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PubMed1999

Sexually dimorphic hemodynamic effects of intragastric ethanol in conscious rats.

This study investigated the gender-related differences in hemodynamic effects of small to moderate doses of intragastrically (i.g.) administered ethanol in conscious rats. Changes evoked by ethanol (0.25, 0.5 or 1 g/kg) in mean arterial pressure (MAP), heart rate, cardiac index (CI), stroke volume (SV), and total peripheral resistance (TPR) were followed for 90 min in age-matched male and female Sprague-Dawley rats. Baseline values of MAP (121+/-2 vs. 124+/-2 mm Hg) were similar whereas CI (55+/-2 vs. 43+/-2 ml/min/100 g) and TPR (2.2+/-0.1 vs. 3.0+/-0.1 mm Hg/ml/min/100 g) were significantly (P<0.05) higher and lower, respectively, in female compared with male rats. In male rats, the middle dose (0.5 g/kg) of ethanol caused a slight increase in MAP due to significant (P<0.05) increases in CO whereas the other two doses (0.25 and 1 g/kg) had no effect on MAP. In female rats, MAP was not affected by ethanol (0.25 and 0.5 g/kg) and showed a significant reduction by the higher dose (1 g/kg) that was associated with decreases in CO and SV while TPR did not change. The hypotensive effect of ethanol (1 g/kg) in female rats started after 50 min, was maximal (13+/-1.7 mm Hg) at 70 min and remained so for the remaining 20 min of the study. Blood ethanol concentrations were similar in male and female rats. These findings suggest that the hemodynamic responses to i.g. ethanol are gender-related and that ethanol-evoked hypotension in female rats appears to involve a reduction in cardiac output.

Animals↗

PubMed1995

Effect of felodipine on systemic hemodynamics of spontaneous mild-hypertensive aged rats.

The aim of the present study was to examine the effects of felodipine, a dihydropyridinic calcium ions channels blocker, on mean arterial blood pressure (MAP), cardiac output (CO), peripheral resistances (TPR) and blood flow distribution in spontaneously mildly hypertensive female Wistar 30-34 months old rats. Under pentobarbital anesthesia, CO and regional organ blood flow were measured by the radioactive microspheres method, before and 30 min after administration of felodipine 0.5 mumol/kg b. w. by gastric gavage. They were compared to the corresponding values in normotensive rats of the same strain and age. Fifteen (from twenty five) rats were hypertensive with a MAP averaging 139 +/- 2 mm Hg. CO and TPR were slightly higher in these hypertensive rats. Cerebral blood flow (CBF) was lower, though the difference did not reach significant values. MAP significantly decreased after felodipine with no significant changes in CO and TPR in hypertensive as well as in normotensive animals. Renal blood flow (RBF) was similar before and after felodipine which significantly decreased renal vascular resistance in both groups. Felodipine administration did not induce significant changes in CBF but a significant increase in portal venous inflow (PVI) in hypertensive rats only. In conclusion, in old female rats with mild spontaneously hypertension, acute felodipine oral administration reduced arterial blood pressure without diminishing CBF.

Aging↗

PubMed1994

Effect on pressor and vascular responsiveness in rabbits of drugs that decrease norepinephrine uptake.

The purpose of this study was to determine if decreases in norepinephrine (NE) uptake would result in pressor and vascular hyperresponsiveness to vasoconstrictor substances. These experiments examined the effects of cocaine and imipramine, drugs known to decrease NE uptake, on the changes in arterial pressure and total peripheral resistance (TPR) in response to NE and arginine vasopressin (AVP) in conscious rabbits. The infusion of graded doses of NE resulted in significantly greater increases in mean arterial pressure at all dose levels following the administration of cocaine (0.6 mg/kg iv) or imipramine (0.5 mg/kg) than following the administration of the vehicle alone. The infusion of NE also resulted in greater increases in TPR as well as blood pressure following cocaine or imipramine administration than occurred prior to the administration of these drugs. The infusion of AVP caused significantly larger increases in arterial pressure and in TPR following cocaine or imipramine administration than was seen after the administration of AVP to control rabbits not treated with these drugs. These studies demonstrated that cocaine and imipramine, substances known to decrease NE uptake by the sympathetic nerve terminals, will induce pressor and vascular hyperresponsiveness to NE and AVP in rabbits. These results are in keeping with the concept that pressor and vascular hyperresponsiveness in renal prehypertensive rabbits may be the result of decreases in NE uptake by sympathetic fibers supplying vascular smooth muscle cells.

Animals↗

PubMed1994

Changes in arterial smooth muscle contractility, contractile proteins, and arterial wall structure in spontaneous hypertension.

Heart disease, stroke, and kidney failure are leading causes of death. Essential hypertension is the major predisposing risk factor of cardiovascular disease. Yet, after several decades of intensive investigation, the initiating causative mechanism of essential hypertension is still unknown. However, investigators in the field generally agree that an increased total peripheral resistance (TPR) is the fundamental hemodynamic disorder in essential hypertension. This review addresses the hypothesis that the increased TPR of essential hypertension is due to a defective mechanism in the contractility of arterial smooth muscle. Force-velocity and length-tension studies have shown that both caudal arterial muscle and mesenteric resistance arterial muscle from spontaneously hypertensive rats (SHR) can shorten more and faster than muscle from normotensive control Wistar-Kyoto rats (WKY). In addition, the SHR muscle relaxation rate is slower compared with the WKY muscle. These alterations in mechanical behavior of SHR arterial muscle appear to be primary to the high blood pressure since MK-421 (enalapril maleate)-treated SHR arterial muscle shows the same increased velocity of shortening, increased shortening ability, and decreased relaxation rate as the untreated SHR muscle. MK-421 is an angiotensin-converting enzyme blocker. SHR maintained on MK-421 treatment have normal blood pressures in spite of being of the genetically hypertensive strain. While these findings are encouraging, several other important issues supporting the hypothesis require resolution and warrant review. Firstly, structural alterations of blood vessel walls in hypertension cause the walls to thicken and encroach on the vessel lumens contributing to the increased TPR. Whether such wall thickening is the cause or consequence of high blood pressure has been controversial in the literature. In this report, data are presented from a study in which MK-421-treated SHR were utilized as a model of prehypertensive SHR. Light micrograph observations and morphometric analyses were made of cross-sections of mesenteric resistance arteries from SHR, MK-421-treated SHR, and WKY. Results show that the MK-421-treated SHR resistance arteries had media thicknesses and a number of smooth muscle cell layers that were significantly less than in the untreated SHR and not different from the WKY. Secondly, velocity of shortening is dependent on actomyosin ATPase activity, and, since maximum velocity of shortening has been shown to be increased in SHR arterial muscle, it became necessary to know whether or not an increased actomyosin ATPase activity might be responsible. Therefore, data from a study of SHR and WKY caudal arterial myofibrillar ATPase activities are compared.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2006

Differences in beneficiary assessments of health care between TRICARE prime and TRICARE prime remote.

OBJECTIVES: We examined differences in health care ratings and reported health care experiences for active duty uniform services personnel using health care plans other than military treatment facilities. METHODS: We used a cross-sectional mail survey of a stratified sample of 3,871 beneficiaries enrolled in TRICARE Prime (TP) and TRICARE Prime Remote (TPR). The adjusted plan mean composite and global ratings were compared between TP and TPR participants. RESULTS: There were few significant differences between the two groups. Patient satisfaction was higher when patients chose their providers (TPR), and use of some preventive services was higher in managed-care plans (TP). Respondents in metropolitan locations differed significantly from those in nonmetropolitan locations in ratings of plans, quality of health care received, and access to services. CONCLUSIONS: The military health system is achieving some success in delivering uniform benefits but faces challenges in delivering high-quality uniform benefits in rural communities.

Adolescent↗

PubMed2000

Tetratricopeptide repeat domain of Yarrowia lipolytica Pex5p is essential for recognition of the type 1 peroxisomal targeting signal but does not confer full biological activity on Pex5p.

Peroxins are proteins required for peroxisome assembly and are encoded by the PEX genes. The Yarrowia lipolytica pex5-1 mutant fails to import a subset of peroxisomal matrix proteins, including those with a type 1 peroxisomal targeting signal (PTS1). Pex5p family members interact with a PTS1 through their characteristic tetratricopeptide repeat (TPR) domain. We used binding assays in vitro to investigate the nature of the association of Y. lipolytica Pex5p (YlPex5p) with the PTS1 signal. A purified recombinant YlPex5p fusion protein interacted specifically, directly and autonomously with a protein terminating in a PTS1. Wild-type YlPex5p translated in vitro recognized functional PTS1s specifically. This activity is abrogated by the substitution of an aspartic residue for a conserved glycine residue in the TPR domain (G455D) of YlPex5p encoded by the pex5-1 allele. Deletion analysis demonstrated that an intact TPR domain of YlPex5p is necessary but not sufficient for both interaction with a PTS1 and functional complementation of a strain lacking YlPex5p.

Acetic Acid↗

PubMed2000

Ethnicity and socioeconomic status: impact on cardiovascular activity at rest and during stress in youth with a family history of hypertension.

OBJECTIVE: The purpose of the present study was to examine the potential interaction of ethnicity and SES on hemodynamic functioning at rest and during acute stress in normotensive adolescents with a family history of essential hypertension (EH). DESIGN: The influences of ethnicity and socioeconomic status (SES) on cardiovascular function were evaluated at rest and in response to five different laboratory stressors. METHODS: 110 (50 female) Caucasian and 162 (85 female) African-American normotensive youth (initial age 11.2+/-2.4 years) with a family history of essential hypertension (EH) were tested on two occasions, an average of 2.5 years apart. Based on previous findings, it was predicted that African Americans, particularly those of low SES, would exhibit higher resting blood pressure (BP) and greater cardiovascular reactivity to acute laboratory stressors than would Caucasians. RESULTS: As predicted, African-American youth exhibited higher resting diastolic blood pressure (DBP) and total peripheral resistance (TPR) than Caucasians on both visits (both Ps<.04). African Americans exhibited greater systolic blood pressure (SBP) reactivity than did Caucasians to the video game stressor during both lab visits (both Ps<.02) and greater heart rate reactivity during the first lab visit (P<.01). African Americans exhibited greater SBP and/or DBP, and TPR reactivity to the cold pressor during the first lab visit and the parent-child discussion during the second visit (all Ps<.03). CONCLUSION: As predicted, African Americans exhibited higher resting BP and TPR, and greater cardiovascular reactivity than Caucasians. Although not in the predicted direction, a pattern of interactions began to emerge on the second evaluation. For example, upper SES youth exhibited greater heart rate reactivity compared to all other groups on the social competence interview and parent-child discussion stressors. Further study is needed to clarify the role cardiovascular reactivity may play in the link between ethnicity, SES, and cardiovascular disease risk.

Adolescent↗

PubMed2001

Repetitive apneas reduce nonlinear dynamical complexity of the human cardiovascular control system.

We tested the hypothesis that intermittent apneas performed by awake subjects simulate obstructive sleep apnea (OSA) and change dynamic complexity of the cardiovascular control system by repetitive short time stimulation of arterial chemoreceptors. Correlation dimension (CD) and reccurent plot quantification calculated as ratio % determinism versus % recurrence (RDR) were used.as indices of chaotic dynamics. Thirty three normotensive subjects of mean age 21,58 +/- 4,1 performed 10 voluntary apneas 1 min. each separated by 1 min free breathing period. Systolic (SYS), diastolic (DIAS) arterial blood pressure was continuously recorded by finger volume clamp. Stroke volume (SV) was estimated by pulse pressure analysis. Cardiac output (CO) and total peripheral resistance (TPR) were calculated by Portapress system. Cardiac inter-beat interval (IBI) was measured from R-R intervals of ECG. Standard deviation (SD), an index of linear variability, was calculated in 1 min epoch. Dynamics of cardiovascular variables was computed in each subject during 20 min. rest (C), 20 min. of 10 apneas, 1 min each, separated by 1 min free breathing (A), and in 20 min. recovery free breathing (R). In A period CD of all circulatory variables was significantly reduced and RDR augmented. In 23 out of 33 subjects decreased nonlinear dynamics of TPR was carried over from A to R. In contrast, SD increased significantly in A. In conclusion, intermittent brief chemoreflex stimulations by repetitive apneas increase blood pressure and TPR and decrease chaotic behaviour and complexity of the cardiovascular autonomic control system, presumably by inhibition of some regulatory loops such as baroreflex, less vital for survival at oxygen deprivation. Reduced complexity could be implicated in the mechanism of arterial hypertension linked with OSA.

Adolescent↗

PubMed1990

Hemodynamics and exercise tolerance after bisoprolol, nifedipine, and their combination in patients with angina pectoris.

The different mechanisms of action of beta-blockers and calcium antagonists could result in an additive therapeutic effect in patients with angina pectoris. Twenty-one male patients aged between 41 and 68 years and suffering from chronic stable angina pectoris and coronary artery disease confirmed by angiography took part in a randomized, double-blind study to examine the acute effect of 10 mg of bisoprolol, 20 mg of nifedipine, and a combination of the two drugs on hemodynamics at rest and during exercise [heart rate (HR), systolic blood pressure (SBP), rate-pressure product (RPP), cardiac index (CI), total peripheral resistance (TPR), and pulmonary capillary wedge pressure (PCP)], the behavior of the ST segment (ST), and exercise tolerance until occurrence of an ST-segment depression of 0.1 mV (W-ST01) and until onset of anginal pain (W-AP1). Following a baseline exercise test, 11 patients were given 10 mg of bisoprolol orally, whereas 10 patients received placebo. Two hours later, a second exercise test was carried out. All patients in both groups then received 20 mg of N orally. A third exercise test was performed 2 h later. On exercise, bisoprolol resulted in significant changes in HR (-16%), RPP (-22%), and CI (-16%), as well as in TPR (+ 13%); PCP was not significantly affected. Nifedipine led to significant changes in CI (+9%) and PCP (-34%). The effects of bisoprolol on HR and RPP and of nifedipine on PCP were retained in the combination. Competition was detectable as regards the opposing effects on CI and TPR. Measured by W-ST01 and ST, bisoprolol had a marked anti-ischemic effect, whereas that of nifedipine was distinctly less. There was an increase in effect after combination of the drugs (not significant). In patients with chronic angina pectoris due to coronary artery disease, bisoprolol and nifedipine had different hemodynamic profiles after acute administration; when the two drugs were combined, these effects were partly intensified and partly canceled out. There was a tendency for the effect of bisoprolol to be intensified by nifedipine in the combination. The combination of bisoprolol and nifedipine was well tolerated in the doses selected.

Adrenergic beta-Antagonists↗

PubMed1993

Hemodynamic responses to passive body tilts.

To investigate the relationship between the effects of gravity and hemodynamic responses to body tilts in the early steady-state, twelve healthy young adult males were passively tilted from the supine control position (SCP) to the 15 degrees, 30 degrees and 60 degrees head-up position (HU), and then the -15 degrees and -30 degrees head-down position (HD). Cardiac output (Q), stroke volume (SV), acceleration index (ACI) of the heart, thoracic fluid volume (TFV), blood pressure (BP), heart rate (HR), total peripheral vascular resistance (TPR) and ECG were measured. In the postural changes from SCP to the 15 degrees, 30 degrees and 60 degrees HU, the SV gradually decreased and the Q also decreased. The HR and TPR gradually increased. On the contrary, in the -15 degrees and -30 degrees HD, the SV increased and the Q increased and the HR and TPR decreased. The ACI increased in the HD, but decreased in the HU. The mean BP increased in the HU, but decreased in the HD. The TFV increased in the HD, and decreased in the HU. The average QRS vector was 56.1 degrees on the SCP and it increased in the HU, but decreased in the HD. In conclusion, the changes of hemodynamic parameters except in BP were linearly related to the sine of the tilt angle in regardless of HU or HD.

Adolescent↗

PubMed2001

[Role of phosphate in recurrent calcium lithiasis. A current view].

OBJECTIVE: To analyze the biochemical impact of treatment with phosphates in patients with recurrent calcium lithiasis and hypercalciuria. METHODS: 20 patients were selected according to the following criteria: normal renal function, recurrent calcium nephrolithiasis, hypercalciuria, hypophosphatemia, normal calcium and low tubular phosphate reabsorption (TPR). The mean duration of treatment was 7.5 +/- 3.8 months. The pre and post-treatment phosphatemia, calciuria, phosphaturia and TPR were analyzed. The results were analyzed by the Wilcoxon statistical method. RESULTS: We found a moderate but significant decrease of calciuria (326.5 +/- 52-4 to 266.4 +/- 31.7 mg/24 h), while phosphatemia (2.21 +/- 0.09 to 2.52 +/- 0.30 mg/24 h) and TPR (65.7 +/- 6.3 to 71.3 +/- 4.1) increased significantly. Overall treatment was well-tolerated and no patient abandoned treatment. CONCLUSIONS: The short-term biochemical results obtained are similar to those reported in the literature. However, definitive conclusions cannot be made since treatment application is not standardized and studies that demonstrate its clinical efficacy are scanty.

Calcium↗

PubMed2002

Pulmonary hemodynamic and tidal volume changes during exercise in heart failure.

BACKGROUND: Impairment of lung mechanics, increase of pulmonary artery pressure and limitation of exercise capacity are common findings in chronic heart failure. The objective of the present study was to evaluate whether pulmonary mechanics are correlated with pulmonary hemodynamics, whether both are correlated with the functional capacity and whether the time course of their changes during exercise correlates with the exercise capacity. METHODS: We performed a cardiopulmonary exercise test (breath by breath analysis of ventilation and gas exchange, cycloergometer, 25 W increments every 3 min) with pulmonary hemodynamic monitoring in 38 heart failure patients. The parameters were analyzed at rest, 1 min after the work rate increase and at peak exercise. RESULTS: A significant linear correlation with peak oxygen consumption was found at rest for: mean pulmonary artery pressure (mPAP, r = -0.56), right atrial pressure (RAP, r = -0.42), pulmonary wedge pressure (PWP, r = -0.53), and total pulmonary (TPR, r = -0.53) and pulmonary vascular resistances (PVR, r = -0.45); after 1 min of exercise for: cardiac index (CI, r = 0.49), mPAP (r = -0.57), RAP (r = -0.60), PWP (r = -0.45), and TPR (r = -0.67) and PVR (r = -0.38); at peak exercise for: tidal volume (r = 0.63), CI (r = 0.63), RAP (r = -0.43), TPR (r = -0.65) and PVR (r = -0.43). A significant linear correlation with peak oxygen consumption was found, for the increment between rest and 1 min of exercise, for RAP (r = -0.58) and CI (r = 0.42) and, for the increments between rest and peak exercise, for tidal volume (r = 0.79) and CI (r = 0.61) and, for the ratio between the increment between rest and 1 min of exercise/increment between rest and peak exercise, for mPAP (r = -0.42), RAP (r = 0.51) and CI (r = -0.54). The same ratio of increment of mPAP (r = 0.39) and CI (r = 0.36) correlated with that of tidal volume. CONCLUSIONS: This study provides evidence of a strong correlation between the respiratory function and pulmonary vascular pressure changes during exercise in heart failure.

Adult↗

PubMed1998

[Effects of dopexamine on cardiac hemodynamics during myocardial ischemia in rats and in comparison with fenoldopam and procaterol].

The effect of dopexamine hydrochloride(DPX) on cardiac hemodynamics during acute myocardial ischemia (AMI) was studied in rats and compared with those of fenoldopam hydrochloride(FODA) and procaterol hydrochloride (PCT). The results showed that i.v. DPX remarkably attenuated the increases of total peripheral resistance(TPR) and left ventricular end-diastolic pressure and the decreases of + dp/dt max caused by ischemia, while DPX showed no significant effect on mean arterial pressure(MAP). Although FODA was more potent than DPX in attenuating the increase of TPR and the decrease of myocardial contractility caused by ischemia, it significantly decreased MAP. The effects of PCT on all these variables were the smallest among the 3 agents. The results suggest that DPX has a better prospect in the treatment of ischemic heart disease in view of its actions of decreasing TPR, mild increase of myocardial contractility, without MAP decrease and myocardial oxygen consumption increase.

Adrenergic beta-2 Receptor Agonists↗

PubMed2002

[Cardiovascular responses to G-suits with 3 levels of positive pressure breathing using different chest counter pressures].

OBJECTIVE: To observe cardiovascular responses to positive pressure breathing (PPB) using different counter pressures. METHOD: Cardiovascular responses of 7 male healthy subjects (aged 18-20 years) wearing two kinds of Jerkin-G-suit were observed under three levels of ground-level PPB (30, 50, 70 mmHg) for 3 min. RESULT: All subjects completed the experiment successfully. While during PPB at 50, 70 mmHg levels within 3 min, HR, MAP, TPR elevated significantly, while SV declined significantly. At all 3 PPB levels Q-Z time was not significantly changed. There were significant difference (P<0.05) between delta SV and delta TPR with the two Jerkin-G-suits under PPB of 70 mmHg. CONCLUSION: PPB resulted in elevation of MAP, TPR, HR and decline of SV significantly using two kinds of Jerkin-G-suit. PPB had no effect on contractile function of cardiac muscle. Under PPB, SV increased significantly when chest counter pressure was equal to the mask pressure.

Adolescent↗

PubMed2003

Identification and characterization of TPARM gene in silico.

Several tumor suppressor genes are located within human chromosome 11q23 region. We have cloned and characterized MFRP and RNF26 genes at 11q23.3. We also identified and characterized KIAA1735/MTHDIX gene at 11q23.1 and CLDN24 gene at 11q23.2 by using bioinformatics. Here, a novel human gene corresponding to a 5'-truncated FLJ20535 cDNA was identified. FLJ20535 corresponded to nucleotide position 55-2255 of FLJ13859, and nucleotide position 52-2169 of FLJ13859 was the coding region. Because of tetratricopeptide repeat (TPR) and armadillo repeat (ARM) domains within its gene product, the novel human gene was designated TPARM. Mouse E330017O07Rik cDNA was derived from mouse Tparm gene. Human TPARM (705 aa) and mouse Tparm (704 aa), showing 75.4% total-amino-acid identity, consist of TPR domain and three ARM domains. TPR domain of TPARM was most homologous to that of SMAP1, while ARM1-ARM3 domains of TPARM were most homologous to ARM7-ARM9 domains of CTNNB1 (also known as beta-catenin). TPARM might be implicated in the WNT-beta-catenin signaling pathway. TPARM mRNA was expressed in testis, prostate, lung, germinal center B-cells, and also in neuroblastoma, teratocarcinoma, colon cancer, and gastric cancer. Human TPARM gene was found to consist of 22 exons. TPARM gene, located between NCAM1 and DRD2 genes, was mapped to human chromosome 11q23.2. TPARM as well as NCAM1 and DRD2 were predicted to be candidate tumor suppressor genes within the commonly deleted region of malignant melanoma on 11q23.1-q23.2 (between microsatellite markers D11S1347 and D11S4122).

Amino Acid Sequence↗

PubMed2000

A noninvasive method for total peripheral resistance baroreflex identification.

We developed a noninvasive method for estimating the static gains of the arterial and cardiopulmonary total peripheral resistance (TPR) baroreflexes. The method involves a system identification analysis of beat-to-beat fluctuations in arterial blood pressure (ABP), cardiac output (CO), and stroke volume (SV) in order to identify two transfer functions relating CO fluctuations to ABP fluctuations and SV fluctuations to ABP fluctuations. The static gains of each of the TPR baroreflexes may then be computed from the static gains of the two identified transfer functions. In order to evaluate the method, we constructed a computer model of the human cardiovascular system. We applied the method to data generated from the computer model and found close agreement between the estimated and actual static gains of the model TPR baroreflexes. We also applied the method to experimental human data and obtained encouraging results. These results motivate the experimental validation of the method.

Baroreflex↗

PubMed2004

Comparison of methods to quantitate 18F-FDG uptake with PET during experimental acute lung injury.

UNLABELLED: PET with 18F-FDG may be useful for quantifying neutrophilic activation. We previously demonstrated that pulmonary neutrophil sequestration could be detected during acute lung injury (ALI), even without migration into the alveolar compartment. Using the influx constant Ki as the method to quantify lung 18F-FDG uptake, we also showed that Ki correlated positively with in vitro assays of 3H-deoxyglucose (3H-DG) uptake in cells harvested via bronchoalveolar lavage. In the present study, we have reanalyzed data from that study to determine if simpler nonkinetic methods of quantifying the pulmonary uptake of 18F-FDG could be as powerful as calculating Ki. METHODS: 18F-FDG uptake was quantified as Ki, calculated by 3-compartmental model analysis (used as the gold standard) and Patlak graphical analysis, with and without normalization for initial volume of tracer distribution; the standardized uptake value; and the tissue-to-plasma activity ratio (TPR). RESULTS: Values for Ki, determined either from a 3-compartmental model analysis of the time-activity data or by Patlak graphical analysis, were highly correlated (R2 = 0.97). The correlation was worse if these variables were normalized for the initial volume of tracer distribution. TPR was highly correlated with Ki determined by the compartmental model (R2 = 0.96) and with in vitro measurements of 3H-DG uptake (R2 = 0.63). CONCLUSION: The TPR is a simple and equally effective alternative to dynamic imaging in determining net 18F-FDG uptake during ALI. Normalization of the kinetic data for differences in the initial volume of tracer distribution does not contribute significantly to signal interpretation during ALI.

Animals↗

PubMedDate not supplied

[Alterations of cardiac output during bicarbonate hemodialysis and its relationship with other hemodynamic parameters].

PURPOSE: Time course of cardiac output (CO) and other hemodynamic parameters were measured during hemodialysis (HD). Our aims were to identify a characteristic CO profile and investigate the relationship with other hemodynamic parameters. PATIENTS AND METHODS: CO was measured with ultrasound dilution method in 45 chronic hemodynamically stable HD patients. Diabetics and patients with heart diseases were excluded. Ultrafiltration rate (UFR) was fixed at 649 +/- 244 mL/min. Pre/post statistical comparisons were performed for CO, cardiac index (IC), central blood volume (CBV) and total peripheral resistance (TPR). RESULTS: CO was pre 5.7 +/- 1.8 and post 4.5 +/- 1.4 L/min (p=0.001); IC was pre 3.2 +/- 0.9 and post 2.6 +/- 0.7 L/m2 (p=0.001); CBV was pre 1.28 +/- 0.39 and post 1.09 +/- 0.32 L (p=0.001). TPR increased from 18.7 +/- 5.6 to 22.7 +/- 6.1 mmHg/L/min (p=0.001). Maximal CO reduction rate was found at 60 min, thereafter it reduced progressively. Log(CO1) increased in a non-linear way with body weight gain and similarly it decreased during UFR. A negative correlation was found between log(TPR1) and log(CO1-QA). CO reduction was associated with UFR and not with age, dialysis duration, left ventricular hypertrophy, sex and hemoglobin (Hb) in a multiple regression model (r2 =0.31, p=0.05). Qa/CO1 was 0.16 +/- 0.12. CBV/CO increased from 0.23 +/- 0.06 to 0.25 +/- 0.07%. CONCLUSIONS: Progressive CO reduction and TPR increase appear to be the typical hemodynamic features of bicarbonate HD with a UFR of moderate degree. Volume overload and CO increase were related in a non-linear way. TPR1 was strongly correlated with CO1-Qa, suggesting that a large arterovenous shunt was associated with increased resistance.

Adult↗