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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was investigated for the effects of pulsatile flow on retrograde cerebral perfusion under profound hypothermic circulatory arrest. Fifteen adult mongrel dogs were placed cardiopulmonary bypass and induced profound hypothermia of 20 degrees C at nasopharyngeal temperature. Five dogs were performed non-pulsatile retrograde cerebral perfusion (NP-RCP) and 5 were pulsatile retrograde cerebral perfusion (P-RCP) for 60 minutes each group. The rest of 5 dogs were performed hypothermic circulatory arrest (HCA) without any circulatory assist. Retrograde cerebral perfusion flow rate was regulated to maintain an external jugular vein pressure of 20 mmHg by infusing oxygenated blood by way of bilateral maxillary vein. Regional cerebral blood flow (rCBF), cerebrospinal fluid pressure (CSFP), adenosine triphosphate (ATP) concentration of cerebral tissue, and water content of cerebral tissue were measured. The rCBF were no statistical difference between the two groups. CSFP and ATP concentration in both of NP-RCP and P-RCP were significantly higher than those of HCA. Water content of cerebral tissue in P-RCP were significantly lower than those of NP-RCP. We concluded that retrograde cerebral perfusion for 60 minutes protects the brain as the assistances of circulatory arrest and retrograde cerebral perfusion with pulsatile flow has the possibility to control brain edema as compared with non-pulsatile flow in dogs.
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PMID:[Experimental studies of pulsatile retrograde cerebral perfusion]. 813 83

Retrograde cerebral perfusion through a superior vena caval cannula is a new technique used to protect the brain during operations on the aortic arch. We measured cerebral tissue blood flow, oxygen consumption, and cerebrospinal fluid pressure under various perfusion conditions in hypothermic (20 degrees C) mongrel dogs (n = 18, 12.8 +/- 0.6 kg) to determine the optimum conditions for retrograde cerebral perfusion. Retrograde cerebral perfusion was performed by infusion via the superior vena caval cannula and drainage via the ascending aortic cannula while the inferior vena cava and azygos vein were clamped. Retrograde cerebral perfusion was performed as the external jugular venous pressure was changed from 15 to 35 mm Hg in increments of 5 mm Hg. Cerebral tissue blood flow was measured by the hydrogen clearance method. Hypothermic retrograde cerebral perfusion with an external jugular venous pressure of 25 mm Hg provided about half the cerebral tissue blood flow of hypothermic (20 degrees C) cardiopulmonary bypass with a flow rate of 1000 ml/min (13.7 +/- 7.9 versus 32.7 +/- 8.5 ml/min per 100 gm). It decreased significantly as the external jugular venous pressure was decreased from 25 to 15 mm Hg but did not increase significantly as the external jugular venous pressure was increased from 25 to 35 mm Hg. Whole-body oxygen consumption during hypothermic retrograde cerebral perfusion with an external jugular venous pressure of 25 mm Hg was one quarter of that during hypothermic cardiopulmonary bypass (3.4 +/- 0.7 versus 12.7 +/- 5.6 ml/min) and varied in proportion to external jugular venous pressure. The cerebrospinal fluid pressure was a little lower than the external jugular venous pressure (19.2 +/- 4.5 mm Hg versus 24.8 +/- 2.4 mm Hg) but also varied with the external jugular venous pressure. The cerebrospinal fluid pressure remained lower than 25 mm Hg so long as the external jugular venous pressure remained lower than 25 mm Hg. High external jugular venous pressure was associated with high intracranial pressure, which restricts cerebral tissue blood flow and may cause brain edema. We believe that a venous pressure of 25 mm Hg is the optimum condition for retrograde cerebral perfusion.
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PMID:Determination of optimum retrograde cerebral perfusion conditions. 796 89

Past over two years, thirteen cases of aortic arch aneurysm, including 5 proximal arch aneurysms, 5 transverse arch aneurysms and 3 distal arch aneurysms, were operated under retrograde cerebral perfusion with deep hypothermia. In the operation, tympanic temperature, rectal temperature and SEP were monitored. When the rectal temperature fell to 20 degrees C, circulatory arrest was done and retrograde cerebral perfusion was started through SVC venous cannula, at the rate of 200-300 ml/min. During cerebral perfusion, PGE1, Mannitol, Solumedrol were administered and defroxamine as radical scavenger was injected before reperfusion for protection of the brain edema. The duration of retrograde cerebral perfusion was from 28 min to 67 min. (mean 42.8 min). In the retrograde cerebral perfusion, cerebral embolization was prevented and good operative field without cannulation was obtained. Of 13 patients, 3 patients were died of intraoperative myocardial infarction and acute renal failure. Ten patients were alive and recovery of consciousness was complete. In conclusion, retrograde cerebral perfusion method is very simple and useful for the operation of aortic arch aneurysm.
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PMID:[Retrograde cerebral perfusion with circulator arrest for aortic arch aneurysm]. 837 29

It is controversial whether profound hypothermia (15 degrees C) provides adequate cerebral protection during a limited period of total circulatory arrest during pediatric cardiac surgery. In the present study, transcranial Doppler echography was used to monitor the blood flow velocity (BFV) pattern in the middle cerebral artery (MCA). The purpose of the study was to investigate the influence of a period of circulatory arrest on MCA BFV, as judged from the reperfusion flow velocity pattern. The MCA BFV was studied in 22 small children undergoing profound hypothermic cardiac operations after induction of anesthesia. Twelve of the children had a period of profound hypothermic circulatory arrest (15 to 74 minutes; arrest group). Circulation was maintained in the remaining 10 children (nonarrest group). Time-averaged MCA BFV was decreased and diastolic BFV was absent immediately after cardiopulmonary bypass in 10 of 12 children in the arrest group. In contrast, only 1 of 10 patients in the nonarrest group (p < 0.05) showed this pattern. Diastolic BFV normalized 54 to 328 minutes after the arrest in the arrest group. Circulatory arrest during profound hypothermia is followed by a period of low cerebral perfusion, whereby time-averaged MCA BFV is decreased and MCA BFV is absent during diastole. We speculate that this can be explained by an increase in intracranial pressure after brain edema.
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PMID:Absent diastolic cerebral blood flow velocity after circulatory arrest but not after low flow in infants. 837 25

The "therapeutic window" of neuroprotective intervention due to hypoxic-ischemic brain injuries are initial disturbances of the neuronal function in regions of only moderate decrease of local cerebral blood flow (ICBF). Because of limited effects of single therapeutic principles therapeutic combinations should be tested. Neuroprotective effects of mild hypothermia and the nootropic drug Cerebrolysin (Cerebrolysin, EBEWE, Austria) on ICBF and development of brain edema were used. Four groups of adult Wistar rats (untreated and Cerebrolysin treated animals with 35 degrees C and 37 degrees C rectal temperature) were subjected to moderate forebrain ischemia by permanent bilateral carotid artery ligation for 6 h. The ICBF was measured continuously in the frontal and the occipital cortex by a 2-channel Laser Doppler flowmeter. The ECoG was derived from 4 ECoG leads above the frontal and occipital cortex and quantified by spectral analysis. Six hours after the onset of ischemia, the function of the blood-brain barrier to proteins was determined by staining with Evans Blue, the animals were sacrificed and the brain water content was estimated by gravimetry. Permanent bilateral carotid artery ligation led to an abrupt ICBF reduction to between 40-50% of baseline levels. Within a few minutes, however, the ICBF increased again to 50-80% of the baseline. The reduced spectral band power of the ECoG was correlated with the decreased ICBF values (p < 0.05) that indirectly indicated changes in the energy state of the neurons (p < 0.05). Changes in the ECoG appeared only with a delay of approximately 4 sec after the onset of ICBF reduction. Six hours after the onset of ischemia, a cytotoxic brain edema was shown in the frontoparietal cortex and hippocampus. Reducing the temperature by 2 degrees C diminished the decrease in ICBF between 10 min and 2 h after the onset of ischemia (p < 0.05). This effect was noted in the frontal but not in the occipital cortex. Furthermore, mild hypothermia prevented the loss of ECoG spectral power in the beta, alpha and theta bands (p < 0.05) as well as the development of cytotoxic brain edema. Cerebrolysin prevented the development of brain edema, too, both under normo- and hypothermic conditions. The ICBF was restored to higher levels in the occipital cortex in comparison both to the normothermic Cerebrolysin treated and hypothermic untreated rats (p < 0.05). This effect of Cerebrolysin was associated with only slight changes in ECoG, indicating that the neuronal activity state and the energy supply was obviously not decisively influenced. In conclusion, moderate ICBF reduction in rats to about 50-80% of baseline values was detectable in the ECoG by using spectral analysis. This reduction led to the development of cytotoxic brain edema in rats within 6 h. Thus, hypothermia prevents the development of cytotoxic brain edema. Cerebrolysin enhanced the effects of hypothermia on ICBF reduction and on the development of brain edema.
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PMID:Physiological effects and brain protection by hypothermia and cerebrolysin after moderate forebrain ischemia in rats. 908 84

Polyamines and N-methyl-D-aspartate (NMDA) receptors are both thought to play an important role in secondary neuronal injury after cerebral ischemia. Ifenprodil, known as a noncompetitive inhibitor of polyamine sites at the NMDA receptor, was studied after transient focal cerebral ischemia occurred. Spontaneously hypertensive male rats, each weighing between 250 and 350 g, underwent 3 hours of tandem middle cerebral artery (MCA) and common carotid artery occlusion followed by reperfusion for a period of 3 hours or 21 hours. Intravenous ifenprodil (10 microg/kg/minute) or saline infusion was started immediately after the onset of MCA occlusion and continued throughout the ischemic period. Physiological parameters including blood pressure, blood gas levels, blood glucose, hemoglobin, and rectal and temporal muscle temperatures were monitored. Six rats from each group were evaluated at 6 hours postocclusion for brain water content, an indicator of brain edema, and Evans blue dye extravasation for blood-brain barrier breakdown. Infarct volume was also measured in six rats from each group at 6 and 24 hours postocclusion. Ifenprodil treatment significantly reduced brain edema (82.5 +/- 0.4% vs. 83.5 +/- 0.4%, p < 0.05) and infarct volume (132 +/- 14 mm3 vs. 168 +/- 25 mm3, p < 0.05) compared with saline treatment, with no alterations in temporal muscle (brain) or rectal (body) temperature (35.9 +/- 0.4 degrees C vs. 36.2 +/- 0.2 degrees C; 37.7 +/- 0.4 degrees C vs. 37.6 +/- 0.6 degrees C; not significant). These results demonstrate that ifenprodil has neuroprotective properties after ischemia/reperfusion injury in the absence of hypothermia. This indicates that antagonists selective for the polyamine site of the NMDA receptors may be a viable treatment option and helps to explain some of the pathophysiological mechanisms involved in secondary injury after transient focal cerebral ischemia has occurred.
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PMID:Effects of ifenprodil, a polyamine site NMDA receptor antagonist, on reperfusion injury after transient focal cerebral ischemia. 938 5

Recently, P/Q-type Ca2+ channels have been shown to be involved in neurotransmission in the central nervous system in mammals. We evaluated the effects of the P/Q-type Ca2+ channel blocker omega-agatoxin IVA (omega-Aga-IVA) on brain edema formation and infarct size determined after 24 h of reperfusion following 1 h of middle cerebral artery (MCA) occlusion in rats. Intracerebroventricular (i.c.v.) treatment with omega-Aga-IVA significantly attenuated the postischemic increase of brain water content. omega-Aga-IVA also significantly reduced the size of the infarct area determined by triphenyltetrazolium chloride staining after 24 h of reperfusion. omega-Aga-IVA (30 pmol, i.c.v.), which exhibited a neuroprotective effect, had no significant effect on the magnitude of intra- and postischemic brain temperature when compared with vehicle-treated rats. This indicates that the postischemic neuroprotective effect of omega-Aga-IVA is produced by a direct and not an indirect effect via hypothermia. These results suggest that P/Q-type Ca2+ channels may be involved in the development of focal ischemic brain injury and that blockers of these channels may be therapeutically useful against ischemic injury.
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PMID:P/Q-type Ca2+ channel blocker omega-agatoxin IVA protects against brain injury after focal ischemia in rats. 943 6

The objective of this study was to improve the ability to detect cerebrovascular complications in patients undergoing complicated neurosurgical procedures using on-line monitoring of cerebral pH with in vivo microdialysis. We employed on-line pH monitoring in patients with a variety of neurosurgical procedures including high-flow bypass surgery, aneurysm clipping, and temporal resection in epilepsy treatment. The pH was monitored with a microdialysis probe, usually inserted into the frontal cortex and pH of the dialysate was measured on-line with a pH electrode. We monitored 17 cases: 12 high-flow extracranial-intracranial (EC-IC) bypass procedures, 3 surgeries to clip large basilar tip aneurysms under protection of hypothermic circulatory arrest, and 2 surgeries for intractable seizure disorders. In the patients undergoing high-flow bypass, the pH remained stable in 5 patients and all had an uneventful outcome. In 3 patients, the pH decreased during surgery. One patient had a severe hemiparesis on awaking from anesthesia. The fall in pH in another patient was corrected when the blood pressure was raised during surgery. The pH was also responsive to changes in intraoperative ventilation and probably also to brain edema with elevation of pH values. In the three patients undergoing basilar tip aneurysm clipping under hypothermic circulatory arrest, the pH fell to 6.41 in one patient. This patient awoke with a mild hemiparesis. In the other two patients, the pH was stable during the hypothermia and neither patient had complications. In the patients undergoing temporal lobectomy and hippocampectomy, the pH fell rapidly with the onset of ischemia. We conclude that it is possible to monitor the cerebral extracellular pH with on-line microdialysis. The information obtained may alert the surgeon to the possibility of impending cerebral ischemia or other complications. However, further experience is needed before the technique can be recommended for general use.
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PMID:Intraoperative on-line monitoring of cerebral pH by microdialysis in neurosurgical procedures. 952 50

Hypothermia maintains the impermeability of the blood-brain barrier to proteins and, therefore, presumably the development of vasogenic brain edema after brain ischemia. We intended to determine whether mild hypothermia would have a protective effect against cytotoxic brain edema, the early stage of ischemic brain edema. Two groups of Wistar rats (37 degrees C and 35 degrees C body temperature) were subjected to 6 h of moderate decrease of cerebral blood flow (CBF) by means of permanent bilateral carotid artery ligation, and compared to a third group of unaffected animals. Carotid artery ligation induced a local cerebral blood flow (LCBF) reduction to 50-80% of baseline values. LCBF in the frontal cortex was restored to a higher level in hypothermic animals than in normothermic ones (P < 0.05). In normothermic animals, an increase of brain water content was detected in the frontoparietal and occipital cortex as well as in the hippocampus (P < 0.05), but only in one region of the frontoparietal cortex in hypothermic animals. The impermeability of the blood-brain barrier to proteins was shown by the absence of staining with Evans blue as an indicator of vasogenic brain edema. We conclude that mild hypothermia offers protection against the development of cytotoxic brain edema.
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PMID:Mild hypothermia prevents the occurrence of cytotoxic brain edema in rats. 958 85

The recovery of injured neurons in primely brain damage, neuroprotection to the secondary brain damage (such as brain edema, brain ischemia, free radicals, neuroexcitation and ICP elevation), activation of gene-tropic regeneration, and prevention of apobiosis are major targets on the management of severe brain injury. However, excess release of catecholamines (catecholamine surge) make a very difficult to control of cerebral hypoxia by changes of systemic blood circulations. Mild cerebral hypothermia is only one method to prevent of these catecholamines surge. We developed new technique, cerebral hypothermia that control brain tissue temperature at 32-34 degrees C with more than 800 ml/min. oxygen delivery at acute stage. Combination therapy with these cerebral hypothermia and replacement of cerebral dopamine-pituitary hormone-estrogen was very successful to prevent of vegetation after severe brain injury.
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PMID:[The control of brain tissue temperature and stimulation of dopamine-immune system to the severe brain injury patients]. 964 93


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