Hypothermia treatment

In addition, any proposed treatment with other agent(s) in conjunction with hypothermia will require very careful scrutiny of efficacy in preclinical models because of the marked benefit of hypothermia alone reported in many experimental studies. The addition of the alternative agent(s) must result in a clear-cut additional benefit compared with hypothermia treatment alone. Moreover, as previously discussed, it would be helpful to prove in both clinical and preclinical studies that each agent individually has some degree of benefit, as neither hypothermia nor neuroprotective pharmaceuticals have yet been definitively proven to be beneficial in clinical studies of acute stroke treatment. 

In addition, there is the added complexity of finding the optimal dose of neuroprotective and hypothermia treatment that will result in the optimal degree of neural protection. Because of the possibility of treatment interactions, significant preclinical testing will be necessary to identify the most clinically feasible and neurologically potent therapeutic regimen. This may be quite difficult, as the translation of preclinical research to human subjects is inexact. Added testing in phase I (safety) and phase II (dose escalation) human trials will be necessary, with a special emphasis on possible adverse interactions between the treatments. 

Hypothermia is known to cause cardiac dysfunction, particularly arrhythmias (36,37). Careful temperature control and optimal antiar-rhythmic therapy can minimize this problem. However, to avoid severe circulatory dysfunction, knowledge of arrhythmias is required. Hypothermia may be associated with a suppression of the immunological system, which exposes patients to the danger of severe infections. Schwab et al. reported that 7 of 25 stroke patients undergoing hypoth-ermiatherapy suffered a septic syndrome (17). In our hypothermic study, none of the 13 patients who underwent hypothermia therapy for 3-7 d developed severe infectious diseases. However, the remaining patient, who underwent 10 d of hypothermia because of massive cerebral edema, developed septic shock on the 10th day of hypothermia treatment. The immunosuppressive effect appears to be correlated with the depth and... 

Atkins CM, Oliva AA Jr, Alonso OF, Chen S, Bramlett HM, Hu BR, Dietrich WD (2007b) Hypothermia treatment potentiates ERKl/2 activation after traumatic brain injury. Eur J Neurosd 26 810-819... 

One of the possible alternative methods for non-invasive temperature sensing and monitoring that is completely passive and inherently safe is microwave radiometry (MWR).. We proposed a multi-fl equency microwave radiometry as a non-invasive monitoring method of deep brain temperature and fabricated a five-band receiver system and reported its measurement performance of about 1.6 K 2o-confidence interval at 5 cm depth from the surface of a water-bath phantom with similar temperature distribution as infant s brain [6]. Because the clinical requirement is less than 1 K, further improvement of MWR system were essential for a successful hypothermia treatment. We have done a couple of actions to reduce background noise in order to obtain the better temperature resolutions of five microwave receivers and tried to retrieve the temperature profile in the phantom. This paper describes the current feasibility of the MWR system for clinical hypothermic treatment. 

Gaohua, L., and H. Kimura, A Mathematical Model of Intracranial Pressure Dynamics for Brain Hypothermia Treatment, J. Theor. Biol, 238,882 (2006). 

Schwab S, Schwarz S, Spranger M, Keller E, Bertram M, Hacke W. Moderate hypothermia in the treatment of patients with severe middle cerebral artery infarction. Stroke 1998 29 2461-2466. 

Wagner KR, Zuccarello M. Local brain hypothermia for neuroprotection in stroke treatment and aneurysm repair. Neurol Res 2005 27(3) 238-245. 

There is a good deal of evidence that the therapeutic effects of antidepressants could involve adaptive changes in 5-HTia receptors. Postsynaptic 5-HTia receptor responses became implicated because the hyperpolarisation of hippocampal CA3 pyramidal neurons that follows ionophoretic administration of 5-HT was found to be increased after chronic treatment with most (but not all) antidepressants (Chaput, de Montigny and Blier 1991). Others suggested that antidepressants attenuate postsynaptic 5-HTja responses because the hypothermia, evoked by their activation, is diminished by antidepressants (Martin et al. 1992). 

SuccessM treatment of PEA and asystole depends almost entirely on diagnosis of the underlying cause. Potentially reversible causes include (1) hypovolemia, (2) hypoxia, (3) preexisting acidosis, (4) hyperkalemia, (5) hypothermia, (6) hypoglycemia, (7) drug overdose, (8) cardiac tamponade, (9) tension pneumothorax, (10) coronary thrombosis, (11) pulmonary thrombosis, and (12) trauma. 

In the first 2 weeks post-MI, caution is advised and careful dose titration is especially important, particularly in patients with markedly impaired ventricular function. Intraoperative and postoperative tachycardia and hypertension Do not use esmolol as the treatment for hypertension in patients in whom the increased blood pressure is primarily caused by the vasoconstriction associated with hypothermia. Renal/Hepatic function impairment Use with caution. 

Solanine hydrochloride has been used as a commercial pesticide. It has sedative and anticonvulsant properties, and has sometimes been used for the treatment of asthma, as well as for cough and common cold. However, gastrointestinal and neurological disorders result from solanine poisoning. Symptoms include nausea, diarrhoea, vomiting, stomach cramps, burning of the throat, headaches and dizziness. Other adverse reactions, in more severe cases, include hallucinations, loss of sensation, paralysis, fever, jaundice, dilated pupils and hypothermia. Solanine overdose can be fatal. 

In CONCLUSION, the future drug treatment of stroke will probably depend on a combination of both neuroprotection (e.g. hypothermia, glutamate receptor antagonists, free radical scavengers, etc.) with thrombolysis which attempts to re-establish normal blood flow. Such treatments may help to expand the window between the initial ischaemic episode and brain damage. Whether any of the drugs mentioned here will ultimately be of any value in the prevention and / or treatment of stroke is still a matter of conjecture. 

Direct cardiac delivery into adults can be performed via the vector transfer procedure described by Ikeda et al. (2002). Briefly, animals are anesthetized with an intraperitoneal injection of sodium pentobarbital (75 mg/kg), and ventilated. The right carotid artery is then cannulated with a catheter placed at the aortic root. The animal is then placed under induced hypothermia until the body core temperature drops to below 26 °C. The ascending aorta and pulmonary arteries are occluded and histamine pre-treatment is delivered to the aorta (20 mmol/1, volume 2.5 ul/g, body weight) for 3 min. The vector solution is then injected, the occlusions released 30 s later and the animal is resuscitated. 

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