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PubMed1994

Myocardial blood flow at rest and during pharmacological vasodilation in cardiac transplants during and after successful treatment of rejection.

BACKGROUND: The relative intracoronary flow reserve has been found to be reduced during acute transplant rejection, but the effects of rejection on absolute flows at rest and during hyperemia have not been established previously. This has now become possible through noninvasive quantification of myocardial blood flow with positron emission tomography. METHODS AND RESULTS: Myocardial blood flow (MBF) at rest and during dipyridamole-induced hyperemia was quantified in 10 transplant patients (group A) during an acute, biopsy-proven rejection episode and again after successful immunosuppressive treatment and in 6 transplant patients (group B) without prior rejection episode. In group A patients, MBF during rejection averaged 1.7 +/- 0.3 mL.min-1.g-1 at rest and 2.5 +/- 0.9 mL.min-1.g-1 during hyperemia; after recovery, MBF at rest had declined to 1.2 +/- 0.3 mL.-1.g-1 (P < .001) but had increased to 3.9 +/- 1.1 mL.-1.g-1 (P < .001) during hyperemia. Flows after recovery from rejection were similar to those in the group B patients (0.9 +/- 0.2 and 3.9 +/- 0.7 mL.min-1.g-1). Flow reserve in the group A patients was only 1.5 +/- 0.5 during rejection but improved to 3.4 +/- 0.9 at recovery (P < .001) and thus remained lower than in the control patients (4.5 +/- 0.7, P < .05). Minimal coronary resistance during dipyridamole vasodilation was elevated during rejection (40 +/- 11 mm Hg.mL-1.min-1.g-1); after recovery, it no longer differed from that in the group B patients (26 +/- 11 versus 22 +/- 4 mm Hg.mL-1.min-1.g-1). MBF during rejection was increased relative to cardiac work, as demonstrated by significantly higher ratios of blood flow to rate-pressure product than those at recovery and in the control patients. CONCLUSIONS: A decrease in hyperemic and an increase in resting myocardial blood flow, in excess to cardiac work, account for the previously reported reduction in coronary flow reserve. Because both alterations improve with antirejection treatment, they may reflect reversible alterations, presumably of endothelial function, local coagulation, and edema. The compromise in flow reserve and hyperemic flows may contribute to acute and chronic injury from rejection and thus provides a rationale for exercise restriction during rejection. The results further suggest a potential role for serial noninvasive flow measurements to guide immunosuppressive therapy.

Adult↗
PubMed1997

Dobutamine echocardiography and quantitative rest-redistribution 201Tl tomography in myocardial hibernation. Relation of contractile reserve to 201Tl uptake and comparative prediction of recovery of function.

BACKGROUND: The purposes of this study were to evaluate the comparative accuracy of dobutamine echocardiography and quantitative rest-redistribution 201Tl tomography in the prediction of recovery of function after revascularization and to assess the relation of contractile reserve to thallium uptake. METHODS AND RESULTS: Thirty-four patients with stable coronary disease and regional dysfunction underwent dobutamine echocardiography (2.5 up to 40 micrograms.kg-1.min-1) and rest-redistribution 201Tl tomography 1 day before revascularization. Resting echocardiography and scintigraphy were repeated at > or = 6 weeks. Before revascularization, resting 201Tl uptake was similar in segments demonstrating biphasic or sustained improvement and was higher than in those exhibiting no change or worsening function during dobutamine. After revascularization, 201Tl uptake increased only in segments that showed a biphasic response (from 66 +/- 12% to 78 +/- 13%; P < .05). Biphasic response had a sensitivity of 74% and specificity of 89% for prediction of recovery. The use of biphasic or sustained improvement responses increased the sensitivity to 86% with a decrease in specificity to 68%. Qualitative thallium assessment provided a high sensitivity (98%) but poor specificity (27%). Quantification of thallium uptake, however, improved its accuracy: a maximal uptake (at rest or redistribution) of > or = 60% yielded a 90% sensitivity and a 56% specificity. CONCLUSIONS: In patients with myocardial hibernation, biphasic response during dobutamine is less sensitive but more specific for recovery of function, whereas indexes of 201Tl scintigraphy are in general more sensitive and less specific, the least accurate being a qualitative assessment of thallium uptake. The sensitivity and specificity of both methods, however, can be altered depending on the quantitative criteria of thallium uptake or combination of responses of the myocardium to dobutamine.

Aged↗
PubMed1997

Cardiac atrophy after bed-rest deconditioning: a nonneural mechanism for orthostatic intolerance.

BACKGROUND: The cardiovascular adaptation to bed rest leads to orthostatic intolerance, characterized by an excessive fall in stroke volume (SV) in the upright position. We hypothesized that this large fall in SV is due to a change in cardiac mechanics. METHODS AND RESULTS: We measured pulmonary capillary wedge pressure (PCWP), SV, left ventricular end-diastolic volume (LVEDV), and left ventricular mass (by echocardiography) at rest, during lower-body negative pressure, and after saline infusion before and after 2 weeks of bed rest with -6 degrees head-down tilt (n=12 subjects aged 24+/-5 years). Pressure (P)-volume (V) curves were modeled exponentially by P=ae(kV)+b and logarithmically by P=-Sln[(Vm-V)/(Vm-V0)], where V0 indicates volume at P=0, and the constants k and S were used as indices of normalized chamber stiffness. Dynamic stiffness (dP/dV) was calculated at baseline LVEDV. The slope of the line relating SV to PCWP during lower-body negative pressure characterized the steepness of the Starling curve. We also measured plasma volume (with Evans blue dye) and maximal orthostatic tolerance. Bed rest led to a reduction in plasma volume (17%), baseline PCWP (18%), SV (12%), LVEDV (16%), V0 (33%), and orthostatic tolerance (24%) (all P<.05). The slope of the SV/PCWP curve increased from 4.6+/-0.4 to 8.8+/-0.9 mL/mm Hg (P<.01) owing to a parallel leftward shift in the P-V curve. Normalized chamber stiffness was unchanged, but dP/dV was reduced by 50% at baseline LVEDV, and cardiac mass tended to be reduced by 5% (P<.10). CONCLUSIONS: Two weeks of head-down-tilt bed rest leads to a smaller, less distensible left ventricle but a shift to a more compliant portion of the P-V curve. This results in a steeper Starling relationship, which contributes to orthostatic intolerance by causing an excessive reduction in SV during orthostasis.

Adaptation, Physiological↗
PubMed1991

Prognostic significance of exercise versus resting blood pressure in hypertensive men.

The outcome of 143 male hypertensive patients, investigated in the period 1972-1982, was ascertained in 1989 to determine if brachial artery pressure measured during a progressive graded exercise test on the bicycle ergometer is a better predictor of mortality and cardiovascular events than pressure at rest. During the total follow-up time of 1,573 patient years, 27 patients suffered at least one fatal or nonfatal cardiovascular event and 13 patients died. Using the Cox regression model, the age-adjusted relative hazard rates of systolic pressure at supine rest, at 50 W, at peak work load, and at 50% of peak exercise capacity were significant for total mortality (p less than or equal to 0.01) and for cardiovascular events (p less than or equal to 0.03). Pressure during exercise, however, did not significantly (p = 0.11-0.97) predict the outcome of the patients when age and pressure at rest were taken into account. The results were similar for diastolic pressure. In conclusion, intra-arterial pressures at rest and during submaximal and peak exercise significantly predict mortality and the incidence of cardiovascular events in hypertensive men, independent of age. However, there is no additional prognostic precision of the exercise pressures when age and the rest pressure are taken into account.

Adolescent↗
PubMed1997

Region-specific neuropeptide Y overflows at rest and during sympathetic activation in humans.

Neuropeptide Y coexists with norepinephrine in sympathetic nerves and is coreleased into the circulation on sympathetic activation. Little is known about the regional release of neuropeptide Y in humans under normal conditions or in pathophysiological situations of sympathetic activation or denervation. We measured plasma neuropeptide Y-like immunoreactivity and norepinephrine concentrations in samples taken from the brachial artery; coronary sinus; and internal jugular, antecubital, or hepatic veins in volunteers aged 20 to 64 years. Regional neuropeptide Y overflow at rest was calculated from venoarterial plasma concentration differences and plasma flow, and norepinephrine spillover was determined by [3H]norepinephrine infusion techniques. Cardiac release of neuropeptide Y and norepinephrine was examined in response to various stressors as well as in clinical models of sympathetic activation, cardiac failure, and denervation after cardiac transplantation. In healthy volunteers, cardiac, forearm, and jugular venous sample neuropeptide Y concentrations were similar to arterial levels. Hepatic vein plasma neuropeptide Y was greater than arterial both at rest (119 +/- 5% of arterial, n = 7) and after a meal (132 +/- 12%, n = 7), with neuropeptide Y overflows of 6 +/- 2 and 11 +/- 2 pmol/min, respectively. In contrast, hepatomesenteric norepinephrine spillover was not significantly increased by feeding. Although coronary sinus plasma norepinephrine concentrations increased significantly with the cardiac sympathetic activation accompanying mental arithmetic, coffee drinking, isotonic exercise, and bicycle exercise, only the latter powerful sympathetic stimulus increased neuropeptide Y overflow. Cardiac failure was associated with increased resting release of both norepinephrine and neuropeptide Y from the heart, whereas postcardiac transplant norepinephrine spillover from the heart was reduced. The net overflow of neuropeptide Y to plasma observed at rest across the hepatic circulation, but not the cardiac, forearm, or cerebral circulations, indicates that the gut, the liver, or both make a major contribution to systemic plasma neuropeptide Y levels in humans. Sympathetic activation by exercise produced a modest increase in cardiac neuropeptide Y overflow but to only approximately 25% of the resting input from the gut and without a change in arterial neuropeptide Y concentration. Plasma neuropeptide Y measurements are less sensitive than those of plasma norepinephrine concentrations as an index for quantifying sympathetic neural responses regulating the systemic circulation.

Adult↗
PubMed1978

Pressure-flow characteristics of coronary stenoses in unsedated dogs at rest and during coronary vasodilation.

The pressure-flow characteristics of 100 left circumflex stenoses in 10 chronically instrumented unsedated dogs were studied under resting conditions and during pharmacological coronary vasodilation. At rest, the pressure loss (deltaP) due to a stenosis and arterial flow velocity (V) were related by the equation, deltaP = FV + SV2, where F is the coefficient of pressure loss due to viscous friction in the stenotic segment and S is the coefficient of pressure loss due to flow separation at the diverging end of the stenosis. The linear term due to viscous friction accounted for 65% and the nonlinear term due to flow separation accounted for 35% of the total pressure loss at resting coronary flow. At peak coronary flow after coronary vasodilation, the pressure loss due to viscous friction accounted for 33% and pressure loss due to flow separation accounted for 67% of the total pressure loss. The pressure gradient-velocity relationship at high flows was characterized by the same general equation but with proportionately larger values of the coefficient S and therefore greater pressure loss associated with flow separation than predicted by the resting gradient-velocity relationship. The pressure loss predicted for high coronary flow velocities on the basis of the gradient-velocity equation at rest was only 64% of the actual experimentally observed pressure gradient at peak coronary flow. The augmented separation loss following coronary vasodilation probably was due to dilation of the epicardial artery adjacent to the fixed stenotic segment which caused more severe relative percent narrowing and a larger divergence angle at the distal end of the stenosis, the primary geometric determinants of separation losses.

Animals↗
PubMed1995

Effects of rest interval on the release of calcium from the sarcoplasmic reticulum in isolated guinea pig ventricular myocytes.

Guinea pig cardiac myocytes were loaded with the fluorescent dye indo 1, and cell contraction was measured by a video edge-detection system. Ca2+ was released from the sarcoplasmic reticulum (SR) by rapidly cooling the myocytes or by rapid application of 10 mmol/L caffeine. Estimates of the amount of Ca2+ released from the SR after different rest intervals (ie, under different loading conditions) were obtained by measuring the current evoked by rapid application of 10 mmol/L caffeine, which we call Na+/Ca2+ exchange current. This current is completely inhibited by removal of extracellular Na+ and Ca2+ or by application of 5 mmol/L Ni2+. SR Ca2+ release after rest intervals of 5 to 120 seconds (assuming cell volume to be 30 x 10(-12) L) was estimated to be 57.8 +/- 5.7 to 25.7 +/- 4.5 mumol/L accessible cell volume, respectively, equivalent to 23 to 10 mumol/kg wet wt, respectively. There was an exponential decline in Ca2+ release from the SR after rest intervals of 2 to 120 seconds (rate constant, 0.029 s-1; t1/2, 24 seconds); thereafter, there remained a portion (56%) of Ca2+ releasable to caffeine application. We found a similar exponential decay (rate constant, 0.020 s-1; t1/2, 35 seconds) of the size of rapid cooling contractures with increasing rest intervals. The time to peak of the Na+/Ca2+ exchange current in the presence of caffeine slowed at long rest intervals, ie, at smaller SR loads. A decrease in SR load of 50% increased the time to peak of the exchange current by 213 +/- 37% (n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Ventilatory mechanics at rest and during exercise in patients with cystic fibrosis.

Ventilatory mechanics were measured at rest and during steady-state (25%, 50%, 75%) and maximal exercise (W-Max) on a cycle-ergometer in eight adult patients (FEV1 22 to 114% of predicted) with cystic fibrosis (CF). Tidal flow-volume loops were measured at rest and during exercise and placed within the maximal pre- and postexercise flow-volume loops, based on measured end-expiratory lung volume (EELV). The degree of flow limitation was expressed as the percentage of the tidal flow-volume loop that met the expiratory boundary of the maximal loop (TFVL%). Pressure-volume relationships were assessed by measurement of transpulmonary pressure (PTP). Peak inspiratory PTP was compared with maximal inspiratory pressures at rest and during exercise (Pcap(i)) at the equivalent lung volume. The maximal effective expiratory pressure (Pmax(e)) was determined using the orifice technique. Three patients with milder disease (FEV1 114, 98, 89% of predicted) did not show any flow limitation at rest or 50% W-Max but two did show some flow limitation at W-Max (0, 3, 23 TFVL%) with a decrease in EELV (-400, -200, -300 ml). There was considerable reserve for inspiratory and expiratory pressure generation at W-Max. Flow limitation was noted at rest in three patients and at 50% W-Max in the five patients with more severe airways obstruction. The increased flow was achieved by an increase in EELV in all five patients (+400, +430, +330, +150, +700 ml at W-Max). Pcap(i) was reached in two patients (-28, -36 cm H2O), while Pmax(e) was exceeded by four patients suggesting inefficient pressure generation. Expiratory flow limitation, hyperinflation, and pressure swings approaching capacity severely compromised the capacity to generate ventilation in some patients with CF.

Adolescent↗
PubMed1975

The relationship between regional myocardial perfusion at rest and arteriographic lesions in patients with coronary atherosclerosis.

Measurements of mean left ventricular (LV) and regional myocardial blood flow rates were made at rest in 161 patients with 133Xe and a multiplecrystal scintillation camera. Myocardial perfusion rates were correlated with assessments of the degree of coronary artery disease made from the arteriograms obtained during the same studies. In patients with normal coronary arteries without heart failure, the presence of hypertension, aortic stenosis, or aortic insufficiency was not associated with changes in mean LV perfusion from the control value of 61+/-7 ml/100 g-min. However, mean LV perfusion was significantly reduced in patients with normal coronary arteries who had cariomyopathy and impaired ventricular performance. Mean LV perfusion was not significantly different from control values in patients with "mild" coronary artery disease (less than 50% obstruction) or in patients with significant isolated disease (greater than 50% obstruction) of the left anterior descending (lad) artery. Significant reductions in mean LV perfusion were found in patients with greater than 50% obstruction of two coronary arteries (LAD + right or LAD + circumflex) and in patients with triple-vessel disease. The average perfusion rate for regions distal to LAD obstructions in patients with isolated LAD disease was not lower than the LAD perfusion in control patients, but was significantly reduced in patients with LAD + right coronary artery disease (43+/-14 ml/100 g-min). In the latter group average perfusion distal to the LAD lesion was significantly lower than the average regional perfusion rate for the remainder of the LV. However, the mean blood flow rate for the remainder of the LV was also significantly lower than control values despite the lack of significant circumflex disease. The data demonstrate that the presence of radiographically "mild" or significant isolated LAD coronary disease is not associated with reductions in mean LV perfusion at rest, but that mean LV perfusion is reduced in the presence of significant disease of two or three coronary artieries. None of the patients experienced angina during the resting studies and most had clinical evidence of ventricular failure. The observation of depressed LV perfusion in this group, as in the patients with cardiomyopathy, raises the possibility that a lowered resting blood supply may be adequate for a reduced level of performance of a diseased ventricle. The lack of selective reductions of regional perfusion at rest in the majority of the patients with LAD lesions suggests that regional myocardial blood flow must be measured during an intervention which increases myocardial oxygen consumption in order to assess the physiological significance of lesions which are observed at coronary arteriography.

Adult↗
PubMed1984

Turnover and splanchnic metabolism of free fatty acids and ketones in insulin-dependent diabetics at rest and in response to exercise.

Nine insulin-dependent diabetics and six healthy controls were studied at rest, during, and after 60 min of bicycle exercise at a work load corresponding to 45% of their maximal oxygen intake. The catheter technique was employed to determine splanchnic and leg exchange of metabolites. FFA turnover and regional exchange was evaluated using [14C]oleate infusion. Basal glucose (13.8 +/- 1.1 mmol/l), ketone body (1.12 +/- 0.12 mmol/l), and FFA (967 +/- 110 mumol/l) concentrations were elevated in the diabetics in comparison with controls. In the resting state, splanchnic ketone acid production in the diabetics was 6-10-fold greater than in controls. Uptake of oleic acid by the splanchnic bed was increased 2-3-fold, and the proportion of splanchnic FFA uptake converted to ketones (61%) was threefold greater than in controls. In contrast, splanchnic fractional extraction of oleic acid was identical in diabetics and controls. A direct relationship was observed between splanchnic uptake and splanchnic inflow (plasma concentration X hepatic plasma flow) of oleic acid that could be described by the same regression line in the diabetic and control groups. During exercise, splanchnic ketone production rose in both groups. In the control group the increase in ketogenesis was associated with a rise in splanchnic inflow and in uptake of oleic acid, a rise in splanchnic fractional extraction of oleate, and an increase in the proportion of splanchnic FFA uptake converted to ketone acids from 20-40%. In the diabetic group, the increase in ketogenesis occurred in the absence of a rise in splanchnic inflow or uptake of oleic acid, but was associated with an increase in splanchnic fractional extraction of oleic acid and a marked increase in hepatic conversion of FFA to ketones, so that the entire uptake of FFA was accountable as ketone acid output. Splanchnic uptake of oleic acid correlated directly with splanchnic oleic acid inflow in both groups, but the slope of the regression line was steeper than in the resting state. Plasma glucagon levels were higher in the diabetic group at rest and during exercise, while plasma norepinephrine showed a twofold greater increment in response to exercise in the diabetic group (to 1,400-1,500 pg/ml). A net uptake of ketone acids by the leg was observed during exercise but could account for less than 5% of leg oxidative metabolism in the diabetics and less than 1% in controls. Despite the increase in ketogenesis during exercise, a rise in arterial ketone acid levels was not observed in the diabetics until postexercise recovery, during which sustained increments to values of 1.8-1.9 mmol/l and sustained increases in splanchnic ketone production were observed at 30-60 min. The largest increment in blood ketone acids and in splanchnic ketone production above values observed in controls thus occurred in the diabetics after 60 min of recovery from exercise. We concluded that: (a) In the resting state, increased ketogenesis in the diabetic is a consequence of augmented splanchnic inflow of FFA and increased intrahepatic conversion of FFA to ketones, but does not depend on augmented fractional extraction of circulating FFA by the splanchnic bed. (b) Exercise-induced increases in ketogenesis in normal subjects are due to augmented splanchnic inflow and fractional extraction of FFA as well as increased intrahepatic conversion of FFA to ketones. (c) When exercise and diabetes are combined, ketogenesis increases further despite the absence of a rise in splanchnic inflow of FFA. An increase in splanchnic fractional extraction of FFA and a marked increase intrahepatic conversion of FFA to ketones accounts for the exaggerated ketogenic response to exercise in the diabetic. (d) Elevated levels of plasma glucagon and/or norepinephrine may account for the increased hepatic ketogenic response to exercise in the diabetic. (e) Ketone utilization by muscle increases during exercise but constitutes a quantitatively minor oxidative fuel for muscle even in the diabetic. (f) The accelerated ketogenesis during exercise in the diabetic continues unabated during the recovery period, resulting in an exaggerated postexercise ketosis.

Adult↗
PubMedDate not supplied

High-dose dipyridamole and gated sestamibi SPECT imaging provide diagnostic resting and stress ejection fractions useful for predicting extent of coronary artery disease.

A decline in ejection fraction at stress compared with rest images has been associated with increased severity of coronary artery disease (CAD) and suggests a poorer prognosis. Myocardial perfusion imaging (MPI) using high-dose dipyridamole (HDD) has been shown to more accurately detect CAD than either standard dose dipyridamole (SDD) or exercise-induced stress (EST), but has not been looked at to determine its usefulness in detecting changes in stress and rest ejection fractions. To determine the relationship between changes in left ventricular ejection fraction (LVEF) and the severity of CAD, 36 Individuals underwent gated single photon emission computed tomography (SPECT) MPI using HDD. In each case resting and stress LVEFs were determined along with MPI results. Subjects with single-vessel CAD demonstrated an increase in LVEF from 77.8% (sd +/-8.8%) to 85.6% (sd +/-8.4%) resulting in a statistically significant increase in LVEF of 7.8% (p = 0.009). Patients with two-vessel disease showed a smaller increase from 73.2% (sd + 8.3%) to 79.8% (sd + 9.8%) following HDD stress. This increase was statistically (p = 0.008) significant. Patients with triple-vessel CAD showed a reduction in LVEF from 67.4% (sd +/-14.07) to 65.1% (sd +/-16.5%) which represented a decrease in LVEF of 2.7% and approached (p = 0.25) but did not reach statistical significance. Both the resting and stress LVEFs were statistically lower (p<0.05) in patients with triple-vessel CAD. Changes in resting LVEF (REF) and HDD pharmacologically induced stress LVEF (SEF) provide a valuable diagnostic marker as to the number of significantly diseased coronary arteries and can be acquired from gated SPECT sestamibi images.

Adult↗
PubMed2004

Induction of beta-cell rest by a Kir6.2/SUR1-selective K(ATP)-channel opener preserves beta-cell insulin stores and insulin secretion in human islets cultured at high (11 mM) glucose.

In health, most insulin is secreted in pulses. Type 2 diabetes mellitus (TTDM) is characterized by impaired pulsatile insulin secretion with a defect in insulin pulse mass. It has been suggested that this defect is partly due to chronic overstimulation of beta-cells imposed by insulin resistance and hyperglycemia, which results in depletion of pancreatic insulin stores. It has been reported that in TTDM overnight inhibition of insulin secretion (induction of beta-cell rest) leads to quantitative normalization of pulsatile insulin secretion upon subsequent stimulation. Recently, decreased orderliness of insulin secretion has been recognized as another attribute of impaired insulin secretion in TTDM. In the current studies we sought to address at the level of the isolated islet whether chronic elevated glucose concentrations induce both defects involved in impaired insulin secretion in TTDM: deficiency and decreased orderliness of insulin secretion. We use the concept of beta-cell rest, induced by a novel beta-cell selective K(ATP)-channel opener (KCO), NN414 (6-chloro-3-(1-methylcyclopropyl)amino-4H-thieno[3,2-e]-1,2,4-thiadiazine 1,1-dioxide), to test whether preservation of insulin stores leads to normalization of both processes in response to glucose stimulation. Human islets were isolated from three cadaveric organ donors and studied in perifusion experiments and static incubation. Acute activation of K(ATP)-channels suppressed insulin secretion from perifused human islets by approximately 90% (P < 0.0001). This KCO also inhibited glucagon secretion in a dose-dependent manner (P = 0.01). Static incubation at 11 and 16 vs. 4 mM glucose for 96 h decreased islet insulin stores by approximately 80% and 85% (P < 0.0001, respectively). In subsequent perifusion experiments, total insulin secretion ( approximately 30%; P < 0.01) from these islets and insulin pulse mass ( approximately 40%; P < 0.05) were both decreased (11 vs. 4 mM). The inhibition of insulin secretion during static incubation with KCO reduced the loss of islet insulin stores in a dose-dependent manner (P < 0.0001) and resulted in increased total insulin secretion (2.6-fold; P < 0.01) and insulin pulse mass (2.5-fold; P < 0.05) during subsequent perifusion. The orderliness of insulin secretion was significantly reduced after chronic incubation of human islets at 11 mM glucose (P = 0.04), but induction of beta-cell rest at 11 mM failed to normalize the regularity of insulin secretion during subsequent perifusion. We conclude that physiological increased glucose concentrations (11 mM), which are frequently observed in diabetes, lead to a loss of islet insulin stores and defective pulsatile insulin secretion as well as reduced orderliness of insulin secretion. Induction of beta-cell rest by selective activation of beta-cell K(ATP)-channels preserves insulin stores and pulsatile insulin secretion without restoring the orderliness of insulin secretion. Therefore, the concept of beta-cell rest may provide a strategy to protect beta-cells from chronic overstimulation and to improve islet function. Impaired glucose-regulated insulin secretion in TTDM may, however, partially involve mechanisms that are distinct from insulin stores and insulin secretion rates.

Adenosine Triphosphate↗
PubMed2005

Effects of high-dose growth hormone on glucose and glycerol metabolism at rest and during exercise in endurance-trained athletes.

CONTEXT: Recombinant human-GH (r-hGH), in supraphysiological doses, is self-administered by athletes in the belief that it is performance enhancing. OBJECTIVE: The objective of this study was to determine whether r-hGH alters whole-body glucose and glycerol metabolism in endurance-trained athletes at rest and during and after exercise. DESIGN: This was a 4-wk double-blind placebo-controlled trial. SETTING: This study was conducted at St. Thomas Hospital (London, UK). PARTICIPANTS: Twelve endurance-trained male athletes were recruited and randomized to r-hGH (0.2 U/kg.d) (n = 6) or identical placebo (n = 6) for 4 wk. One (placebo group) withdrew after randomization. INTERVENTION: Intervention was conducted by randomization to r-hGH (0.2 U/kg x d) or identical placebo for 4 wk. MAIN OUTCOME MEASURES: Whole-body rates of appearance (Ra) of glucose and glycerol (an index of lipolysis) and rate of disappearance of glucose were measured using infusions of d-[6-6-2H2]glucose and 2H5-glycerol. RESULTS: Plasma levels of glycerol and free fatty acids and glycerol Ra at rest and during and after exercise increased during r-hGH treatment (P < 0.05 vs. placebo). Glucose Ra and glucose rate of disappearance were greater after exercise during r-hGH treatment (P < 0.05 vs. placebo). Resting energy expenditure and fat oxidation were greater under resting conditions during r-hGH treatment (P < 0.05 vs. placebo). CONCLUSIONS: r-hGH in endurance-trained athletes increased lipolysis and fatty acid availability at rest and during and after exercise. r-hGH increased glucose production and uptake rates after exercise. The relevance of these effects for athletic performance is not known.

Adult↗
PubMed1999

Testosterone administration preserves protein balance but not muscle strength during 28 days of bed rest.

Decrements in muscle strength as a result of prolonged bed rest are well defined, but little is known about potential countermeasures for preventing loss of strength under this condition. The purpose of this study was to determine whether testosterone administration would preserve protein balance and muscle strength during prolonged bed rest. Ten healthy men (age, 36 +/- 2 yr; height, 177.2 +/- 3.4 cm; weight, 80.5 +/- 3.9 kg; mean +/- SE) were admitted to our in-patient metabolic unit. After a 1-week ambulatory run-in period, each subject was confined to bed for 28 days at 6 degree head-down tilt while receiving a daily oral dose of T3 (50 microg/day). During the bed rest/T3 period, six of the men were randomized to receive testosterone enanthate by i.m. injection (T; 200 mg/week) while four received placebo in a double blind fashion. Nitrogen balance was determined throughout, and whole body [13C]leucine kinetics were assessed at baseline and on day 26 of bed rest. Before bed rest and on the third day of reambulation, the muscle strength of the knee extensors and flexors and shoulder extensors and flexors was determined at 60 degrees/s on a Cybex isokinetic dynamometer. Despite improved [13C]leucine kinetics and maintenance of nitrogen balance and lean body mass in T-treated subjects, little preservation of muscle strength, particularly in the knee extensors, was noted. Muscle strength [reported as the best work repetition in foot-pounds (FtLb)] for right knee extensors declined (P = 0.011) similarly in both groups; from 165 +/- 15 to 126 +/- 18 FtLb in T-treated men and from 179 +/- 22 to 149 +/- 13 FtLb in placebo-treated men. Overall, there was less of a decline in extension and flexion strength of the shoulder compared to the knee, with no benefit from T. These results suggest that in the absence of daily ambulatory activity, T administration will not increase or, in the case of this bed rest model, preserve muscle strength.

Adult↗
PubMed1985

Effects of nifedipine and diltiazem on hemodynamic responses at rest and during exercise in hypertensive patients.

Twelve patients with uncomplicated systemic hypertension were treated with nifedipine (30 mg/day) and diltiazem (180 mg/day) for 1 month each, and performed two stage (50 watt and 100 watt) of bicycle ergometer exercise before and after each period of administration. Both drugs produced significant reduction in systolic and diastolic blood pressure at rest and during exercise, while the mean values of systolic blood pressure tended to be less with nifedipine than with diltiazem. Nifedipine caused a nonsignificant increase in heart rate at rest and during exercise, but diltiazem significantly decreased it at rest and during exercise. Cardiac output was significantly increased at rest and during mild exercise (50 watt), but not during more strenuous exercise (100 watt) with both drugs. Thus, different actions in arterial vasodilation and chronotropism between nifedipine and diltiazem in usual clinical doses were noted. However, nifedipine and diltiazem may be effective in hypertensive patients, probably with left ventricular dysfunction, because both drugs reduced systemic blood pressure even during exercise with simultaneous increase in cardiac output at rest and during mild exercise.

Adult↗
PubMed1995

Relationship between insufficient redistribution in exercise thallium-201 myocardial single-photon emission computed tomography and reverse redistribution at rest.

It is widely accepted that perfusion defects in 3 to 4-h delayed images in exercise thallium-201 (201Tl) myocardial scintigraphy underestimate the viability of myocardium in the infarct region. In the present study, to examine the contribution of the condition of myocardium which demonstrates reverse redistribution in resting scintigraphy to the insufficiency of redistribution in the 4-h delayed image in exercise scintigraphy, we performed exercise and resting 201Tl myocardial single-photon emission computed tomography in 58 patients with acute myocardial infarction and a single diseased coronary artery. Twenty eight patients demonstrated reverse redistribution (group RR) and 28 showed a fixed defect (group FD) in resting scintigraphy. Redistribution in the 4-h delayed image in exercise scintigraphy was significantly more insufficient in group RR than in group FD (p < 0.01), and the degree of the insufficiency of redistribution in exercise scintigraphy closely correlated with the degree of reverse redistribution in resting scintigraphy (r = 0.79, p < 0.001). We conclude that in patients with acute myocardial infarction, the condition of myocardium which demonstrates reverse redistribution in resting myocardial scintigraphy is related to the insufficiency of redistribution in the delayed image in exercise scintigraphy.

Adult↗
PubMed1997

Decrease in CD4 lymphocyte counts with rest; implications for the monitoring of HIV infection.

Measurement of the CD4 lymphocyte count is widely used as a prognostic marker and guide for the institution of antiretroviral therapy in patients infected with HIV (human immunodeficiency virus). CD4 counts are known to fluctuate with strenuous physical activity and diurnal variation but there is no information on the effects of rest or normal daily activity. We investigated the effects of rest on the absolute CD4 lymphocyte count in 20 healthy laboratory workers. Blood samples were obtained in 20 subjects upon arrival in the laboratory (CD4 0), following 30 and 60 min rest (CD4 30 and CD4 60 respectively) and 8 h into a normal working day (CD4 8). A significant decrease in the CD4 lymphocyte count was observed following 60 min rest; mean CD4 count at 0 min 1060 x 10(6)/L, mean CD4 count at 60 min 660 x 10(6)/L (P = 0.0017). These results demonstrate a significant effect of rest on CD4 lymphocyte counts in healthy volunteers. This biological variation may be important in HIV-infected patients and needs to be addressed by further studies.

Activities of Daily Living↗
PubMed2007

Is supine rest necessary before blood sampling for plasma metanephrines?

BACKGROUND: The impact of blood sampling in sitting vs supine positions on measurements of plasma metanephrines for diagnosis of pheochromocytoma is unknown. METHODS: We compared plasma concentrations of free metanephrines in samples from patients with primary hypertension obtained after supine rest with those obtained in the sitting position without preceding rest. We also assessed the effects on diagnostic test performance retrospectively in patients with and without pheochromocytoma, and we calculated cost-effectiveness for pheochromocytoma testing. RESULTS: Upper reference limits of plasma free metanephrines were higher in samples obtained from seated patients without preceding rest than from supine patients with preceding rest. Application of these higher upper reference limits to samples from supine patients with pheochromocytoma decreased the diagnostic sensitivity from 99% to 96%. In patients without pheochromocytoma, adjusting the plasma concentration for the effects of sitting while preserving the 99% sensitivity by use of the supine upper reference limits increased the number of false-positive test results from 9% to 25%. CONCLUSIONS: To preserve high diagnostic sensitivity we recommend the use of upper reference limits determined from blood samples collected in the supine position. Under these conditions, negative test results for blood samples obtained with patients sitting are as effective for ruling out pheochromocytoma as negative results from samples obtained after supine rest. Repeat testing with samples obtained in the supine position offers a cost-effective approach for dealing with the increased numbers of false-positive results expected after initial sampling in the sitting position.

Adrenal Gland Neoplasms↗