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At least 145 records · Page 8Linked to original sources
PubMed1995

Renal reserve in patients with high blood pressure.

The mechanism by which hypertension produces renal damage remains poorly defined. Experimental evidence suggests that glomerular hypertension/hyperfiltration constitutes a potential mechanism by which hypertension leads to chronic renal failure. Renal functional reserve has been used to investigate the presence or absence of hyperfiltration, both in experimental animals and humans. Micropuncture studies using the two-kidney, one-clip hypertension model have shown that glomerular hypertension/hyperfiltration is associated with loss of renal functional reserve. However, loss of renal functional reserve in this experimental model is not always indicative of hyperfiltration because some antihypertensive agents (Verapamil, Losartan) correct glomerular hypertension/hyperfiltration, but do not restore renal reserve. Renal reserve has also been evaluated in patients with essential hypertension. Some investigators have shown that hypertension is associated with loss of renal functional reserve which can be restored in some studies with antihypertensive therapy. However, normal renal reserve has also been shown in hypertensive patients. Altogether, these data suggest that renal functional reserve cannot be used to assess the role of hemodynamic mechanisms in hypertension-induced renal injury. Long-term follow-up studies are required to establish if loss of renal reserve is indicative of risk factors leading to renal failure in patients with systemic hypertension.

Animals↗
PubMed2026

Post-intervention effectiveness of a computerized personalized cognitive stimulation program adapted according to cognitive reserve in older adults without cognitive impairment in Primary Care: A randomized clinical trial.

BACKGROUND: Cognitive reserve may influence responsiveness to cognitive interventions, yet it is rarely used to tailor computerized stimulation. OBJECTIVE: To evaluate the effectiveness of a computerized cognitive stimulation program personalized according to cognitive reserve on cognition, reserve-related activities, and digital competence in community-dwelling older adults without cognitive impairment in Primary Care. METHODS: In this randomized clinical trial, 102 adults aged ≥65 years with normal cognitive performance were recruited from three primary care centers in Zaragoza, Spain, and stratified by cognitive reserve level before random allocation to intervention or control. The intervention comprised digital literacy sessions followed by 8 weeks of home-based computerized cognitive stimulation tailored to participants' cognitive reserve profiles and life history. Controls received a single group-based health education session focused on maintaining everyday cognitive activity. Outcomes were assessed at baseline and post-intervention using global cognition (MEC-35), the Cognitive Reserve Questionnaire, the Mobile Device Proficiency Questionnaire-16, and domain-specific neuropsychological tests. A total of 100 participants completed the final evaluation and were included in complete-case analyses. RESULTS: Compared with controls, the intervention group showed greater adjusted post-intervention improvements in global cognition (MEC-35 between-group difference: 1.8 points) and several cognitive measures, including temporal orientation, calculation, attention, praxis, verbal fluency, processing speed, executive functions, and verbal learning. CRQ scores and digital competence also improved, with small-to-large effect sizes. CONCLUSIONS: A computerized cognitive stimulation program adapted according to cognitive reserve appears feasible in Primary Care and may improve cognition, engagement in reserve-related activities, and digital competence in older adults without cognitive impairment.

Humans↗
PubMed2005

Marine reserves demonstrate trophic interactions across habitats.

Several infaunal bivalve taxa show patterns of decreased biomass in areas with higher densities of adjacent reef-associated predators (the snapper, Pagrus auratus and rock lobster, Jasus edwardsii). A caging experiment was used to test the hypothesis that patterns observed were caused by predation, using plots seeded with a known initial density of the bivalve Dosinia subrosea to estimate survivorship. The caging experiment was replicated at several sites inside and outside two highly protected marine reserves: predators are significantly more abundant inside these reserves. Survivorship in fully caged, partially caged and open plots were then compared at sites having either low (non reserve) or high (reserve) predator density. The highest rates of survivorship of the bivalve were found in caged plots inside reserves and in all treatments outside reserves. However, inside reserves, open and partially caged treatments exhibited low survivorship. It was possible to specifically attribute much of this mortality to predation by large rock lobsters, due to distinctive marks on the valves of dead D. subrosea. This suggests that predation by large rock lobster could indeed account for the distributional patterns previously documented for certain bivalve populations. Our results illustrate that protection afforded by marine reserves is necessary to investigate how depletion through fishing pressure can change the role of upper-level predators and trophic processes between habitats.

Animals↗
PubMed1991

Relationship of left ventricular mass to impairment of coronary vasodilator reserve in hypertensive heart disease.

An impaired coronary vasodilator reserve has been demonstrated in all stages of hypertensive heart disease but is most likely in the setting of hypertrophy. The decrease in coronary flow reserve has, however, not been predictable previously. We postulated that flow reserve depression might be related to a left ventricular mass threshold. Seventy-two patients (82% with hypertension) with suspected ischemic heart disease who were found to be free of significant coronary artery disease at cardiac catheterization were evaluated utilizing the intracoronary Doppler catheter and two-dimensional directed M-mode echocardiography for determination of coronary flow reserve and left ventricular mass. For left ventricular mass indexed (LVMI) by body surface area (BSA) greater than or equal to 50% above normal using established gender-specific norms, American Society of Echocardiography (ASE) and PENN methods (correction of LV mass by regression equation agreeing with necropsy estimates of mass) predicted impairment of flow reserve (p = 0.005 and 0.009, respectively). Unindexed left ventricular mass and LVMI by height were not helpful in this regard. Using the ASE method for LV mass determination, coronary flow reserve was moderately depressed (2.4 +/- 1.0) for those with LVMI greater than or equal to 50% above normal; in comparison, flow reserve was normal (3.5 +/- 1.3) for those with LVMI less than 50% above normal. A rare patient was able to maintain a normal flow reserve when ASE- and Penn-indexed mass estimates were greater than or equal to 50% above normal, but only in the setting of a markedly elevated mean arterial pressure.

Adult↗
PubMed1988

Normalization of coronary flow reserve by percutaneous transluminal coronary angioplasty.

Fifteen patients undergoing routine follow-up angiography 5 months after successful percutaneous transluminal coronary angioplasty (PTCA) without angina and with normal exercise thallium scintigraphy were selected for analysis. The coronary flow reserves of these patients were compared with those of 24 patients with angiographically normal coronary arteries to establish whether PTCA can restore to normal the coronary flow reserve of patients with chronic coronary artery disease. The quantitative cineangiographic changes and the concomitant alterations in coronary flow reserve as an immediate result of the PTCA and the subsequent changes 5 months later are described. Coronary flow reserve was measured with digital subtraction cineangiography. PTCA resulted in an increase in minimal obstruction area (mean +/- standard deviation) from 0.8 +/- 0.3 to 3.4 +/- 0.7 mm2 and in coronary flow reserve from 1.0 +/- 0.3 to 2.5 +/- 0.6. Five months later a further substantial and significant (p less than 0.05) late increase in obstruction area (3.8 +/- 0.9 mm2) and flow reserve (3.6 +/- 0.5) had occurred. In 11 of 15 patients coronary flow reserve was restored to normal. Changes in stenosis geometry are likely to be 1 of the major determinants of this late normalization of coronary flow reserve.

Adult↗
PubMed1993

Coronary vasodilator reserve in untreated and treated hypertensive patients with and without left ventricular hypertrophy.

OBJECTIVES: This study was initiated to compare the coronary reserve in treated hypertensive patients with and without left ventricular hypertrophy with that in untreated patients. BACKGROUND: Coronary reserve is impaired in hypertensive patients with left ventricular hypertrophy and normal coronary arteries. Moreover, basal coronary resistance is elevated in hypertensive patients without left ventricular hypertrophy. METHODS: Coronary reserve was measured with a coronary Doppler catheter before and after a maximally vasodilating dose of intracoronary papaverine (peak/rest flow velocity ratio) in 16 control subjects and 37 hypertensive patients with normal epicardial coronary arteries. Among 20 untreated hypertensive patients, myocardial mass was increased in 11 (group 2a) and normal in 9 (group 2b). Seventeen patients had been treated effectively for at least 1 year; nine (group 3a) had persistent left ventricular hypertrophy, and eight (group 3b) had no left ventricular hypertrophy before treatment. Left ventricular volumes and ejection fraction were normal in all groups. RESULTS: Coronary reserve was moderately reduced in group 2b (3.5 +/- 0.6 vs. 5.2 +/- 0.8 in control subjects, p < 0.001) and markedly diminished in groups 2a and 3a (2.5 +/- 0.5 and 2.7 +/- 0.4, respectively; all p < 0.001 vs. control subjects). In group 3b, coronary reserve was comparable to that of control subjects (5.1 +/- 1.4). CONCLUSIONS: The reduction in coronary reserve observed in untreated hypertensive patients with normal myocardial mass suggests that structural abnormalities of the coronary microvasculature may occur before left ventricular hypertrophy. Treated patients with normal mass before treatment had a coronary reserve comparable to that of normotensive control subjects, whereas normalization of arterial pressure with persistent left ventricular hypertrophy was associated with a marked impairment of coronary reserve.

Adult↗
PubMed1995

Coronary blood flow reserve in acute aortic regurgitation.

OBJECTIVES: This study sought to determine the impact of acute aortic regurgitation on coronary blood flow reserve and phasic epicardial coronary blood flow in closed-chest dogs. BACKGROUND: Hemodynamic changes in acute aortic regurgitation are known to precipitate myocardial ischemia. Coronary blood flow reserve has not been studied in closed-chest experimental preparations with acute aortic regurgitation. METHODS: Graded temporary acute aortic regurgitation was produced in 11 mongrel dogs. Phasic coronary blood flow velocities were measured using a Doppler guide wire. Coronary flow reserve was defined as the ratio of the time average of spectral peak velocity after administration of papaverine to that of the baseline state. RESULTS: Under control conditions (mean [+/- SEM] diastolic blood pressure 82.2 +/- 4.5 mm Hg), coronary flow reserve was 3.51 +/- 0.27 with predominantly diastolic epicardial coronary blood flow. With mild acute aortic regurgitation (diastolic blood pressure 61.8 +/- 3.0 mm Hg), coronary flow reserve decreased to 2.38 +/- 0.27, with an increase in phasic systolic epicardial coronary blood flow. At the onset of moderate acute aortic regurgitation (diastolic blood pressure 42.1 +/- 0.9 mm Hg), coronary flow reserve declined further to 1.46 +/- 0.12, and the phasic systolic epicardial coronary blood flow became more prominent. With severe aortic regurgitation (diastolic blood pressure 29.2 +/- 2.2 mm Hg), coronary flow reserve reached 1.20 +/- 0.05, and the phasic epicardial coronary blood flow pattern was found to be predominantly systolic with retrograde diastolic flow. The ratio of diastolic to systolic pressure-time indexes with severe aortic regurgitation suggested subendocardial underperfusion. CONCLUSIONS: This study demonstrates a marked decline in coronary blood flow reserve and documents a progressive change in the phasic epicardial blood flow to a predominantly systolic pattern with increasing degrees of acute aortic regurgitation.

Animals↗
PubMed1995

Noninvasive quantification of regional myocardial flow reserve in patients with coronary atherosclerosis using nitrogen-13 ammonia positron emission tomography. Determination of extent of altered vascular reactivity.

OBJECTIVES: The aim of this study was to evaluate patients with coronary artery disease to 1) determine the relation between flow reserve measured by nitrogen-13 (N-13) ammonia kinetic modeling and stenosis severity assessed by quantitative angiography, and 2) examine whether flow reserve is impaired in regions supplied by vessels without significant angiographic disease. BACKGROUND: With the advent of new therapeutic approaches for coronary disease, an accurate noninvasive approach for absolute quantification of flow and flow reserve is needed to evaluate functional severity and extent of atherosclerosis. Nitrogen-13 ammonia kinetic modeling may permit such evaluation. METHODS: Twenty-seven subjects were classified into three groups: group 1 = 5 young volunteers: group 2 = 7 middle-aged volunteers; and group 3 = 15 patients with coronary artery disease. Dynamic N-13 ammonia positron emission tomographic imaging was performed at rest and during adenosine infusion. A three-compartment model was fit to regional N-13 ammonia kinetic data to determine myocardial flow. Group 3 patients underwent quantitative coronary angiography. RESULTS: The regional blood flow results in patients with coronary disease were classified into four subgroups: no significant detectable disease and mild (50% to 69.9% area stenosis), moderate (70% to 94.9% area stenosis) or severe (95% to 100% area stenosis) coronary disease. Flow reserve was 2.95 +/- 0.65; 2.09 +/- 0.47; 2.02 +/- 0.51; 1.3 +/- 0.32, respectively (p < or = 0.01 except mild vs. moderate). Flow reserve was correlated with percent area stenosis (r = -0.56) and minimal lumen diameter (r = 0.75). In volunteers (groups 1 and 2), flow reserves were greater than in segments without detectable disease in group 3 patients (4.10 +/- 0.71 and 3.79 +/- 0.42, respectively, vs. 2.88 +/- 0.56, p < or = 0.02). CONCLUSIONS: The functional severity of coronary disease measured by N-13 ammonia positron emission tomography varied for a given stenosis but was significantly related to angiographic severity. Among patients with coronary disease, myocardial regions without significant angiographic stenoses displayed reduced flow reserve than did regions in control subjects, indicating that vascular reactivity was more diffusely impaired in group 3 than was suggested by angiography. Noninvasive quantification of myocardial flow reserve using dynamic N-13 ammonia positron emission tomography yields important functional data that permit definition of the extent of disease even when disease is not apparent by angiography.

Adenosine↗
PubMed2006

Cut-off value of coronary flow velocity reserve by transthoracic Doppler echocardiography for the assessment of significant donor left anterior descending artery stenosis in patients with spontaneously visible collaterals.

We evaluated the influence of collateral circulation on a donor left anterior descending artery and an appropriate cut-off value of coronary flow velocity reserve for the diagnosis of significant donor left anterior descending artery stenosis. Measurement of coronary flow velocity reserve by transthoracic Doppler echocardiography provides noninvasive assessment of significant left anterior descending artery stenosis. The cut-off value of coronary flow velocity reserve for the diagnosis of significant donor left anterior descending artery stenosis has not been well studied. We retrospectively examined 64 patients who had no significant left anterior descending artery stenosis and who had other coronary artery stenosis. Seventeen patients had collaterals from the left anterior descending artery (group A) and 47 patients did not have collaterals (group B). We prospectively examined 23 consecutive patients who had collaterals from the left anterior descending artery to other coronary arteries. Eight patients had a significant donor left anterior descending artery stenosis. Coronary flow velocity reserve assessment was performed by transthoracic Doppler echocardiography in the 2 protocols. Coronary flow velocity at baseline in group A was significantly higher than that in group B. Coronary flow velocity reserve in group A was significantly lower than that in group B (2.6 +/- 0.8 vs 3.2 +/- 0.9, p < 0.05). Coronary flow velocity during hyperemia and coronary flow velocity reserve were significantly lower in patients with significant stenosis. A cut-off value of 2.0 of coronary flow velocity reserve had a sensitivity of 88% and a specificity of 93% for the diagnosis of significant donor left anterior descending artery stenosis. In conclusion, coronary flow velocity reserve of a donor left anterior descending artery was decreased by the presence of collaterals. However, a cut-off value < 2.0 was appropriate for the diagnosis of significant donor left anterior descending artery stenosis in a population that included patients with collaterals.

Blood Flow Velocity↗
PubMed2006

Recovery of global systolic function after primary angioplasty. Influence of coronary flow velocity reserve measured by transthoracic echocardiography.

BACKGROUND: Our objective were to know whether coronary flow velocity reserve measured by transthoracic Doppler echocardiography, as marker of microvascular integrity, affects the recovery of global systolic function. Secondly, we intended to define the best cut-off point of coronary flow velocity reserve to predict recovery of global systolic function. METHODS: We studied 57 patients with coronary flow recorded by transthoracic Doppler echocardiography, after suffering a first anterior acute myocardial infarction and undergoing a successful primary percutaneous coronary intervention (TIMI 3 flow). We measured, at discharge and at 1 month: ejection fraction, volume indexes and anterior wall motion score index. Coronary flow in left anterior descending artery was detected by transthoracic Doppler echocardiography and coronary flow velocity reserve was calculated. RESULTS: After applying ROC curves, 1.54 was the best cut-off value of coronary flow velocity reserve for detection of recovery of global systolic function. Ejection fraction only increased significantly in patients with normal coronary flow velocity reserve. Only end-systolic volume index increased significantly at 1 month in patients with impaired coronary flow velocity reserve. CONCLUSION: We showed that coronary flow velocity reserve, measured by transthoracic Doppler echocardiography, influence the recovery of global systolic function, mainly by ventricular dilation. Furthermore, a quite lower value of coronary flow velocity reserve than that used for diagnostic purpose should be used to predict improvement of systolic function.

Angioplasty, Balloon, Coronary↗
PubMed1976

Vascular and cardiac contractile reserve in the dog heart with chronic multiple coronary occlusions.

Nineteen mongrel dogs survived chronic occlusion of the left circumflex and of the right coronary artery without infarction due to the timely development of a collateral circulation. Only 38 per cent of the conductance of the arteries before occlusion was restored by collateral vessels. In these animals and in 15 control dogs with normal coronary arteries myocardial contractility, contractility reserve, and myocardial blood flow were studied. The same was done in dogs with chronic coronary artery occlusion after aortocoronary bypass. Myocardial blood flow was determined woth the tracer microsphere technique. Contractility reserve was tested and defined as isovolumetric left ventricular pressure and dp/dt max with norepinephrine infusion and cross-clamping of the aorta. Contractile reserve was not significantly different between normal dogs and dogs with chronic coronary artery occlusion before and after aortocoronary bypass. Myocardial blood flow during control conditions was homogenously distributed in all three groups studied. The ratio of blood flow to the endocardium and the epicardium was not significantly different from inity. Coronary reserve was determined at peak reactive hyperemia following a 20 second period of coronary artery occlusion, with ongoing norepinephrine infusion. Under these conditions subendocardial fow in normal dogs rose by a factor of 7.9 while subepicardial flow increased 7.4 times. In dogs with chronic occlusion of two coronary arteries the increase of myocardial flow was nonnomogenous; subendocardial flow to areas supplied by a normal coronary artery rose by a factor of 7.0 while subepicardial flow increased 5.7 times control. Subendocardial collateral flow rose by a factor of 2.4 and subepicardial collateral flow increased 3.5 times control. In normal dogs norepinephrine alone did not result in maximal coronary flow but only 57 per cent thereof. Dogs with chronic coronary occlusion, however, required the entire coronary reserve in areas that were supplied by a normal coronary artery, whereas areas supplied by collaterals became ischemic. Opening of an aortocoronary bypass restored normal flow to previously ischemic areas, and reduced the flow to areas supplied by a normal artery. With the bypass open no differences existed between normal dogs and those with two occluded coronary arteries. We conclude that the norepinephrine-stimulated contractile reserve of hearts with chronic coronary occlusion was comparable to that of normal hearts; however, norepinephrine forced these hearts to spend the entire flow reserve of the remaining normal artery while producing ischemia in collateral-dependent areas. The same dose of norepinephrine did not require the entire flow reserve of normal dogs.

Animals↗
PubMed1983

Coronary vascular reserve in left ventricular hypertrophy secondary to chronic aortic regurgitation.

Coronary vascular reserve was studied in 11 patients with severe chronic aortic regurgitation (AR). Nineteen patients with the chest pain syndrome and normal findings on cardiac catheterization served as control subjects. Resting coronary sinus flow and contrast-agent-induced hyperemia were measured by continuous thermodilution. Left ventricular (LV) dimensions and mass were obtained echocardiographically. All patients had normal coronary arteries. Resting coronary flow was increased and coronary reserve was decreased in patients with AR compared with the control subjects: 310 +/- 38 versus 121 +/- 13 ml/min and 56 +/- 9 versus 86 +/- 7.5%, respectively. The decrease in coronary vascular reserve correlated with the increase in LV mass (r = -0.86, p = 0.001) and LV wall thickness (r = -0.83, p = 0.002) and with the decrease in LV volume/mass ratio (r = 0.761, p = 0.007). There was no significant correlation between the decrease in coronary vascular reserve and LV volume (r = 0.255), LV peak wall stress (r = 0.292), LV systolic pressure (r = -0.495), aortic or LV diastolic pressure (r = 0.322 and -0.318, respectively), or aortic-LV diastolic gradient, nor with the voltage on the electrocardiogram (limb leads r = -0.60, precordial leads r = -0.118). Thus, coronary vascular reserve is decreased in proportion to the degree of left ventricular hypertrophy in patients with chronic AR. Patients with angina pectoris tended to have a lower coronary vascular reserve than those without angina (median 26 versus 76%, difference not significant). LV wall thickness and not LV volume is the critical component of left ventricular mass related to coronary reserve. No significant correlation between the decrease in coronary vascular reserve and the presence of angina pectoris was demonstrated.

Adult↗
PubMed1996

Time course of impaired coronary flow reserve after reperfusion in patients with acute myocardial infarction.

To evaluate the time course of coronary flow reserve after reperfusion, 14 patients with a first anterior wall acute myocardial infarction who underwent successful coronary angioplasty within 6 hours after symptom onset were studied. After angioplasty, coronary flow reserve of the left anterior descending artery was measured with a coronary Doppler guidewire and intravenous dipyridamole (0.56 mg/kg over 4 minutes). Measurements were repeated at predischarge (16 +/- 3 days, n = 12) and at follow-up (6 +/- 3 months, n = 9). Patients with restenosis at the time of repeat catheterization were excluded. An additional 13 patients with normal angiograms served as reference patients. Coronary flow reserve was 1.33 +/- 0.29 after angioplasty. It increased to 1.88 +/- 0.36 at predischarge (p <0.01) and further to 2.34 +/- 0.38 at follow-up (p <0.01 vs after angioplasty and at predischarge, respectively). However, compared with reference patients (3.15 +/- 0.48), coronary flow reserve was significantly reduced in the infarct patients even at follow-up (p <0.01). In infarct patients, the infarct region wall motion was initially -3.86 +/- 0.67 SD/chord. It significantly improved to -2.07 +/- 1.04 SD/chord at predischarge (p <0.01) and to -1.67 +/- 1.43 SD/chord at follow-up (p <0.01). However, there was no significant relation between coronary flow reserve and region wall motion after angioplasty (r = 0.10), at predischarge (r = 0.35), and at follow-up (r = 0.28). Thus, coronary flow reserve is severely impaired early after reperfusion. Coronary flow reserve improves over 2 weeks, but the impairment persists at 6 months after acute myocardial infarction. The impairment of coronary flow reserve cannot be predicted by left ventricular function. Small sample size is a potential limitation of this study, and a larger study should be performed to confirm these findings.

Aged↗
PubMedDate not supplied

Cerebrovascular reactivity and reserve capacity in type II diabetes mellitus.

The aim of the study was to test the hypothesis that cerebrovascular reserve capacity and cerebrovascular reactivity are impaired in patients suffering from non insulin-dependent diabetes mellitus. We also intended to investigate factors which may influence resting cerebral blood flow velocity and cerebrovascular reserve capacity. A total of 28 patients suffering from type II diabetes mellitus and 20 healthy control subjects were studied. Based on diabetes duration patients were divided into two groups: subjects with > 10 years and those with < or = 10 years disease duration. Middle cerebral artery mean blood flow velocities were measured at rest and after intravenous administration of 1g acetazolamide. Cerebrovascular reactivity and reserve capacity were calculated. Blood glucose, insulin, glycosylated hemoglobin, hemostatic factors (fibrinogen, alpha-2 macroglobulin and von Willebrand factor antigen) were determined. Cerebrovascular reactivity and reserve capacity values were compared between the two diabetic subgroups and controls. Correlations between laboratory parameters and cerebrovascular reserve were investigated by linear regression analysis. Resting cerebral blood flow velocity was similar in controls and in the two diabetic subgroups. Cerebrovascular reactivity was elevated for a shorter time in patients with > 10 years disease duration than in controls and short-term diabetic patients. Cerebrovascular reserve capacity was lower in the long-term diabetes group (means +/- SD: 39.6 +/- 20.7%) than in patients with < or = 10 years disease duration (63.3 +/- 17.4%, p < 0.02 after Bonferroni correction). Cerebrovascular reserve capacity was inversely related to the duration of the disease (R = 0.53, p < 0.003). None of the determined laboratory factors had any relation with resting cerebral blood flow and cerebrovascular reserve capacity. The vasodilatory ability of cerebral arterioles is diminished in long-standing type II diabetes mellitus.

Aged↗
PubMedDate not supplied

Agreement and disagreement between "metabolic viability" and "contractile reserve" in akinetic myocardium.

BACKGROUND: In patients with chronic coronary artery disease and depressed left ventricular function, assessment of residual viability in akinetic myocardium is important for therapeutic management. Intact perfusion, preserved metabolism, and presence of contractile reserve are different aspects of cellular viability. However, not all viable cells exhibit all characteristics; it is thought that contractile reserve is less often preserved compared with metabolic activity or intact perfusion. In this study we performed a direct comparison between perfusion imaging with thallium-201 single photon emission computed tomography (SPECT), metabolic imaging with F18-fluorodeoxyglucose SPECT, and assessment of contractile reserve with low-dose dobutamine echocardiography in akinetic myocardium. METHODS AND RESULTS: Forty patients with depressed left ventricular function (mean left ventricular ejection fraction 31% +/- 16%) were studied. Resting echocardiography showed akinesis in 165 (32%) segments. Most (n = 154, 93%) of these segments demonstrated resting hypoperfusion. F18-fluorodeoxyglucose imaging revealed a perfusion-metabolism mismatch in 41 segments and a match in 113 segments. Contractile reserve was present in 33 (80%) of the segments with a perfusion-metabolism mismatch and in 7 (6%) segments with a match (P < .0005). Of the 11 segments with normal perfusion, only 5 (45%) showed contractile reserve. The agreement between SPECT and dobutamine echocardiography was 87%. Although 94% of the segments that were nonviable on scintigraphy did not show contractile reserve, the disagreement between SPECT and dobutamine echocardiography was caused mainly by the absence of contractile reserve in 27% of the segments that were viable on scintigraphy. CONCLUSION: This study shows a good agreement between SPECT and dobutamine echocardiography, although a substantial number of segments with preserved viability on SPECT do not exhibit contractile reserve, indicating underestimation of viability by dobutamine echocardiography compared with F18-fluorodeoxyglucose imaging.

Coronary Disease↗
PubMed1982

Role of the endoplasmic reticulum in the synthesis of reserve proteins and the kinetics of their transport to protein bodies in developing pea cotyledons.

Developing pea (Pisum sativum L.) cotyledons were labeled with radioactive amino acids, glucosamine, and mannose in pulse an pulse-chase experiments to study the synthesis, glycosylation, and transport of the reserve proteins vicilin and legumin to the protein bodies. Tissue extracts were fractionated on sucrose gradients to isolate either the endoplasmic reticulum (ER) or the protein bodies. Immunoaffinity gels were used to determine radioactivity in the reserve proteins (legumin and vicilin). After pulse-labeling for 45 min with amino acids, about half the total incorporated radioactivity coincided closely with the position of the ER marker enzyme NADH-cytochrome c reductase at a density of 1.13 g . cm-3 on the sucrose gradient. Both radioactivity and enzyme activity shifted to a density of 1.18 g . cm-3 in the presence of 3 mM MgCl2 indicating that the radioactive proteins were associated with the rough ER. Approximately half of the incorporated radioactivity associated with the rough ER was in newly synthesized reserve protein and this accounted for 80% of the reserve protein synthesized in 45 min. Trypsin digestion experiments indicated that these proteins were sequestered within the ER. In pulse-chase experiments, the reserve proteins in the ER became radioactive without appreciable lag and radioactivity chased out of the ER with a half-life of 90 min. Radioactive reserve proteins became associated with a protein body-rich fraction 20-30 min after their synthesis and sequestration by the ER. Pulse-chase experiments with radioactive glucosamine and mannose in the presence and absence of tunicamycin indicated that glycosylation of vicilin occurs in the ER. However, glycosylation is not a prerequisite for transport of vicilin from ER to protein bodies. Examination of the reserve protein polypeptides by SDS PAGE followed by fluorography showed that isolated ER contained legumin precursors (Mr 60,000-65,000) but not the polypeptides present in mature legumin (Mr 40,000 and 19,000) as well as the higher molecular weight polypeptides of vicilin (Mr 75,000, 70,000, 50,000, and 49,000). The smaller polypeptides of vicilin present in vicilin extracted from protein bodies (Mr 12,000-34,000) were absent from the ER. The results show that newly synthesized reserve proteins are preferentially and transiently sequestered within the ER before they move to the protein bodies, and that the ER is the site of storage protein glycosylation.

Biological Transport↗
PubMed2004

Theory for designing nature reserves for single species.

We examine the question of the optimal number of reserves that should be established to maximize the persistence of a species. We assume that the mean time to extinction of a single population increases as a power of the habitat area, that there is a certain amount of habitat to be reserved, and that the aim is to determine how this habitat is most efficiently divided. The optimal configuration depends on whether the management objective is to maximize the mean time to extinction or minimize the risk of extinction. When maximizing the mean time to extinction, the optimal number of independent reserves does not depend on the amount of available habitat for the reserve system. In contrast, the risk of extinction is minimized when individual reserves are equal to the optimal patch size, making the optimal number of reserves linearly proportional to the amount of available habitat. A model that includes dispersal and correlation in the incidence of extinction demonstrates the importance of considering the relative rate at which these two factors decrease with distance between reserves. A small number of reserves is optimal when the mean time to extinction increases rapidly with habitat area or when risks of extinction are high.

Animals↗
PubMed2005

Reserve selection using nonlinear species distribution models.

Reserve design is concerned with optimal selection of sites for new conservation areas. Spatial reserve design explicitly considers the spatial pattern of the proposed reserve network and the effects of that pattern on reserve cost and/or ability to maintain species there. The vast majority of reserve selection formulations have assumed a linear problem structure, which effectively means that the biological value of a potential reserve site does not depend on the pattern of selected cells. However, spatial population dynamics and autocorrelation cause the biological values of neighboring sites to be interdependent. Habitat degradation may have indirect negative effects on biodiversity in areas neighboring the degraded site as a result of, for example, negative edge effects or lower permeability for animal movement. In this study, I present a formulation and a spatial optimization algorithm for nonlinear reserve selection problems in grid-based landscapes that accounts for interdependent site values. The method is demonstrated using habitat maps and nonlinear habitat models for threatened birds in the Netherlands, and it is shown that near-optimal solutions are found for regions consisting of up to hundreds of thousands grid cells, a landscape size much larger than those commonly attempted even with linear reserve selection formulations.

Algorithms↗