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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolic effects on rat cardiac and skeletal muscle of a strenous program of swimming, of cold acclimation and of isoprenaline treatment (0.3 mg/kg daily for 5 five-day weeks) were compared. Exercised and cold-exposed rats gained less body weight than did controls or isoprenaline-treated rats. In all treated groups the heart and the intercapular brown adipose tissue hypertrophied. The size of the adrenals increased only in isoprenaline-treated animals. Cold-acclimation and physical training increased and isoprenaline treatment reduced or did not affect the activities of succinate dehydrogenase, malate dehydrogenase and citrate synthase of cardiac muscle. In the skeletal muscle all treatments resulted in increased activities of these enzymes. Of the anaerobic enzymes analysed, only the activity of hexokinase increased in response to the treatements used. This increase was the same in cardiac as in skeletal muscle, but it was significantly greater with isoprenaline-treatment than with training or with cold-acclimation. The activities of lactate dehydrogenase and phosphofructokinase did not differ significantly. All treatments improved cold resistance, but only swimming exercise and cold acclimation significantly increased tolerance to exercise. It is concluded that prolonged stimulation of adrenergic beta-receptors by catecholamines is responsible for the metabolic changes observed.
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PMID:Comparison of the effects of physical exercise, cold acclimation and repeated injections of isoprenaline on rat muscle enzymes. 12 87

Rats were treated by daily alprenolol (10, 20 and 50 mg/kg) injections for 5 days a week for 4 weeks. At 20--21 degrees C alprenolol treatment retarded the weight gain of the animals and increased the weight of the adrenals. These changes were not seen at 29 degrees C. The reduction in size and fat content of the interscapular brovin adipose tissue in drug-treated rats was independent of experimental temperature. At 20--21 degrees C prolonged beta-blockade did not cause any changes in the enzymes of the energy metabolism. At 29 degrees C, however, alprenolol treatment antagonized the decrease in activity of oxidative enzymes (succinate dehydrogenase, malate dehydrogenase, citrate synthase) and the decrease in protein concentration of the cardiac muscle. In skeletal muscle alprenolol treatment significantly decreased the activities of oxidative enzymes and antagonized the rise in the activity of lactate dehydrogenase resulting from warm acclimation. The increased activities of oxidative enzymes in interscapular brown adipose tissue of aprenolol treated rats were coupled with an increase in protein concentration of the tissue. Although these changes were more marked at 29 degree C they were observable at 20--21 degree C, too. The difference in the drug effects at 20--21 degrees C and 29 degrees C can be accounted for by the compensatory catecholamine release at the lower temperature, due to impaired thermoregulatory capacity after alprenolol. Prolonged beta blockade decreased the exercise tolerance and cold tolerance of the rats. An increased response of the diastolic blood pressure to an alpha-adrenergic drug, noradrenaline, and a decreased response to a beta-adrenergic drug, isoprenaline, in alprenolol-treated rats indicates a shift from beta- to alpha-receptors.
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PMID:Effect of prolonged beta-blockade on energy metabolism and adrenergic responses in the rat. 59 3

Short-term adaptation to cold (-17-19 degrees) results in evident changes of energy metabolism of gerbiles. In cold-adapted Meriones unguiculatus, tissue oxygen consumption increases in all the tissues investigated. In M. tamariscinus, respiratory rate increased only in the cardiac muscle, whereas that in other organs and muscles remained unaffected. In contrast to these two cold-resistant species, M. erythrourus is less resistant to cooling. In the latter case, no changes were observed in total and tissues respiration after cold adaptation of animals.
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PMID:[The effect of cold adaptation on total gaseous metabolism and tissue respiration in gerbils]. 121 8

Cold exposure (6 weeks at 4 degrees C) of normotensive (Wistar-Kyoto) and stroke-prone spontaneously hypertensive female rats led to cardiac hypertrophy (in stroke-prone spontaneously hypertensive rats), increased the level of plasma thyroxine, and increased the alpha-myosin heavy chain expression in the left ventricle. In contrast, myosin heavy chain expression of both main mesenteric artery and uterus was not affected by cold stress and chronic hypertension, suggesting different regulation of myosin heavy chain expression in smooth and cardiac muscle in vivo.
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PMID:The influence of cold stress on the myosin heavy chain expression of cardiac and smooth muscle in normotensive and spontaneously hypertensive female rats. 183 32

The commonly used methods of determining Ca fluxes in smooth and cardiac muscle are scrutinized for their appropriateness. These methods include an incubation of the tissue in 45Ca, followed by a washout period either in ice-cold EGTA-containing Ca-free solutions or in lanthanum-containing Ca-free solutions. The amount of 45Ca remaining in the tissue at the end of the washout phase is taken as Ca2+ influx during the labeling period. Procedures including longer washout periods cannot yield information on Ca2+ influx, since the Ca store relevant for contractile activation rapidly adapts to changes in the extracellular Ca2+ concentrations.
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PMID:Critical remarks on the Ca-flux determinations in smooth and cardiac muscle. 244 18

1. We measured intracellular Ca2+ transients during rapid cooling contractures (RCCs) in guinea-pig ventricular myocytes using the fluorescent Ca2+ indicator, Indo-1. 2. Rapid cooling of myocytes from 22 to 0-1 degrees C induced a rapid increase in [Ca2+]i which preceded the peak of the contraction and was sometimes large enough to saturate Indo-1. This indicates that [Ca2+]i may reach greater than 10 microM during an RCC. 3. The [Ca2+]i during the RCC slowly declined from its peak value and most of this decline in [Ca2+]i can be attributed to slow reaccumulation of Ca2+ by the sarcoplasmic reticulum (SR) in the cold. RCCs induced in the absence of Cao2+, were not different from control, supporting previous conclusions that RCCs depend exclusively on intracellular Ca2+ stores. 4. RCCs are depressed by long rest periods (rest decay) or by exposure to ryanodine or caffeine, which supports conclusions that RCCs are due to Ca2+ release from the SR. The rest decay of RCCs can be almost completely prevented by applying Nao(+)-free solution during the rest period. This implies that the loss of SR Ca2+ during rest depends on the sarcolemmal Na(+)-Ca2+ exchange (and not the sarcolemmal Ca2(+)-ATPase pump). 5. Rapid rewarming during an RCC normally leads to an additional transient contraction (or rewarming spike), without any increase in [Ca2+]i. Thus, the rewarming spike might be attributable to an increase in myofilament Ca2+ sensitivity induced by rewarming. 6. A second RCC is used to assess the fraction of Ca2+ which is re-sequestered by the SR during relaxation from the first RCC. In control solution progressive RCCs decline in amplitude, but in Na(+)-free, Ca2(+)-free solution they are of constant amplitude. We conclude that the SR Ca2+ pump and Na(+)-Ca2+ exchange are responsible for relaxation and that the latter may account for 20-50% of relaxation. 7. These results support the use of RCCs as a useful means of assessing SR Ca2+ content in intact cardiac muscle cells.
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PMID:Intracellular Ca2+ transients during rapid cooling contractures in guinea-pig ventricular myocytes. 262 9

The effect of Na-octanoate (NaC8) on the development of twitch and tetanic tension of a striated muscle (m. longitudinalis linguae) of Lampetra fluviatilis was tested at different temperatures. The muscle exhibited posttetanic potentiation as well as cold potentiation similar to other poikilotherme animals. The sensitivity to NaC8 was higher than that of striated frog or rat muscles but similar to that of mammalian smooth or cardiac muscle preparations. A decrease of temperature remarkably reduced the effect of NaC8 on the tension development. Also the fatigue of muscles during tetanic stimulation was smaller if the temperature was lower. It seems that both the process of fatigue and the action of NaC8 are delayed by the cold.
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PMID:Twitch and tetanic contraction of lamprey muscle exposed to fatty acid at different temperatures. 275 28

This study tests the hypothesis that retrograde/antegrade cardioplegic delivery can overcome the limitations of poor cardioplegic distribution resulting from either technique alone and, potentially, may expand the safety of using internal mammary artery grafts in cardiac muscle in jeopardy of inadequate cardioplegic protection. Jeopardized myocardium was produced in 20 dogs by ligating the left anterior descending coronary artery for 15 minutes before starting cardiopulmonary bypass and by 1 hour of aortic clamping with multidose 6 degrees C cold blood cardioplegia. Five dogs received antegrade cardioplegia via the aortic root. Ten dogs received retrograde cardioplegia via the coronary sinus. Five additional dogs received retrograde/antegrade cardioplegia via both routes. The ligature on the left anterior descending coronary artery was removed after aortic unclamping, and regional myocardial temperature (thermistor probe), segmental shortening (ultrasonic crystals), and global left ventricular and right ventricular myocardial function were evaluated. Antegrade cardioplegia produced excellent right ventricular cooling (14 degrees C) and allowed complete right ventricular functional recovery. However, it failed to cool muscle supplied by the left anterior descending coronary artery (only 31 degrees versus 12 degrees C, p less than 0.05), postischemic global left ventricular function recovered only 38% (p less than 0.05), and segmental shortening in the region supplied by the left anterior descending coronary artery recovered only 22% (p less than 0.05). Retrograde cardioplegia produced homogeneous cooling (17 degrees C) and allowed near normal recovery of global and regional left ventricular function (99% and 86%), but right ventricular cooling was variable (19 degrees to 30 degrees C) and right ventricular function recovered inconstantly (range 64% to 100%, average 82%). The best myocardial protection occurred after retrograde/antegrade cardioplegia; myocardial cooling was homogeneous, left ventricular and right ventricular global function recovered completely (95% and 90%), and regional contractility in muscle supplied by the left anterior descending coronary artery returned to 84% of control. We conclude that retrograde/antegrade cardioplegia provides better myocardial protection than either technique alone, ensures good cardioplegic distribution to the left and right ventricles, and allows regional delivery of cardioplegic flow to segments supplied by occluded arteries.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Studies of retrograde cardioplegia. II. Advantages of antegrade/retrograde cardioplegia to optimize distribution in jeopardized myocardium. 292 65

Survival after repair of postinfarction ventricular septal defects remains poor, often due to extensive loss of contractile muscle in the septum or left ventricle. We evaluated whether a contractile flap of right ventricular muscle could be used to repair a similar ventricular septal defect to augment left ventricular performance in 7 fully instrumented mongrel dogs (weight, 23 to 28 kg). By using hypothermic bypass and cold fibrillatory arrest, a trapezoidal right ventricle flap was fashioned from the free wall of the mid to lower right ventricle, basing its widest portion anteriorly on the septum and left ventricle. A large, 2-cm-diameter core of septum was excised beneath this flap to simulate a postinfarct ventricular septal defect. The right ventricular flap was then invaginated through the defect and sewn to the left ventricular side of the septum with pledgeted sutures taken full thickness through the flap and septum in a "vest-over-pants" fashion. Contraction of the right ventricular flap was confirmed visually and by postbypass multiple gated acquisition scans. The right ventricular defect was closed with fascia lata. All dogs were weaned from bypass without inotropes. Precardiac and postcardiac outputs of 2.5 +/- 0.5 versus 2.3 +/- 0.4 L/min and left ventricular end-diastolic pressures of 4 +/- 2 versus 4 +/- 3 mm Hg were identical. No shunts were detected by oxygen saturation. Autopsies confirmed the integrity of the repair. We conclude that septal defects can be repaired by using contractile right ventricular muscle, thus preserving left ventricular function. This technique offers promise for repair of postinfarction ventricular septal defects by using autologous, already conditioned to contract, cardiac muscle, but its application in humans must await long-term testing.
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PMID:Experimental repair of ventricular septal defects using autologous right ventricular muscle flaps: preliminary report. 304 20

Apomorphine and LY 171555, but not SKF 38393 displaced [3H]Dopamine binding to membranes of guinea-pig heart. Domperidone and 1-sulpiride but not SCH 23390 competitively antagonize the [3H]Dopamine binding performed with 100 microM cold dopamine as displacer. In conclusion the DA2 receptor agonists and antagonists used are able to interfere with the receptors labelled by [3H]Dopamine in cardiac muscle.
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PMID:Evidence that dopamine receptors identified by [3H]dopamine in the ventricles of guinea-pig heart are of DA2 type. 349 56


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