Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether cold could activate the kallikrein-kinin system in vivo as it does in vitro, the circulating systemic concentrations of bradykinin were serially measured in 10 cyildren with congenital diseases of the heart undergoing corrective cardiac surgery. Bradykinin was measured by radioimmunoassay in blood samples obtained before, during and after profound hypothermia (to 18 degrees C) and cardiopulmonary bypass. The circulating concentrations of bradykinin increased significantly as body temperature decreased during surface cooling. The increase in circulating bradykinin was associated with a decrease in the circulating level of bradykininogen, the precursor of bradykinin. With the onset of cardiopulmonary bypass and hence, removal of the lung and pulmonary converting enzyme from the circulation, there was a further rise in the already elevated concentrations of bradykinin. This is the first in vivo demonstration that hypothermia leads to an increase in the circulating concentrations of bradykinin.
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PMID:Increased circulating bradykinin during hypothermia and cardiopulmonary bypass in children. 49 78

Despite the widespread safe application of cardiopulmonary bypass (CPB) for cardiac surgery, it is inherently a pathologic state. CPB produces a generalized inflammatory reaction involving at least the complement, coagulation, kallikrein, and fibrinolytic cascades. Marked alterations in organ perfusion and metabolism occur during CPB which are further affected by the perfusion flow rate. During hypothermic CPB at 20 degrees C, there is a progressive decrease in perfusion of the microcirculation at flow rates less than 1.2 liters/min/m2. Experimental studies suggest that brain oxygen consumption and resistance remain relatively constant as flow rates are reduced during hypothermia, and the brain becomes the passive recipient of proportionally more blood flow. Recent ultrafiltration studies have demonstrated a specific increase in microvascular permeability to proteins after 2 h of normothermic CPB. This provides experimental support to the well-known clinical observation of increased interstitial fluid following CPB. The development of uniformly safe CPB depends upon prevention of the abnormalities of the microcirculation and upon neutralization of the deleterious effects of inflammatory mediators.
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PMID:Cardiopulmonary bypass: studies on its damaging effects. 349 47

Plasma kallikrein activity and plasma serotonin were studied during and after open-heart surgery in 15 patients with extracorporeal circulation and in 15 patients with surface-induced deep hypothermia. Following results were obtained: 1) Plasma kallikrein activity which reflects the activation of the kinin system, showed no significant change during extracorporeal circulation, and significantly increased three hours after the termination of perfusion. However, there was no significant difference in plasma kallikrein activity between the patients with and without low cardiac output syndrome (LOS). In surface-induced deep hypothermia, plasma kallikrein activity showed no significant change during and after operation. 2) Plasma serotonin significantly decreased during both extracorporeal circulation and hypothermia. Moreover, there was no significant difference in plasma serotonin between the patients with and without postoperative LOS or pulmonary hypertension. It is assumed that plasma serotonin may not play an important role in regulating blood pressure during or after open-heart surgery with either extracorporeal circulation or surface-induced deep hypothermia.
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PMID:Changes of kallikrein and serotonin in plasma during and after open-heart surgery. 690 72

The purpose of the present work was to evaluate the kallikrein-kinin system and effects of hypothermia during renal ischemia and reperfusion. Male C57BL/KSJmdb mice were subjected to 20 or 60 min ischemia for different periods of reperfusion. Our results demonstrate that short periods of ischemia followed by reperfusion did not cause significant alterations in kallikrein activity, Evans Blue (EB) extravasation, prokallikreins, myeloperoxidase activity or plasma creatinine concentration. Edema was evident at 1 h reperfusion in the treated mice, but returned to basal values after 24 h reperfusion. Kallikrein activities and EB extravasation showed a significant increase in 60 min ischemic mice. Myeloperoxidase activity in the kidney of the mice confirmed net infiltration in the group with 60 min ischemia and 24 h reperfusion. The generation of kinins and activation of matrix degrading enzymes by tissue kallikrein, liberated from both renal and infiltrated leukocytes, could be responsible at least in part for the damage observed in the kidney of mice subject to 60 min ischemia and reperfusion. The hypothermia significantly reduced the inflammatory process in the 60 min ischemic mice, and did prevent an increase in vascular permeability. Nevertheless, the tissue edema was not shown to change between normothermic and hypothermic ischemic mice.
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PMID:Renal ischemia-induced increase in vascular permeability is limited by hypothermia. 1059 59

Postoperative morbidity after coronary artery bypass grafting (CABG) using cardiopulmonary bypass (CPB) can be influenced by pro- and anti-inflammatory cytokines like interleukin 6 (IL-6) and IL-10 triggering and balancing the acute phase response. The extent of cytokine release can be modulated by different methods. This prospective randomized study examines the effect of treatment of patients with steroid (group 1, 250 mg of prednisolone)(Solu-Decortin H)), aprotinin (group 2, 6 Mio. KIU [kallikrein inhibitory units] aprotinin [Trasylol]), and heparine coating of the artificial surface (group 3, Bioline) on the systemic release of IL-6 and IL-10 in four groups of 40 patients with coronary artery disease (CAD) scheduled for CABG. Group 4 (standard medication) served as control. Twenty hemodynamic and biochemical parameters of the CPB were analyzed regarding correlation to cytokine levels measured by enzyme-linked immunosorbent assay (ELISA). In group 1, IL-6 was suppressed compared to the control (P< 0.01). IL-10 was upregulated (P< 0.01). In group 2, cytokine release was similar to group 1. Using heparin-coated circuits in group 3 led to IL-10 upregulation (P < 0.05) and IL-6 suppression (P < 0.05). We found an exponential relationship between IL-10 levels (IL-6 levels) and cardiac ischemia time, duration of CPB, and the extent of negative base excess. An inverse relationship was found for IL-10 (IL-6) levels and venous O2 saturation (SvO2), and mean arterial pressure (MAP). Hypothermia (<34 degrees C) reduced IL-10 and IL-6 release, whereas long duration of hypothermia correlated with higher IL-10 and IL-6 release. Cytokine release after extracorporeal circulation (ECC) can be modulated pharmacologically and by distinct perfusion regimen.
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PMID:Modulating IL-6 and IL-10 levels by pharmacologic strategies and the impact of different extracorporeal circulation parameters during cardiac surgery. 1177 31

Co-treatment of neuroprotective reagents may improve the therapeutic efficacy of hypothermia in protecting neurons during ischemic stroke. This study aimed to find promising drugs that enhance the neuroprotective effect of mild hypothermia (MH). 26 candidate drugs were selected based on different targets. Primary cultured cortical neurons were exposed to oxygen-glucose deprivation and reoxygenation (OGD/R) to induce neuronal damage, followed by either single treatment (a drug or MH) or a combination of a drug and MH. Results showed that, compared with single treatment, combination of MH with brain derived neurotrophic factor, glibenclamide, dizocilpine, human urinary kallidinogenase or neuroglobin displayed higher proportion of neuronal cell viability. The latter three drugs also caused less apoptosis rate in combined treatment. Furthermore, co-treatment of those three drugs and MH decreased the level of reactive oxygen species (ROS) and intracellular calcium accumulation, as well as stabilized mitochondrial membrane potential (MMP), indicating the combined neuroprotective effects are probably via inhibiting mitochondrial apoptosis pathway. Taken together, the study suggests that combined treatment with hypothermia and certain neuroprotective reagents provide a better protection against OGD/R-induced neuronal injury.
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PMID:Combination of mild hypothermia with neuroprotectants has greater neuroprotective effects during oxygen-glucose deprivation and reoxygenation-mediated neuronal injury. 2656 30