UMLS:C0020672 - FACTA Search

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

The function of isolated guinea pig hearts treated with 2,3 butanedione monoxime (BDM) before, during, and initially after 22 h of hypothermic perfusion was examined during 4 h of normothermic reperfusion. BDM is a vasodilatory and negative inotropic agent that reversibly decreases sensitivity of contractile proteins to Ca2+. Also examined were the effects of adenosine (ADE) and nitroprusside (NP) in improving coronary flow (CF) and contractile function when given with BDM during rewarming and during the initial period of normothermic reperfusion. Isovolumetric left ventricular pressure (LVP), CF, and percentage of O2 extraction (%O2E) were measured in Krebs-Ringer-perfused hearts divided into three groups of 11 hearts each: drug-free controls (0 BDM); 10 mM BDM alone; and 10 mM BDM + 10 microM ADE + 100 microM NP. BDM was given 20 min before hypothermia, during hypothermia (3.8 degrees +/- 0.1 degree C) for 22 h, and for 30 min after rewarming to 37 degrees +/- 0.1 degree C; ADE was given with NP for only 20 min before and during rewarming and for 30 min after rewarming. Hearts were perfused at low constant flow with oxygenated Krebs' solution during hypothermia. After 2.5-h normothermic reperfusion, LVP (initial controls 108 +/- 6 mm Hg) increased more with BDM + ADE + NP (80 +/- 4% of control) than with BDM alone (62 +/- 3%) or without BDM (28 +/- 5%). CF (controls 6.0 +/- 0.5 ml/g/min) decreased less with BDM + ADE + NP (77 +/- 4% of control) than with BDM alone (60 +/- 5%) or without BDM (53 +/- 6%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reperfusion with adenosine and nitroprusside improves preservation of isolated guinea pig hearts after 22 hours of cold perfusion with 2,3 butanedione monoxime. 768 3

Many infants who require cardiac surgery have cyanotic heart disease. We assessed the relative tolerances to ischemia of hearts from immature normoxemic rabbits versus hearts from immature rabbits subjected to hypoxemia since birth. Normoxemic animals were raised from birth in an environment where the inspired fractional concentration of oxygen (FIO2) was 0.21; for the hypoxemic studies FIO2 was reduced to 0.09. Hearts (n = 6/group) from normoxemic and chronically hypoxemic rabbits at 7-12, 21-28, 35-44, and 51-56 days of age underwent aerobic "working" perfusion with Krebs bicarbonate buffer, and cardiac function was measured. Hearts were then arrested by a 3-min infusion with either cold (14 degrees C) Krebs buffer (hypothermia alone group) or St. Thomas' Hospital II solution (hypothermia plus cardioplegia group) before 6 h of hypothermic (14 degrees C) global ischemia. Hearts were reperfused, and postischemic creatine kinase leakage and recovery of function were measured. For hearts protected with hypothermia alone, recovery of aortic flow was better in hearts hypoxemic from birth compared with normoxemic controls at 7-12 days (78 +/- 7 vs. 60 +/- 6%, P < 0.05) and 21-28 days old (81 +/- 12 vs. 26 +/- 28%, P < 0.05). Protection with hypothermia plus cardioplegia was also better in hearts hypoxemic from birth compared with normoxemic controls at 7-12 days (74 +/- 8 vs. 63 +/- 10%, P < 0.05) and 21-28 days old (84 +/- 3 vs. 71 +/- 5%, P < 0.05). Protection with hypothermia alone and hypothermia plus cardioplegia was no different within chronically hypoxemic age groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tolerance of the developing heart to ischemia: impact of hypoxemia from birth. 790 Aug 70

Emissions of ultrasonic vocalizations (USVs) by rat pups (Rattus norvegicus) during hypothermia have consequences for recovery and warming. We investigated the effects on dam behavior of USVs emitted by 3- to 11-day-old pups during hypothermia at rectal temperatures between 18 and 22 degrees C. Rat dams were tested in a Y maze with the home cage as a start box. Dams were given, in one condition, a choice between a hypothermic pup emitting USVs or a hypothermic, silent (anesthetized) pup and, in the other, a choice between 2 hypothermic, silent pups. Although differing in some acoustic properties from normal isolation calls, USVs emitted by hypothermic pups both elicited maternal search behavior and acted as directional cues for dams, in comparisons with control dams exposed only to silent pups. Thus USVs of pups recovering from extreme hypothermia have communicative as well as physiological significance.
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PMID:Hypothermic vocalizations of rat pups (Rattus norvegicus) elicit and direct maternal search behavior. 792 60

Because many infants who require cardiac operation have cyanotic heart disease, we determined whether the existing calcium content of St. Thomas' II solution (1.2 mmol/L) is optimal to protect the immature rabbit heart hypoxemic from birth during subsequent ischemia. Modified hypothermic St. Thomas' II solutions (calcium content, 0 to 2.4 mmol/L) were compared with hypothermic Krebs bicarbonate buffer in protecting chronically hypoxemic (PaO2 = 34 +/- 11 mmHg, SaO2 = 63% +/- 3%) versus normoxemic (PaO2 = 76 +/- 11 mmHg, SaO2 = 92% +/- 3%) immature hearts (7 to 12 days old) during ischemia. Hearts (n = 6 per group) underwent aerobic 'working' perfusion with Krebs bicarbonate buffer and cardiac function was measured. The hearts were then arrested with a 3 minute infusion of either cold (14 degrees C) Krebs buffer (1.8 mmol calcium/L) as hypothermia alone or modified St. Thomas' II solution before 6 hours of hypothermic (14 degrees C) global ischemia. Hearts were reperfused and postischemic enzyme leakage and recovery of function were measured. A bell-shaped dose-response profile was observed for recovery of postischemic aortic flow but not for postischemic creatine kinase leakage, with improved protection occurring at lower calcium concentrations. Optimal myocardial protection occurred at a calcium content of 0.4 mmol/L, which was significantly better than with hypothermia alone or standard St. Thomas' II solution. We conclude that the existing calcium concentration of St. Thomas' II solution is responsible, in part, for its inadequate protection of immature myocardium hypoxemic from birth during ischemia.
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PMID:Calcium and cardioplegic protection of the ischemic immature heart: impact of hypoxemia from birth. 794 63

The effects of electrical pacing during the early reperfusion following hypothermic global ischemia (60 min, at 25 degrees C) was studied in the isolated working rat heart model. The hearts were divided into three groups. Hearts in Group I (n = 8) were control without hypothermia, ischemia or pacing. Hearts in Group II (n = 16) were paced with ventricular rate at 300 beats/min with 1 mVolt for 10 min during the Langendorff mode after an initial 5 min of reperfusion. Hearts in Group III (n = 14) were not paced. The recovery of aortic flow (both absolute and percent) was significantly better in Group II than in Group III, but was significantly lower in both groups than in control. No significant differences were noted, however, in heart rate, aortic pressure or coronary flow between Group II and III. In contrast, the tissue concentration of adenosine triphosphate (ATP) in Groups II and III decreased significantly by the end of reperfusion relative to Group I, but no difference in ATP existed between Group II and III. Myocardial ATP concentrations did not correlate with percent recovery of aortic flow. The myocardial concentration of calcium in Groups II and III increased by the end of reperfusion as compared with Group I, but no difference in calcium existed between Group II and III. The myocardial concentration of calcium demonstrated a significant correlation with percent recovery of aortic flow (r = 0.71, n = 30, p < 0.005). Our results indicate that an electrical pacing during early reperfusion in the myocardium improves functional recovery of aortic flow.
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PMID:Effects of electrical pacing to the preischemic rate during rewarming after hypothermic ischemia in the rat heart. 794 61

We determined the influence of perfusate composition and reinfusion during ischemia upon myocardial protection in the immature rabbit heart. Isolated "working" hearts (n = 6 per group) from 7-10-day-old New Zealand White rabbits were perfused with Krebs bicarbonate buffer and function measured. Hearts were then arrested with 3 minutes cold (14 degrees C) perfusion with bicarbonate buffer (as hypothermia-alone group) or St. Thomas' II cardioplegic solution (as hypothermia-plus-cardioplegia group). Hearts were then subjected to hypothermic (14 degrees C) global ischemia for 2 or 6 hours, with and without multiple reinfusion of the coronary vasculature. Following 2 hours ischemia impaired recovery of aortic flow occurred after multiple reinfusion in comparison with a single infusion with the cardioplegic solution (64 +/- 3% versus 72 +/- 4%) but not with bicarbonate buffer (79 +/- 3% versus 83 +/- 4%). However after 6 hours ischemia impaired recovery of function occurred after multiple reinfusion in comparison with single infusion both with the cardioplegic solution (60 +/- 3% versus 68 +/- 3%) and with bicarbonate buffer (57 +/- 4% versus 75 +/- 5%). There were no differences in post-ischemic creatine kinase leakage or myocardial water content between groups. These results suggest (i) that reinfusion itself, regardless of the composition of the perfusate, caused decreased recovery of function after an extended period of ischemia, and (ii) protection of the ischemic immature heart with St. Thomas' II solution remains inadequate and requires improvement.
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PMID:Protection of the ischemic immature heart--effect of perfusate reinfusion and composition. 830 94

Although standard blood cardioplegia provides good myocardial protection for cardiac operations in adults, protection of the cyanotic, immature myocardium remains suboptimal. Calcium, which has been implicated in reperfusion injury and in the development of "stone heart" in mature myocardium, is routinely lowered in standard cardioplegic solutions. Immature, neonatal myocardium has lower intracellular calcium stores and is more reliant on extracellular calcium for contraction. To determine if normocalcemic cardioplegia would result in improved cardiac function in the neonatal heart, we conducted a series of experiments using an isolated, blood-perfused working heart model. Thirty-two neonatal piglet hearts (24 to 48 hours) were excised without intervening ischemia and were placed directly on a blood-perfused circuit. Baseline stroke work index was assessed. Hearts were then arrested with cold cardioplegic solution delivered at 45 mm Hg for 2 minutes: group I, low-calcium blood cardioplegic solution (Ca = 0.6 mmol/L); group II, normal-calcium blood cardioplegic solution (Ca = 1.1 mmol/L); group III, University of Wisconsin solution; and group IV, University of Wisconsin solution with added calcium (Ca = 1.0 mmol/L). Cardioplegic solution was administered every 20 minutes for 2 hours and topical hypothermia was used. Hearts were then reperfused with warm whole blood. Functional recovery, expressed as a percentage of control stroke work index, was determined minutes after reperfusion. Hearts preserved with normocalcemic cardioplegic solution (groups II and IV) had complete functional recovery at 60 minutes, whereas hearts preserved with low-calcium cardioplegic solution (groups I and III) achieved functional recoveries of only 80% and 65%, respectively, at a left atrial pressure of 9 mm Hg. Electron micrographs taken 1 hour after reperfusion showed minimal edema and only mild myofibrillar changes. They were identical in both the low-calcium and normocalcemic groups. Complete functional recovery is possible in immature myocardium when calcium is added to either blood or an intracellular crystalloid cardioplegic solution. The addition of calcium does not result in ultrastructural damage and does result in good functional recovery.
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PMID:Normocalcemic blood or crystalloid cardioplegia provides better neonatal myocardial protection than does low-calcium cardioplegia. 841 79

Hypothermic alkaline pharmacologic cardioplegia used in pediatric cardiac surgery may be less than satisfactory despite its benefits in adults. We determined whether the pH (7.8) of standard St. Thomas' II cardioplegic solution contributes to inadequate protection of the ischemic immature heart and whether the effect is age-related. Modified hypothermic St. Thomas' II solution (pH range, 4.8 to 8.8) was compared with hypothermic bicarbonate buffer alone (pH 7.25) in protecting the ischemic immature (7 to 10 days old) and mature (12 months old) rabbit heart. Isolated hearts (n = 6 per group) were perfused with bicarbonate buffer, and aortic flow was measured before hypothermic (14 degrees C) ischemia (immature hearts: 4 hours; mature hearts: 3 hours). Hearts were reperfused, and enzyme leakage and recovery of function were measured. In the immature heart, a bell-shaped dose-response profile was observed for pH and recovery of aortic flow but not for postischemic creatine kinase leakage. Optimal recovery of aortic flow (98% +/- 3%) occurred at pH 6.8, which was greater than protection with hypothermia alone (82% +/- 4%; p < 0.05) and standard St. Thomas' II solution (72% +/- 2%; p < 0.05). In the mature heart, a bell-shaped dose-response curve existed for recovery of aortic flow and a U-shaped curve existed for creatine kinase leakage. Again, optimal recovery of aortic flow (84% +/- 5%), which was superior to that with standard St. Thomas' II solution (60% +/- 8%; p < 0.05), and minimal enzyme leakage also occurred at pH 6.8, as did the least enzyme leakage (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Age and protection of the ischemic myocardium: is alkaline cardioplegia appropriate? 845 42

Although hypothermia and cardioplegic cardiac arrest provide effective protection during cardiac surgery, ischemia of long duration, poor preoperative myocardial function, and ventricular hypertrophy may lead to heterogeneous delivery of cardioplegic solutions, incomplete protection, and impaired postischemic recovery. Calcium antagonists are potent cardioprotective agents, but their efficacy in the presence of cold cardioplegia is still controversial, especially in heart failure, since it is often believed that failing hearts are more sensitive to their negative inotropic and chronotropic actions. However, recent data have demonstrated that the benzothiazepine-like calcium antagonists diltiazem and clentiazem, in selected dose ranges, elicit significant cardioprotection independently of intrinsic cardiodepression, thus lending support to their use in cardioprotective maneuvers involving the failing heart. We therefore evaluated the cardioprotective interaction of diltiazem, clentiazem, and cold cardioplegia in both normal and failing ischemic hearts. Hearts were excised from 200- to 225-day-old cardiomyopathic hamsters (CMHs) of the UM-X7.1 line and age-matched normal healthy controls. Ex vivo perfusion was performed at a constant pressure (140 cmH2O; 1 cmH2O = 98.1 Pa) according to the method of Langendorff. Heart rate, left ventricular developed pressure (LVDP), and coronary flow were monitored throughout the study. Global ischemia was produced for 90 min by shutting down the perfusate flow, followed by reperfusion for 30 min. Normal and failing CMH hearts were either untreated (control) or perfused at the onset of global ischemia with one of the following combinations: cold cardioplegia alone (St. Thomas' Hospital cardioplegic solution, 4 degrees C, infused for 2 min), cold cardioplegia + 10 nM diltiazem, or cold cardioplegia + 10 nM clentiazem. The cardiac and coronary dilator properties of 10 nM diltiazem and 10 nM clentiazem alone were investigated in separate groups of isolated preparations. Failing CMH hearts had lower basal LVDP (42 +/- 2 vs. 77 +/- 2 mmHg (1 mmHg = 133.3 Pa) for normal hearts, p < 0.05), while coronary flow was only slightly reduced (5.6 +/- 0.2 vs. 6.2 +/- 0.2 mL/min for normal hearts). Following 90 min global ischemia, coronary flow was increased in both groups, but the peak hyperemic response declined only in failing CMH hearts (+50 +/- 17 vs. +82 +/- 17% in normal hearts). In normal hearts, LVDP virtually recovered within 5 min of reperfusion but steadily decreased thereafter (-37 +/- 4% at 30 min). In contrast, in failing CMH hearts, LVDP significantly decreased early during reperfusion but improved over time (-19 +/- 7% at 30 min). In normal hearts, the addition of diltiazem or clentiazem to cold cardioplegic solutions resulted in improved postischemic contractile function for the duration of reperfusion (85 +/- 4% vs. only 71 +/- 6% for cardioplegia, p < 0.05). The post-ischemic increase in coronary flow was similar in all groups. In failing CMH hearts, the addition of diltiazem or clentiazem afforded no significant contractile benefit at reperfusion. In nonischemic normal hearts, infusion of diltiazem or clentiazem (10 nM) alone increased coronary flow (+6 +/- 1% for diltiazem and +24 +/- 3% for clentiazem) without significant negative inotropic or chronotropic effects. In nonischemic failing CMH hearts, infusion of diltiazem or clentiazem did not elicit cardiodepression. In contrast their coronary dilator actions reverted to vasoconstriction (diltiazem) or were significantly attenuated (clentiazem). From these experiments we can conclude that, compared with the normal heart, the failing CMH heart adapted differently to global ischemia.
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PMID:Resistance of the failing dystrophic hamster heart to the cardioprotective effects of diltiazem and clentiazem: evidence of coronary vascular dysfunctions. 856 77

We studied the effects of mild hypothermia on cardiac contractility in isolated rabbit hearts perfused with Krebs-Henseleit solution according to the technique of Langendorff. Isovolumetric left ventricular pressure (LVP) was measured with a fluid-filled balloon. Hearts were paced after induction of atrioventricular block. At low heart rates ( < 30 bpm) mild hypothermia (cooling to 30 degrees C) induced a 32% increase in LVp (146.5 +/- 10 mm Hg at 30 degrees C vs 110.7 +/- 13 mm Hg at 37 degrees C) but this positive inotropic response was progressively lost by increasing heart rate. At pacing rates > or = 90 bpm, lower systolic LVP, higher diastolic LVP, and lower positive and negative LV dP/dt were obtained in hypothermic (93 +/- 12 mm Hg, 55 +/- 18 mm Hg, 584 +/- 137 mm Hg/s, and 323 +/- 57 mm Hg/s at 210 bpm, respectively) compared to normothermic hearts (123 +/- 4 mm Hg, 10 +/- 4 mm Hg, 1705 +/- 145.5 mm Hg/s, and 1155 +/- 78 mm Hg/s at 210 bpm, respectively.) The duration of mechanical diastole was reduced or suppressed in these hearts. Exposure to the beta-adrenoreceptor agonist, isoproterenol, improved this diastolic dysfunction during hypothermia and pacing at high rates, suggesting that the sarcoplasmic reticulum Ca2+ uptake might be involved. Our data are also consistent with an increase in myofilament Ca2+ sensitivity that is opposed by isoproterenol during hypothermia.
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PMID:Interaction of heart rate and hypothermia on global myocardial contraction of the isolated rabbit heart. 861 Sep 9

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