UMLS:C0599766 - FACTA Search

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Query: UMLS:C0599766 (functional recovery)
13,441 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As the duration of bronchoconstriction induced by inhaled histamine phosphate is greater than five minutes, a study was carried out to determine whether this leads to a cumulative effect when histamine is inhaled at five minute intervals as in standardised procedures. Fourteen clinically stable adult asthmatic subjects were studied. In the first part of the study (the noncumulative stage) they inhaled doubling concentrations of histamine until appreciable bronchoconstriction occurred (changes close to 50% in lung resistance for seven subjects and 15% in forced expiratory volume in one second for seven others). After functional recovery the last concentration of histamine was nebulised on two more occasions, allowing for functional recovery after each nebulisation. In the second part of the study (the cumulative stage) subjects inhaled, depending on their responsiveness, three to eight consecutive doses of the histamine concentration last administered in the non-cumulative stage, these doses being administered at five minute intervals, without recovery. The cumulative effect was assessed by linear regression analysis of the changes in the specific functional indices, all the values obtained during the non-cumulative stage being given the score 0 and those obtained during the cumulative step scores of 1, 2, etc. In all but one instance significant (p less than 0.01) correlations were obtained and the slopes were positive, thus showing a cumulative effect. It is concluded that histamine has a cumulative bronchoconstrictor effect if inhaled at five minute intervals once appreciable bronchoconstriction has been reached.
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PMID:Histamine phosphate has a cumulative effect when inhaled at five minute intervals. 651 99

Morphological and histochemical examinations of the changes induced in the adrenal cortex by the administration of Dexamethasone (Decadron phosphate) to rats for 14 consecutive days were made at intervals during a 28-day post-treatment period, in order to follow the histo-functional recovery of this gland from the changes induced. The modifications that had occurred by the end of the treatment consisted of a decrease in the width of the zona fasciculata and the zona reticularis, an increase in the lipidic content, and degenerative mitochondrial signs in the zona glomerularis. Seven days after discontinuing treatment, we observed the disappearance of the zona intermedia, which reappeared on the 14th day after treatment. From this day on, the adrenal gland tended progressively to complete recovery. Dexamethasone therefore produces both short-term and long-term morphological and histochemical changes in all the adrenocortical zonae.
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PMID:Morphological and histochemical study on the adrenal cortex of the dexamethasone-treated albino rat. 652 5

To determine whether adding blood to a cardioplegic solution affects myocardial preservation, a randomized prospective study was carried out in 60 patients undergoing coronary revascularization to compare the effects of crystalloid potassium cardioplegics (group C) and potassium cardioplegic solutions to which blood has been added (group B) on markers of myocardial metabolism (lactate, inorganic phosphate, base deficit release, glucose and lactate uptake, oxygen extraction), myocardial damage (creatine kinase [CK]-MB levels), and cardiac performance (cardiac index and left atrial pressure). The solution with added blood had a significantly (p less than .05) greater oxygen content, a lower pH, and higher concentrations of potassium, calcium, sodium, and glucose. In group B patients there was a suggestion (p less than .06) of greater uptake of oxygen during the beginning of the initial cardioplegic infusion. During reperfusion there was no evidence of differential release of the metabolites of anaerobiosis and myocardial oxygen extraction and glucose and lactate uptake were similarly depressed in both groups. Likewise, CK-MB release after bypass was the same in both groups. Prompt, adequate functional recovery of cardiac index and left atrial pressure was observed in both groups. It was concluded that although there may be more oxygen available from the blood-containing solution during early infusion, there is no evidence that under the conditions of this investigation adding blood to cardioplegic solution improves myocardial preservation.
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PMID:A randomized comparison of crystalloid and blood-containing cardioplegic solutions in 60 patients. 660 19

The isolated working rat heart model of ischemic arrest was used to determine if the addition of carbohydrate substrate to our cardioplegic solution enhanced metabolic and functional myocardial protection. A single-dose cardioplegia technique, as used in earlier studies that showed glucose to have a harmful effect, and a multidose technique similar to that used clinically were studied and compared. Because recent data suggest that fructose-1,6-diphosphate(FDP) may have a protective effect with ischemia, this substrate was also tested and compared to glucose and fructose. In this model, single-dose cardioplegia resulted in poor protection from ischemic injury in all study groups. There was marked improvement in myocardial protection with multidose cardioplegia, and further substantial protection of myocardial function, high-energy phosphate levels, and glycogen stores when carbohydrate substrate was added to the arrest solution. The solution with a higher concentration of glucose (0.5%) provided the best overall metabolic and functional recovery and was clearly superior to fructose and FDP, both of which had about the same protective effect. Improved protection with carbohydrate substrate was accompanied by evidence of substantial increase in glycolytic flux, supporting the idea that increased anaerobic glycolysis can help protect the ischemic myocardium when intermittent reinfusion of cardioplegic solution is done.
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PMID:Metabolic and functional effects of carbohydrate substrate with single-dose and multiple-dose potassium cardioplegia. 661 70

An isolated working rat heart preparation was used to determine the effect of diltiazem, a calcium antagonist, on the myocardial metabolism and functional recovery in the ischemic and reperfused heart, under conditions of 15 degrees C of topical hypothermia. The hearts were divided into two groups according to the solution injected into aortic root at the onset of ischemia. Group I (25 hearts) were given 3 ml of cold Krebs-Henseleit bicarbonate buffer solution (KHB), and Group II (25 hearts) were given the same dose of KHB containing 300 micrograms of diltiazem. After 30 min of reperfusion following 120 min of ischemia, cardiac output (ml/min) was significantly better in Group II (24.1 +/- 3.2) than in Group I (9.5 +/- 2.5). There were no differences between the groups with regard to tissue levels of creatine phosphate, adenosine triphosphate (ATP), total adenine nucleotide (TAN), glucose-6-phosphate and lactate during the ischemia. However, ATP and TAN levels were significantly higher in Group II after 30 min of reperfusion. These data show that, although diltiazem has little effect in preventing the catabolism of high-energy phosphates during hypothermic ischemia, there was an improvement in myocardial metabolism and an enhanced functional recovery during reperfusion in the diltiazem-treated hearts.
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PMID:Effect of diltiazem on functional recovery and myocardial metabolism during hypothermic global ischemia and normothermic reperfusion. 663 97

The efficacy of the addition of verapamil to a cardioplegic solution was evaluated in immature canine hearts subjected to normothermic global ischemia. Two groups of mongrel puppies less than 10 weeks old were subjected to 30 minutes of global myocardial ischemia while on cardiopulmonary bypass. One group (Group K) was arrested with cardioplegic solution containing 20 mEq/L of KCl; the other group (Group K + V) was arrested with the same solution containing 0.2 mg/kg of verapamil. Ultrasonic crystals were placed for measurement of left ventricular dimensions, and micromanometers measured left ventricular pressures. Functional measurements included left ventricular strain, first derivative of left ventricular pressure (dP/dt), and the end-systolic pressure/volume ratio (Emax). Metabolic recovery was assessed by measuring myocardial adenosine triphosphate (ATP) content. Ninety minutes following ischemia, Group K + V exhibited greater minor axis strain at a left ventricular end-diastolic pressure of 15 and 20 mm Hg (p less than 0.05), greater dP/dt (p less than 0.05 to 0.001), and greater Emax (p less than 0.05) than Group K. ATP content in Group K + V was greater at 60 minutes (Group K + V: 12.74 +/- 1.60 mumol/gm; Group K: 8.39 +/- 1.30, p less than 0.05) and 90 minutes (Group K + V: 10.34 +/- 0.46; Group K: 7.55 +/- 1.42, p less than 0.05) after ischemia. The addition of verapamil to a cardioplegic solution containing potassium enhances the recovery of function and high-energy phosphate stores in the immature myocardium following normothermic global ischemia.
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PMID:Global ischemia in the immature canine ventricle. Enhanced protective effect of verapamil and potassium. 669 12

Previous studies from this laboratory utilized mass spectrometry to measure myocardial oxygen (PO2) and carbon dioxide (PCO2) tensions in isolated feline hearts subjected to periods of global ischemia and reperfusion. Myocardial carbon dioxide tension was found to increase during ischemia, and its rate of increase was found to correlate inversely with subsequent recovery of myocardial function following reflow. The present study utilized phosphorus-31 nuclear magnetic resonance (NMR) to assess whether the severity of intracellular acidosis or the depletion of high energy phosphate stores would show a similar correlation with recovery of function. Hyperkalemic cardioplegia employed as a myocardial preservation technqiue in combination with hypothermia was compared with hypothermia alone as the control intervention. The experimental results demonstrated that intracellular pH fell to 6.09 +/- 0.13 with hypothermia alone and to 6.31 +/- 0.09 with cardioplegia plus hypothermia. Furthermore, myocardial ATP content fell to 22% +/- 2% of control with hypothermia alone, while falling to 36% +/- 4% of control with the combined therapy. Recovery of myocardial performance was found to correlate inversely with the severity of intracellular acidosis and depletion of ATP during ischemia. In contrast, no relationship was observed between preservation of phosphoryl-creatinine levels either during ischemia or after reflow and recovery of ventricular function. These results suggest that, similar to mass spectrometry, which allows monitoring of myocardial PCO2, 31P NMR permits the on-line monitoring of intracellular pH as well as high energy phosphate compounds, and thereby provides useful metabolic indices of the severity of ischemia. Since tight coupling was found between changes in these parameters and subsequent recovery of contractile performance, further development of 31P NMR for evaluation of techniques designed to minimize the severity of ischemic damage would seem indicated.
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PMID:Mass spectrometry and phosphorus-31 nuclear magnetic resonance demonstrate additive myocardial protection by potassium cardioplegia and hypothermia during global ischemia. 677 61

Phosphorus-31 nuclear magnetic resonance (31P NMR) can estimate tissue intracellular pH as well as the content of high-energy phosphate metabolites in isolated perfused hearts. We used 31P NMR to examine mechanisms associated with the recovery of ventricular function in hearts subjected to global ischemia and reperfusion, with special emphasis on intracellular pH, a previously unreported variable. Single-dose and multiple-dose administration of a hyperkalemic cardioplegic solution were compared with hypothermia alone in 18 isolated perfused rabbit hearts. Hearts in group 1 were subjected to 24 degrees C hypothermia during 60 minutes of global ischemia; group 2 hearts received a single injection of 37-mM KCL cardioplegic solution at 10 degrees C at the onset of ischemia; and group 3 hearts received a similar initial cardioplegic injection followed by two subsequent 24 degrees C injections at 20-minute intervals during the ischemic period. Using an intraventricular balloon, maximal dP/dt provided a quantitative index of left ventricular performance before and after ischemia. Return of ventricular function expressed as a percentage of control was 54 +/- 11% for group 1, 84 +/- 6% for group 2, and 101 +/- 18% for group 3. Differences in the rate of development of intracellular acidosis were noted during the 60-minute ischemic period. Intracellular pH fell to 6.09 +/- 0.12 in group 1, 6.31 +/- 0.09 in group 2, an 6.79 +/- 0.03 in group 3. In all three groups intracellular pH returned to control (pH 7.20) within 10 minutes of reflow. The metabolic correlates of functional recovery appeared to be the tissue content of ATP at the end of ischemia and after reflow. ATP content at the end of ischemia was 22 +/- 2% of control in group 1 hearts, 31 +/- 4% in group 2 and 64 +/- 2% in group 3. After 45 minutes of reperfusion, ATP levels recovered to 33 +/- 9% of control in group 1, to 71 +/- 9% in group 2 and to 86 +/- 6% in group 3. Although there were no differences between groups in the content of creatine phosphate after 60 minutes of ischemia, the rates of creatine phosphate decline were dissimilar. Further, during the early reflow period, a marked overshoot in tissue creatine phosphate was detected, especially in groups 1 and 2. Histologic damage assessed by light microscopy correlated with the metabolic data, confirming that multidose cardioplegia provided the best preservation of cellular morphology. These results demonstrate that the magnitude of intracellular acidosis and the associated increase in inorganic phosphate correlate inversely with recovery of postischemic ventricular structure and function. ATP, but not creatine phosphate, content correlates with return of contractile performance after reperfusion. The overshoot in creatine phosphate during early reperfusion might impede optimal restoration of ATP content and, as a result, optimal recovery of cell functions.
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PMID:Mechanisms of ischemic myocardial cell damage assessed by phosphorus-31 nuclear magnetic resonance. 679 21

Hypothermic potassium cardioplegia is now commonly used to protect the myocardium during surgically induced ischemia. Because the potassium-related membrane depolarization has been shown to increase calcium influx, we undertook this study to define the effects of varying the calcium content in hyperkalemic perfusates and the effects of using magnesium instead of or in addition to potassium as the arresting agent on the ability of hearts to recover normal function after ischemic arrest. We subjected isolated perfused working rat hearts to 60 minutes of cardioplegic arrest followed by 30 minutes of reperfusion, and measured high-energy phosphate levels every 2 1/2 minutes by phosphorus-31 nuclear magnetic resonance spectroscopy. These data were correlated with postischemic recovery of function. Our results show that potassium cardioplegia may be harmful when the calcium concentration is greater than 1 mM. The kalemic injury is significantly reduced when the calcium content is lowered to 0.25 mM and the greatest extent of preservation is provided by a calcium-poor perfusate (0.25 mM) containing 13 mM magnesium. The beneficial effects of magnesium are not enhanced by subsequent addition of potassium. Close correlations were found between all observed metabolic changes during arrest and the degree of recovery of contractile performance after reperfusion. We conclude that the ability of the myocardium to maintain or resynthesize high-energy phosphate after cardioplegic arrest may be an important determinant of postischemic mechanical performance. These results show that phosphorus-31 nuclear magnetic resonance spectroscopy is a valuable method for evaluating interventions to reduce the severity of ischemic damage.
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PMID:Evaluation of high-energy phosphate metabolism during cardioplegic arrest and reperfusion: a phosphorus-31 nuclear magnetic resonance study. 685 Oct 24

The calcium channel blocker, diltiazem, has been studied in the same model used for evaluation of cold blood-potassium cardioplegia. Six dogs (Group 1) had one hour of myocardial ischemia with topical ice (myocardial temperature, 7 degrees +/- 2 degrees C) after coronary perfusion with 200 ml of cold blood (5 degrees +/- 1 degree C) containing diltiazem, 400 micrograms per kilogram of body weight. Seven dogs (Group 2) had two hours of ischemia after perfusion with 200 ml of cold blood containing 200 micrograms/kg and reperfusion every 30 minutes with 100 ml of cold blood and diltiazem, 100 micrograms/kg. Baseline studies were repeated after rewarming and 40 minutes of reperfusion. No inotropic agents or calcium were used. Heart rate, peak systolic pressure, velocity of the contractile element, peak + rate of rise of left ventricular pressure (dP/dt), peak - dP/dt, dP/dt over common peak isovolumic pressure, left ventricular compliance and stiffness, and heart water were unchanged in Group 1. In Group 2, heart rate slowed (p less than 0.025) and compliance decreased (p less than 0.02). In both groups, coronary vascular resistance declined (p less than 0.001) and recovery of adenosine triphosphate (p less than 0.001), adenosine diphosphate (p less than 0.025), and the adenosine pool (p less than 0.001) was impaired. Ultrastructure was well preserved, but myofibrillar lesions were noted in Group 2. Diltiazem cardioplegia was associated with good functional recovery, but there was impairment of high-energy phosphate metabolism.
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PMID:Cold blood-diltiazem cardioplegia. 706 65

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