiva: 1) verificar a viabilidade da hipotermia encefálica exclusiva através de um sistema de resfriamento nasofaríngeo concomitante ao de preservação da temperatura corpórea em suínos e 2) investigar os efeitos da hipotermia encefálica exclusiva nas variáveis fisiológicas sistêmicas e encefálicas. MÉTODOS: Dez suínos híbridos foram submetidos a resfriamento nasofaríngeo durante 60 minutos e subsequente reaquecimento espontâneo. Foram obtidos dados referentes a: pressão arterial média, débito cardíaco, temperatura encefálica, pressão parcial de oxigênio do tecido encefálico (PbtO2, do inglês, pressure of brain tissue O2), velocidade do fluxo sanguíneo nas artérias encefálicas, índice de resistência e índice de pulsatilidade. RESULTADOS: O resfriamento nasofaríngeo associou-se à um decréscimo gradual da temperatura encefálica, que foi mais marcante no hemisfério cerebral esquerdo (p < 0,01). Neste hemisfério, houve redução de 1,47 ± 0,86°C nos primeiros 5 minutos (p < 0,01), 2,45 ± 1,03°C aos 10 minutos e 4,45 ± 1,36°C após 1 hora (p < 0,01). A diferença entre as temperaturas cerebral sistêmica foi 4,57 ± 0,87°C (p < 0,01). As temperaturas centrais (retal, esofágica e da artéria pulmonar), assim como a hemodinâmica encefálica e sistêmica, mantiveram-se estáveis durante o procedimento. Houve diminuição significativa da PbtO2, concomitantemente ao decréscimo da temperatura encefálica. CONCLUSÕES: A indução de hipotermia encefálica exclusiva é possível através de resfriamento nasofaríngeo associado a medidas de preservação da temperatura sistêmica. O resfriamento encefálico exclusivo não influencia as funções hemodinâmicas sistêmicas e encefálicas, contudo reduz significativamente a PbtO2 / INTRODUCTION: Relevant evidences for the use of therapeutic hypothermia derive from studies using whole body cooling methods. These methods can lead to serious complications. To avoid such complications, selective brain cooling methods were developed. The objective of this study was: 1) to verify the feasibility of exclusive brain hypothermia by means of nasopharyngeal cooling along with measures of systemic temperature preservation in an experimental swine model, and 2) to investigate the influence of the exclusive brain cooling on cerebral and systemic hemodynamics as well as on cerebral oxygenation. METHODS: Ten hybrid swine underwent nasopharyngeal cooling for 60 minutes, followed by spontaneous rewarming. A number of physiological variables were monitored: arterial blood pressure, cardiac output, temperature in the right and left cerebral hemispheres, pressure of brain tissue O2, cerebral blood flow velocities, resistance index, and pulsatility index. RESULTS: Nasopharyngeal cooling was associated with decrease in brain temperature, which was more significant in the left cerebral hemisphere (p < 0,01). There was a reduction of 1.47 ± 0.86°C in the first 5 minutes (p < 0.01), 2.45 ± 1.03°C within 10 min, and 4.45 ± 1.36°C after 1 hour (p < 0.01). The brain-core gradient was 4.57 ± 0.87°C (p < 0,001). Rectal, esophageal, and pulmonary artery temperatures, as well as brain and systemic hemodynamics, remained stable during the procedure. PbtO2 values significantly decreased following the brain cooling. CONCLUSION: Achievement of exclusive brain hypothermia is feasible by means of nasopharyngeal cooling associated with measures of systemic temperature preservation. Selective brain cooling does not influence both systemic and cerebral hemodynamics, except PbtO2, which decreased significantly

INTRODUÇÃO: Evidências relevantes acerca dos benefícios da hipotermia terapêutica provieram da utilização de técnicas de resfriamento sistêmico. Essas técnicas, no entanto, podem causar complicações graves que poderiam ser evitadas com métodos de hipotermia encefálica seletiva. O presente estudo objetiva: 1) verificar a viabilidade da hipotermia encefálica exclusiva através de um sistema de resfriamento nasofaríngeo concomitante ao de preservação da temperatura corpórea em suínos e 2) investigar os efeitos da hipotermia encefálica exclusiva nas variáveis fisiológicas sistêmicas e encefálicas. MÉTODOS: Dez suínos híbridos foram submetidos a resfriamento nasofaríngeo durante 60 minutos e subsequente reaquecimento espontâneo. Foram obtidos dados referentes a: pressão arterial média, débito cardíaco, temperatura encefálica, pressão parcial de oxigênio do tecido encefálico (PbtO2, do inglês, pressure of brain tissue O2), velocidade do fluxo sanguíneo nas artérias encefálicas, índice de resistência e índice de pulsatilidade. RESULTADOS: O resfriamento nasofaríngeo associou-se à um decréscimo gradual da temperatura encefálica, que foi mais marcante no hemisfério cerebral esquerdo (p < 0,01). Neste hemisfério, houve redução de 1,47 ± 0,86°C nos primeiros 5 minutos (p < 0,01), 2,45 ± 1,03°C aos 10 minutos e 4,45 ± 1,36°C após 1 hora (p < 0,01). A diferença entre as temperaturas cerebral sistêmica foi 4,57 ± 0,87°C (p < 0,01). As temperaturas centrais (retal, esofágica e da artéria pulmonar), assim como a hemodinâmica encefálica e sistêmica, mantiveram-se estáveis durante o procedimento. Houve diminuição significativa da PbtO2, concomitantemente ao decréscimo da temperatura encefálica. CONCLUSÕES: A indução de hipotermia encefálica exclusiva é possível através de resfriamento nasofaríngeo associado a medidas de preservação da temperatura sistêmica. O resfriamento encefálico exclusivo não influencia as funções hemodinâmicas sistêmicas e encefálicas, contudo reduz significativamente a PbtO2 / INTRODUCTION: Relevant evidences for the use of therapeutic hypothermia derive from studies using whole body cooling methods. These methods can lead to serious complications. To avoid such complications, selective brain cooling methods were developed. The objective of this study was: 1) to verify the feasibility of exclusive brain hypothermia by means of nasopharyngeal cooling along with measures of systemic temperature preservation in an experimental swine model, and 2) to investigate the influence of the exclusive brain cooling on cerebral and systemic hemodynamics as well as on cerebral oxygenation. METHODS: Ten hybrid swine underwent nasopharyngeal cooling for 60 minutes, followed by spontaneous rewarming. A number of physiological variables were monitored: arterial blood pressure, cardiac output, temperature in the right and left cerebral hemispheres, pressure of brain tissue O2, cerebral blood flow velocities, resistance index, and pulsatility index. RESULTS: Nasopharyngeal cooling was associated with decrease in brain temperature, which was more significant in the left cerebral hemisphere (p < 0,01). There was a reduction of 1.47 ± 0.86°C in the first 5 minutes (p < 0.01), 2.45 ± 1.03°C within 10 min, and 4.45 ± 1.36°C after 1 hour (p < 0.01). The brain-core gradient was 4.57 ± 0.87°C (p < 0,001). Rectal, esophageal, and pulmonary artery temperatures, as well as brain and systemic hemodynamics, remained stable during the procedure. PbtO2 values significantly decreased following the brain cooling. CONCLUSION: Achievement of exclusive brain hypothermia is feasible by means of nasopharyngeal cooling associated with measures of systemic temperature preservation. Selective brain cooling does not influence both systemic and cerebral hemodynamics, except PbtO2, which decreased significantly

Paraplegia or paraparesis caused by temporary cross-clamping of the aorta is a devastating sequela in patients after surgery of the thoracoabdominal aorta. No effective clinical method is available to protect the spinal cord from ischemic reperfusion injury. A small animal (rat) model of spinal cord ischemia is established to better understand the pathophysiological events and to evaluate potential treatments. Eighty-one male Sprague-Dawley rats weighing 300 g to 350 g were used for model development (45) and treatment evaluation (36). The heparinized and anesthetized rat was supported by a respirator following tracheostomy. The thoracic aorta was cannulated via the left carotid artery for post-clamping intra-aortic treatment solution administration. After thoracotomy, the aorta was freed and temporarily clamped just distal to the left subclavian artery and just proximal to the diaphragm for different time intervals: 0, 5, 10, 15, 20, 25, 30, 35, and 40 minutes (five animals per group). The motor function of the lower extremities postoperatively showed consistent impairment after 30 minutes clamping (5/5 rats were paralyzed), and this time interval was used for treatment evaluation. For each treatment, six animals per group were used, and direct local intra-aortic infusion of physiologic solution (2 mL) at different temperatures with or without buffer substances was given immediately after double cross-clamp to protect the ischemic spinal cord. Arterial blood (2 mL) was infused in the control group. The data indicate that the addition of HCO3-(20 mM) to the hypothermic (15 degrees C) solution offered complete protection of the spinal cord from ischemic injury.(ABSTRACT TRUNCATED AT 250 WORDS)