The age‐related reduction in cerebral blood flow affects vertebral artery more than internal carotid artery blood flow

Ageing reduces cerebral blood flow (CBF), while mean arterial pressure (MAP) becomes elevated. According to ‘the selfish brain’ hypothesis of hypertension, a reduction in vertebral artery blood flow (VA) leads to increased sympathetic activity and thus increases MAP. In twenty‐two young (24 ± 3 years; mean ± SD) and eleven elderly (70 ± 5 years) normotensive men, duplex ultrasound evaluated whether the age‐related reduction in CBF affects VA more than internal carotid artery (ICA) blood flow. Pulse‐contour analysis evaluated MAP while near‐infrared spectroscopy determined frontal lobe oxygenation and transcranial Doppler middle cerebral artery mean blood velocity (MCA V_mean). During supine rest, MAP (90 ± 13 versus 78 ± 9 mmHg; P<0·001) was elevated in the older subjects while their frontal lobe oxygenation (68 ± 7% versus 77 ± 7%; P<0·001), MCA V_mean (49 ± 9 versus 60 ± 12 cm s^?1; P = 0·016) and CBF (754 ± 112 versus 900 ± 144 ml min^?1; P = 0·004) were low reflected in VA (138 ± 48 versus 219 ± 50 ml min^?1; P<0·001) rather than in ICA flow (616 ± 96 versus 680 ± 120 ml min^?1; P = 0·099). In conclusion, blood supply to the brain and its oxygenation are affected by ageing and the age‐related decline in VA flow appears to be four times as large as that in ICA and could be important for the age‐related increase in MAP.     

Middle cerebral artery velocity during head-up tilt induced hypovolemic shock in humans

Summary. Middle cerebral artery mean velocity (V_mean) and pulsatility index (PI) were followed during head-up tilt induced hypovolaemic shock in nine subjects. Mean arterial pressure (MAP), heart rate (HR), central venous pressure (CVP) and thoracic (TI) electrical impedance were also recorded. V_mean, PI, and CVP did not change during head-up tilt to 50°, while MAP increased from 92 (81–106) (median and range) to 100 (97–112) mmHg, HR from 63 (53–74) to 84 (68–89) beats min^-1 and Tl_100kHz from 30 (27–36) to 32 (30–39) Ohm (P < 0.01) (n= 8). During maintained tilt, V_mean decreased from 52 (32–72) to 34 (16–59) cms^-1, whereas HR increased to 87 (52–108) beats min^-1 and Tl_100kHz to 33 (31–39) Ohm (P < 0.01). Presyncopal symptoms appeared after 33 (3–46) min and were associated with a MAP of 65 (32–84) mmHg (P < 0.01) and a HR of 58 (52–71) beats min^-1 (P < 0.05).V_mean decreased to 25 (16–36) cms^-1, and cerebral conductance index (V_mean/MAP_brain) and PI increased (P < 0.01). Arterial collapse was observed (diastolic velocity of zero) in one subject at a brain (diastolic) blood pressure of 21 mmHg and he developed tachycardia (131 beats min^-1) during presyncope. P_aCO₂ did not change. Maintained tilt resulted in central volume depletion reflected by changes in MAP, HR, and thoracic electrical impedance but not in CVP. Transcranial Doppler derived indices of cerebral perfusion demonstrated critically low values despite marked increase in conductance index.     

Cerebrovascular and cardiovascular responses to the Valsalva manoeuvre during hyperthermia

Background

During hyperthermia, the perturbations in mean arterial blood pressure (MAP) produced by the Valsalva manoeuvre (VM) are more severe. However, whether these more severe VM-induced changes in MAP are translated to the cerebral circulation during hyperthermia is unclear.

Methods

Healthy participants (n = 12, 1 female, mean ± SD: age 24 ± 3 years) completed a 30 mmHg (mouth pressure) VM for 15 s whilst supine during normothermia and mild hyperthermia. Hyperthermia was induced passively using a liquid conditioning garment with core temperature measured via ingested temperature sensor. Middle cerebral artery blood velocity (MCAv) and MAP were recorded continuously during and post-VM. Tieck's autoregulatory index was calculated from the VM responses, with pulsatility index, an index of pulse velocity (pulse time) and mean MCAv (MCAv_mean) also calculated.

Results

Passive heating significantly raised core temperature from baseline (37.9 ± 0.2 vs. 37.1 ± 0.1°C at rest, p < 0.01). MAP during phases I through III of the VM was lower during hyperthermia (interaction effect p < 0.01). Although an interaction effect was observed for MCAv_mean (p = 0.02), post-hoc differences indicated only phase IIa was lower during hyperthermia (55 ± 12 vs. 49.3 ± 8 cm s⁻¹ for normothermia and hyperthermia, respectively, p = 0.03). Pulsatility index was increased 1-min post-VM in both conditions (0.71 ± 0.11 vs. 0.76 ± 0.11 for pre- and post-VM during normothermia, respectively, p = 0.02, and 0.86 ± 0.11 vs. 0.99 ± 0.09 for hyperthermia p < 0.01), although for pulse time only main effects of time (p < 0.01), and condition (p < 0.01) were apparent.

Conclusion

These data indicate that the cerebrovascular response to the VM is largely unchanged by mild hyperthermia.     

Brain and muscle oxygen saturation during head-up-tilt-induced central hypovolemia in humans

Summary. Near-infrared spectrophotometry-determined cerebral (ScO₂) and muscle oxygen saturations (SmO₂) were followed in 15 volunteers during passive 50° head-up-tilt-induced central hypovolaemia, and in nine volunteers during ventilatory manoeuvres affecting arterial carbon dioxide tension. During head-up tilt, mean arterial pressure [MAP, 88 (77–118) to 97 (80–136) mmHg, median and range] and heart rate [HR; 66 (49–77) to 87 (42–132) beats min^-1 P<0.01] increased, but after 22 (1–45) min they declined [to 61 (40–91) mmHg and 69 (38–109) beats min^-1, respectively, P=0.001] and pre-syncopal symptoms developed. Central hypovolaemia was indicated by an increased thoracic electrical impedance, and a decreased cardiac output and central venous oxygen saturation. The arterial oxygen saturation, pulmonal oxygen uptake and skin temperatures remained constant. The ScO₂ remained stable at 72 (62–77)% until the pre-syncopal incidence, when it decreased to 62 (31–73)% (P=0–001), and tilt down made it increase to 75 (36–87)% (P<0.05) before the recovery value was established. In contrast, SmO₂ decreased during tilting [75 (70–87) to 65 (53–70)%], and recovered to 70 (53–83)%, P<0.01) during the hypotensive episode. The end-tidal CO₂ tension decreased only during tilt-up. The ScO₂ decreased, and SmO₂ increased during hyperventilation, and ScO₂ increased during breathing of 5% carbon dioxide. Rebreathing from a bag made SmO₂ decrease and resulted in a biphasic ScO₂ response: it first increased and subsequently decreased. Cardiovascular changes during tilt were not reflected in skin temperature. The ScO₂ reflected the maintained autoregulation of cerebral blood flow until the perfusion pressure decreased markedly. In contrast, SmO₂ mirrored muscle vasoconstriction early during tilt, and vasodilatation when pre-syncopal symptoms appeared.     

彩色多普勒超声检测老年高血压患者颈动脉重构与血流动力学变化

目的 探讨老年高血压患者颈动脉结构及血流动力学特征.方法 老年高血压患者81例,按高血压类型分为单纯收缩期高血压组42例(A组),收缩压和舒张压均增高组39例(B组).对照组为30名健康老年人.二维超声测量颈总动脉内膜-中层厚度(IMT)、收缩期、舒张期内径,观察颈总动脉斑块情况;脉冲多普勒超声测量颈总动脉收缩期峰速度(PSV)、舒张末期流速(EDV)、平均流速(Vmean)、阻力指数(RI)、搏动指数(PI).结果 与对照组比较,A、B组颈总动脉IMT、僵硬度、RI升高(P<0.01),扩张性、EDV、Vmean降低(P均<0.05),A组PI升高(P<0.01),B组PSV降低(P<0.05);A组颈总动脉僵硬度、PSV、RI、PI高于B组(P均<0.05),扩张性和EDV低于B组(P<0.01);A、B组斑块发生率均高于对照组(P均<0.05);收缩压、脉压与颈总动脉内径、IMT、EDV、Vmean、RI、PI密切相关.结论 老年高血压患者颈动脉发生重构及血流动力学改变,单纯收缩期高血压患者血管壁顺应性差于收缩压和舒张压均增高患者.收缩压及脉压对颈动脉重构及血流动力学影响较大.     

Cerebral perfusion during human liver transplantation

Summary. During transplantation of the liver cerebral perfusion was monitored by transcranial Doppler determined middle cerebral artery mean flow velocity (V_mean) and pulsatility index (PI) in six fulminant hepatic failure patients and 11 patients with chronic liver disease. In both groups of patients V_mean, PI and central haemodynamic variables were recorded during (1) the last preanhepatic hour; (2) the anhepatic phase; (3) the first 15 min of reperfusion; and (4) for the following 45 min of reperfusion. No significant differences were detected between the two groups of patients with respect to changes of variables with time. The V_mean (40±13 cm s^-1 [mean±SD]), thoracic electrical impedance (TI) (30±7 Ohm), heart rate (97±19 beats min^-1), mean arterial pressure (84±9 mmHg) and arterial carbon dioxide tension (PaCO₂, 4.5±0.4 kPa) remained stable in the anhepatic phase, while cardiac output (CO, 7.6±2.7 to 5.4±1.41 min^-1), stroke volume (SV, 79±26 to 56±15 ml) and PI (1.2±0.3 to 0.9±0.2) decreased (P<0.05). During reperfusion, CO (9.9±4.01 min^-1), SV (105±40 ml), Pa_CO2 (5.5±0.6 kPa), Vmean (57±17 cm s^-1) and PI (1.2±0.2) became elevated. Taken together, during the anhepatic phase of the liver transplantation a maintained central blood volume as indicated by the constant TI served for a stable blood pressure and in turn cerebral perfusion, whereas revascularization of the graft increased cerebral perfusion concomitant with an elevated carbon dioxide tension.     

Protein-kinetic and haemodynamic studies in patients with liver cirrhosis. Evidence of a lymph-imbalance theory of ascites formation

Summary. Lymph drainage, splanchnic vascular pressures, plasma volume (PV), plasma renin (PRC) and aldosterone (PAC) concentrations were studied in different groups of patients with cirrhosis: I, patients who had never had ascites (n=17), II, patients with former but no actual ascites (n= 19), III, patients with slight or moderate ascites (n= 25), and IV, patients with tense ascites (n = 27). Lymph drainage, determined as TER_alb (the fraction of intravascular albumin mass (IVMaib), which leaves/returns into the vascular space per hour) was significantly elevated in cirrhotic patients (11.5% IVM_alb-h^-1) as compared to normal controls (5.9,P<0.001). TER_alb in patients with tense ascites (group IV) was on the average 8-4% IVMaib-h^-1, a value which is significantly above normal (P<0.05), but significantly below those of groups I, II and III (12.5,13.4,12.6,P<0.01). Wedged hepatic venous pressure increased from group I to IV: 16, 22, 25 and 34 mmHg, respectively (P<0.01). Inferior vena caval pressure in group IV (15 mmHg) was significantly above those of group III (8 mmHg) and group I+11 (6 mmHg), (P<0–01). From group I to III, PV increased significantly (3125, 3610, 3870 ml, P<0.01). In the ascitic patients PV was constant or fell slightly in patients with tense ascites (3730 ml). PRC in untreated patients with tense ascites (IV) was 287 mIU-1^-1, as compared to group III, I and normal controls (94, 50, 15, P<0.01). A similar pattern was found with respect to PAC. The results suggest that an imbalance between enhanced protein and fluid filtration (consequent on portal hypertension) on one side, and a relatively insufficient lymphatic drainage on the other side plays a substantial role in the pathogenesis of ascites in cirrhosis. The results do not support a progressive plasma volume expansion as the main cause of cirrhotic ascites.     

Doppler sonography evaluation of flow velocity and volume of the extracranial internal carotid and vertebral arteries in healthy adults

PURPOSE: To measure with Doppler sonography the velocity and volume of blood flow in the extracranial internal carotid artery (ICA) and vertebral artery (VA) of healthy adults and to calculate total cerebral blood flow volume (tCBFV). METHODS: Bilateral ICA and VA were examined sonographically in 180 healthy adults. Angle-corrected peak systolic (Vps), end-diastolic (Ved), and time-averaged maximum blood flow velocity (TAV) were measured in pulsed Doppler mode, and the resistance index (RI) and pulsatility index (PI) were calculated. The cross-sectional area (A) was measured on gray-scale images. Volume flow was calculated as FV = TAV x A, and tCBFV was calculated as the sum of the right and left ICA and VA volume flow. RESULTS: tCBFV was 651 +/- 96 ml/min for the entire population. There was a significant decrease in Vps, Ved, TAV, and tCBFV with age in all arteries. RI and PI values initially declined and then increased with age. Cross-sectional area increased with age in ICA but not in VA. PI and RI were higher in men than in women. Blood flow velocity and volume were higher, and RI was lower in the left than in the right VA. CONCLUSION: The Doppler sonographic assessment of extracranial ICA and VA blood flow volume may be useful for the study of cerebral hemodynamic changes in patients with cerebrovascular disorders. Age-dependent changes should be considered, for instance, in the management of intensive care patients with impaired cerebral perfusion.     

Arterial blood pressure during early sepsis and outcome

Objective  To evaluate the association between arterial blood pressure (ABP) during the first 24 h and mortality in sepsis. Design  Retrospective cohort study. Setting  Multidisciplinary intensive care unit (ICU). Patients and participants  A total of 274 septic patients. Interventions  None. Measurements and results  Hemodynamic, and laboratory parameters were extracted from a PDMS database. The hourly time integral of ABP drops below clinically relevant systolic arterial pressure (SAP), mean arterial pressure (MAP), and mean perfusion pressure (MPP = MAP − central venous pressure) levels was calculated for the first 24 h after ICU admission and compared with 28-day-mortality. Binary and linear regression models (adjusted for SAPS II as a measure of disease severity), and a receiver operating characteristic (ROC) analysis were applied. The areas under the ROC curve were largest for the hourly time integrals of ABP drops below MAP 60 mmHg (0.779 vs. 0.764 for ABP drops below MAP 55 mmHg; P ≤ 0.01) and MPP 45 mmHg. No association between the hourly time integrals of ABP drops below certain SAP levels and mortality was detected. One or more episodes of MAP < 60 mmHg increased the risk of death by 2.96 (CI 95%, 1.06–10.36, P = 0.04). The area under the ROC curve to predict the need for renal replacement therapy was highest for the hourly time integral of ABP drops below MAP 75 mmHg. Conclusions  A MAP level ≥ 60 mmHg may be as safe as higher MAP levels during the first 24 h of ICU therapy in septic patients. A higher MAP may be required to maintain kidney function. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Early SjvO2 monitoring in patients with severe brain trauma

Objective: To investigate early cerebral variables after minimal resuscitation and to compare the adequacy of a cerebral perfusion pressure (CPP) guideline above 70 mmHg, with jugular bulb venous oxygen saturation (SjvO₂) monitoring in a patient with traumatic brain injury (TBI). Design: Prospective, observational study. Setting: Anesthesiological intensive care unit. Patients: 27 TBI patients with a postresuscitation Glasgow Coma Scale score less than 8. Intervention: After initial resuscitation, cerebral monitoring was performed and CPP increased to 70 mmHg by an increase in mean arterial pressure (MAP) with volume expansion and vasopressors as needed. Measurements and results: MAP, intracranial pressure (ICP), CPP, and simultaneous arterial and venous blood gases were measured at baseline and after treatment. Before treatment, 37 % of patients had an SjvO₂ below 55 %, and SjvO₂ was significantly correlated with CPP (r = 0.73, p < 0.0001). After treatment, we observed a significant increase (p < 0,0001) in CPP (78 ± 10 vs 53 ± 15 mmHg), MAP (103 ± 10 vs 79 ± 9 mmHg) and SvjO₂ (72 ± 7 vs 56 ± 12), without a significant change in ICP (25 ± 14 vs 25 ± 11 mmHg). Conclusion: The present study shows that early cerebral monitoring with SjvO₂ is critical to assess cerebral ischemic risk and that MAP monitoring alone is not sensitive enough to determine the state of oxygenation of the brain. SjvO₂ monitoring permits the early identification of patients with low CPP and high risk of cerebral ischemia. In emergency situations it can be used alone when ICP monitoring is contraindicated or not readily available. However, ICP monitoring gives complementary information necessary to adapt treatment. Received: 10 July 1998 Final revision received: 5 January 1999 Accepted: 20 January 1999     

Doppler resistive index to reflect regulation of renal vascular tone during sepsis and acute kidney injury

ABSTRACT: INTRODUCTION: Renal resistive index (RI), determined by Doppler ultrasonography, directly reveals and quantifies modifications in renal vascular resistance. The aim of this study was to evaluate if mean arterial pressure (MAP) is determinant of renal RI in septic, critically ill patients suffering or not from acute kidney injury (AKI). METHODS: This prospective observational study included 96 patients. AKI was defined according to RIFLE criteria and transient or persistent AKI according to renal recovery within 3 days. RESULTS: Median renal RI was 0.72 (0.68-0.75) in patients without AKI and 0.76 (0.72-0.80) in patients with AKI (P=0.001). RI was 0.75 (0.72-0.79) in transient AKI and 0.77 (0.70-0.80) in persistent AKI (P=0.84). RI did not differ in patients given norepinephrine infusion and was not correlated with norepinephrine dose. RI was correlated with MAP (rho= -0.47; P=0.002), PaO2/FiO2 ratio (rho= -0.33; P=0.04) and age (rho=0.35; P=0.015) only in patients without AKI. CONCLUSIONS: A poor correlation between renal RI and MAP, age, or PaO2/FiO2 ratio was found in septic and critically ill patients without AKI compared to patients with AKI. These findings suggest that determinants of RI are multiple. Renal circulatory response to sepsis estimated by Doppler ultrasonography cannot reliably be predicted simply from changes in systemic hemodynamic. As many factors influence its value, the interest in a single RI measurement at ICU admission to determine optimal MAP remains uncertain.     

Doppler tissue imaging of the heart in secondary amyloidosis

Secondary amyloidosis (SA) affects cardiac texture and function by interstitial fibrosis. Doppler tissue imaging (DTI) may quantify heart function through the assessment of myocardial velocities. Echocardiographic findings of early cardiac amyloidosis (CA) without heart failure (HF) caused by SA were determined both by standard methods and DTI. It was then determined whether DTI is superior to conventional echocardiography in documenting early CA due to SA. Twenty-five patients with SA who had CA without HF (group 1) were compared with 25 healthy control subjects (group 2). After standard echocardiography, systolic (s), early (e) and late diastolic (a) velocities of interventricular septum, anterolateral, and anterior and inferior walls were measured from mitral annulus by DTI. The averages were called (s_mean), (e_mean), and (a_mean), respectively. Fractional shortening (FS) and ejection fraction (EF) values of groups 1 and 2 were similar. Standard Doppler echocardiographic values were not typical for a specific diastolic abnormality. The (s_mean) and (e_mean) for group 1 were lower but (a_mean) was higher compared with group 2 (all P < .05). The group 1 (e_mean/a_mean) was lower (P < .0001) and (E/e_mean) was higher (P=.003) than in group 2 (both P < .05). (E/e_mean) and (E/e_{lateral wall}) ratios were positively correlated (r=0.74, P < .05). In patients with early CA due to SA without HF, by DTI, (s_mean) and (e_mean) velocities decrease and (a_mean) velocity increases. These may be markers of subclinical CA of SA when standard echocardiography is not informative. (E/e_mean) ratio may be an alternative index to (E/_{elateral wall}).     

The venoarteriolar response of the skin in healthy legs measured at different depths

The venoarteriolar response (VAR) of the skin in healthy legs of 20 subjects was investigated. The laser Doppler flux (LDF), at an experimental venous hypertension of 30 mmHg, 45 mmHg and 60 mmHg, produced by a pneumatic cuff around the thigh in a recumbent position, was compared with the LDF in a sitting position. The LDF of the skin was measured simultaneously at the same site of the superficial capillary layer (with 543 nm) and of the deeper capillary layer (with 780 nm). At 543 nm the LDF did not differ significantly at any cuff pressure from the LDF recorded in a sitting position, whereas at 780 nm the LDF was significantly higher at the cuff pressure of 30 mmHg than the LDF in a sitting position (P = 0·002). The VAR was much weaker at 543 nm than at 780 nm, and the scatter of the VAR values was high. In a sitting position the VAR at 543 nm was 9·3% and at 780 nm 34·6% (P<0·001). The VAR at 543 nm at the cuff pressure of 30 mmHg did not differ significantly from the VAR caused by the sitting position, whereas at 780 nm the VAR at the cuff pressure of 30 mmHg was significantly less than the VAR caused by the sitting position (P = 0·001). Despite the high scatter of the VAR values, these findings suggest that the VAR in the superficial capillary layer is smaller, and that it reached maximum at lower venous hypertension, than the VAR in the deeper capillary layer.     

The effect of phenylephrine on arterial and venous cerebral blood flow in healthy subjects

Aim: Sympathetic regulation of the cerebral circulation remains controversial. Although intravenous phenylephrine (PE) infusion reduces the near‐infrared spectroscopy (NIRS)‐determined measure of frontal lobe oxygenation (S_cO₂) and increases middle cerebral artery mean blood velocity (MCA V_mean), suggesting α‐adrenergic‐mediated cerebral vasoconstriction, this remains unconfirmed by evaluation of arterial and venous cerebral blood flow. Methods: We determined S_cO₂, MCA V_mean, and right internal carotid artery (ICA) and internal jugular venous (IJV) blood flow (duplex ultrasound) during infusion of PE in eight supine young healthy men [26 (3) years, 177 (7) cm and 74 (8) kg; mean (SD)]. Results: Compared with saline, during infusion of PE, mean arterial pressure increased 26 ± 3% (mean ± SE) and MCA V_mean by 4·8 ± 1·9% (P<0·05), while S_cO₂ decreased by 13·7 ± 3·7% (P<0·05) with no significant changes in the arterial oxygen or carbon dioxide tensions. ICA blood flow did not change significantly in response to PE administration (351 ± 12 versus 373 ± 21 ml min^?1; P = 0·236), while IJV blood flow increased (443 ± 57 versus 507 ± 58 ml min^?1; P = 0·023). Conclusions: These findings confirm that PE induces a reduction in S_cO₂ measured by NIRS and causes an increase in MCA V_mean indicative of cerebral arterial vasoconstriction, although ICA was preserved and IJV increased. These results suggest that a decrease in S_cO₂ during infusion of PE reflects an altered cerebral contribution of arterial versus venous blood to the NIRS signal, although we cannot rule out that an effect of PE on skin blood flow is important.     

Longitudinal Examination of Leisure-Time Physical Activity (LTPA), Participation,and Social Inclusion Upon Joining a Community-based LTPA Program for Adults With Physical Disabilities

ObjectiveFirst, to examine whether participants reported changes in (1) leisure-time physical activity (LTPA) participation and social inclusion variables and (2) well-being outcomes before and after joining a community-based LTPA program for adults with physical disabilities. Second, to explore the longitudinal relationship between LTPA and the other aforementioned outcomes.DesignA double baseline longitudinal design with measurements at 4-6 weeks (baseline 1) and immediately (baseline 2) before and 2 and 4 months after joining the community-based LTPA program.SettingCommunity.ParticipantsAdults (N=43) with a physical disability who reported no cognitive impairment, were new members of the community-based LTPA program, and spoke English or French.InterventionsA community-based physical activity program for adults with physical disabilities. Participants were provided an individualized exercise program and accessed the program at designated times during the week.Main Outcome MeasuresPrimary: LTPA (LTPA Questionnaire for People with Spinal Cord Injury), participation (Patient-Perceived Participation in Daily Activities Questionnaire), and social inclusion. Secondary: depression severity, self-esteem, resilience, and life satisfaction.ResultsAfter joining the program, participants reported an increase in total LTPA (mean_baseline2, 177.80±211.32; mean_2months, 299.31±298.70; mean_4months, 288.14±292.14), moderate-to-vigorous LTPA (mean_baseline2, 83.95±123.95; mean_2months, 142.00±198.38; mean_4months, 163.23±182.08), and participation in health (mean_baseline2, 6.24±1.16; mean_2months, 6.58±1.25; mean_4months, 6.97±0.82) and family-related activities (mean_baseline2, 12.18±2.43; mean_2months, 12.60±2.30; mean_4months, 13.47±2.01). A significant increase (β=3.46, P<.001) in social inclusion before joining the program was followed by a decrease (β=−1.09, P<.05) 4 months later. Improvements related to depression severity were noted (β_{baseline1−baseline2}=−1.51, P<.05; β_{baseline2−4 months}=−0.28, P>.05).ConclusionsThe results support the role of a community-based LTPA program in increasing LTPA levels and enhancing participation in some activities among adults with physical disabilities.     

Inosine causing insulin release and increased myocardial uptake of carbohydrates relative to free fatty acids in dogs

Summary. The aim of the present study was to determine the effect of i.v. inosine on myocardial substrate uptake and function in the in situ dog heart. Inosine was infused i.v. at a rate of 5 mg kg min^-1 in eight closed-chest pentobarbital anaesthetized dogs. Inosine caused a 46% decrease (P<0.01) in plasma free fatty acids (FFA), a 15% decrease (P<0.05) in plasma glycerol, an 18% decrease (P<0.05) in plasma glucose and a 46% increase (P<0.01) in blood lactate. This was associated with a 55% decrease (P<0.01) in myocardial FFA uptake and a 72% increase in lactate uptake, while glucose uptake remained unchanged. These metabolic changes were associated with a five-fold increase (P<0.05) in arterial insulin. Inosine caused an 18% increase (P<0.01) in myocardial blood flow without changing MVO₂. There was a 33% increase (P<0.01) in LV dP/dt_max, a decrease in LVEDP from 4.9 ± 0.9 (mean ± SEM) to 0.9 ± 0.3 mmHg (P<0.05) and a 24% decrease (P<0.01) in systemic vascular resistance. Inosine caused a transient 38% increase (P<0.05) in pulmonary vascular resistance. In conclusion, in addition to a positive inotropic effect and vascular effects inosine was found to cause release of insulin and to shift myocardial metabolism towards increased uptake of carbohydrates relative to FFA.     

Assessment of Global and Regional Left Ventricular Function After Surgical Revascularization in Patients With Coronary Artery Disease by Real‐time Triplane Echocardiography

Objective. The purpose of this study was to evaluate the capability of real‐time triplane echocardiography (RT3PE) for monitoring global and regional systolic function of the left ventricle (LV) after surgical revascularization and for evaluating the effect of surgery and predicting restenosis. Methods. Forty‐nine patients underwent RT3PE before and at 10 days and 1, 3, and 6 months after coronary artery bypass grafting (CABG). The global systolic function of the LV was assessed with the parameters of end‐diastolic volume (EDV), end‐systolic volume (ESV), ejection fraction (EF), and stroke volume (SV). The regional myocardial deformation was detected by triplane strain rate imaging. Recovery of myocardial function after surgery and the correlation between global and regional function were investigated. Results. In 41 of the 49 patients, the EDV and ESV decreased, and the EF and SV increased gradually and showed statistical significance at 3 and 6 months after surgery (P < .05; P < .01). The systolic strain rate (SR_sys) and systolic strain (S_sys) increased, and the postsystolic strain index (PSI) decreased progressively after CABG, with significant changes in almost all studied segments at 6 months (P < .05; P < .01). In addition, recovery of the SR_sys, S_sys, and PSI at each follow‐up stage after surgery correlated well with EF improvement, with a positive correlation between the SR_sys, S_sys, and EF and a negative correlation between the PSI and EF. Restenosis was suspected in the other 8 patients. The sensitivity, specificity, and accuracy of RT3PE to predict restenosis were 75.00%, 89.47%, and 85.19%, respectively. Conclusions. Real‐time triplane echocardiography can be used to quantitatively assess global and regional myocardial function. It may represent a new, powerful method to monitor improvement of myocardial function after CABG and to predict restenosis.     

阴道彩色多普勒对育龄妇女子宫卵巢动脉血流的研究

阴道彩色多普勒对443名健康育龄妇女的子宫、卵巢动脉血流,四个周期间,进行博动指数(PI)、阻力指数(RI)检测,其间有显著性差异(P<0.01),且功能侧子宫动脉与卵巢动脉阻抗参数也有差异(P<0.05),可见这一些测定,对妇科疾病的诊断可提供帮助。     

75例附件肿块彩色多普勒超声检查分析

本文分析我院１９９２年７月～１９９３年１２月期间７５例经彩色多普勒超声检查，且有病理证实的附件肿块。结果显示，内膜样囊肿２２例，炎性肿块１１例，中肾管囊肿７例，良性卵巢肿瘤１８例，恶性卵巢肿瘤２１例。彩色多普勒超声显示良性肿块内部无血管，或很少。恶性肿瘤内部血管分布呈网状或团块状。多普勒频谱分析，恶性卵巢肿瘤搏动指数（ＰＩ）０．７８±０．４７，阻力指数（ＲＩ）０．４７±０．１６，显著低于内膜样囊肿ＰＩ１．５６±１．０９，ＲＩ０．５７±０．２１，中肾管囊肿ＰＩ２．６０±１．７５，ＲＩ０．８０±０．２６，炎性肿块ＰＩ１．２５±０．６９，ＲＩ０．６３±０．１２和良性卵巢肿瘤ＰＩ１．９２±１．０２，ＲＩ０．７５±０．１９（Ｐ＜０．０５），良性病变中阻力指标差异无显著性。以ＰＩ≤１．００诊断卵巢癌敏感性７６．２％，特异性８３．３％，阳性预测值６４％，阴性预测值９０％，ＲＩ≤０．６诊断卵巢癌敏感性７１．４％，特异性７９．６％，阳性预测值５７．７％，阴性预测值８７．８％，提示彩色多普勒超声在早期诊断卵巢癌方面具有一定的价值。     

Cutaneous reactive hyperaemia is unaltered by dietary nitrate supplementation in healthy humans

The purpose of this study was to determine whether nitrate supplementation augments cutaneous reactive hyperaemia. Seven participants were tested pre‐ and postnitrate supplementation (25 ml beetroot juice); participants consumed one shot per day for 3 days. Participants were instrumented with two microdialysis fibres: control (Ringer's solution) and NO synthase inhibition (20 mM L‐NAME). Skin blood flow was measured via laser‐Doppler flowmetry (LDF). A blood pressure cuff was placed on the experimental arm and inflated to 250 mmHg for 5 mins to occlude arterial inflow. The cuff was released, and the resultant reactive hyperaemia was measured. Blood pressure was continuously measured via plethysmography from a finger on the non‐experimental arm. Cutaneous vascular conductance was calculated (LDF/MAP) and normalized to maximal vasodilatation (%CVC_max). Only diastolic blood pressure was reduced following nitrate supplementation (71 ± 2 vs. 66 ± 1 mmHg; P<0·05). There was no effect of nitrate supplementation on peak reactive hyperaemia at control (Pre: 52 ± 3 vs. Post: 57 ± 2%CVC_max) or L‐NAME (Pre: 52 ± 2 vs. Post: 59 ± 4%CVC_max) sites. There was no effect of nitrate supplementation on total reactive hyperaemia at either control (Pre: 4197 ± 943 vs. Post: 4523 ± 1040%CVC_max * sec) or L‐NAME (Pre: 5108 ± 997 vs. Post: 5694 ± 1002%CVC_max * sec) sites. These data suggest cutaneous reactive hyperaemia is unaffected by dietary nitrate supplementation in healthy humans.