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Peripheral Resistance (peripheral + resistance)

Distribution by Scientific Domains
Medical Sciences52%
Life Sciences30%
Distribution within Medical Sciences
Pharmacology & Pharmaceutical Medicine21%
Obstetrics & Gynecology15%
General & Internal Medicine9%

Kinds of Peripheral Resistance

  • total peripheral resistance
    		•

    Selected Abstracts

    Relationship between breathing and cardiovascular function at rest: sex-related differences

    ACTA PHYSIOLOGICA, Issue 2 2010
    B. G. Wallin
    Abstract Aim:, To compare relationships at rest between breathing rate, levels of muscle sympathetic nerve activity, total peripheral resistance and cardiac output among young men and women. Methods:, Recordings were made of respiratory movements, sympathetic nerve activity (peroneal microneurography), intra-arterial blood pressure, electrocardiogram, cardiac output (open-circuit acetylene uptake technique) in 19 healthy men (age 27 ± 2 years, mean ± SEM) and 17 healthy women (age 25 ± 1 years). Total peripheral resistance and stroke volume were calculated. Four minutes epochs of data were analysed. Results:, Breathing rates and sympathetic activity were similar in men and women but compared to men, women had significantly lower blood pressures, cardiac output and stroke volume. In men breathing rate correlated positively with sympathetic activity (r = 0.58, P < 0.05) but not in women (r = 0.12, P > 0.05). Furthermore, in men, respiratory rate correlated positively with total peripheral resistance (r = 0.65, P < 0.05) and inversely with cardiac output (r = ,0.84, P < 0.05) and heart rate (r = ,0.60, P < 0.05) but there were no such relationships in women (P > 0.05 for all). Conclusions:, The positive relationship between breathing and sympathetic activity in men, and the inverse coupling of breathing to cardiac output and heart rate suggest that influences of respiration may be important not only for dynamic but also for ,tonic' cardiovascular function. The lack of relationships among these variables in women shows that there are fundamental differences in basic blood pressure regulation between the sexes. [source]

    Systemic nitric oxide clamping in normal humans guided by total peripheral resistance

    ACTA PHYSIOLOGICA, Issue 2 2010
    J. A. Simonsen
    Abstract Aim:, We wanted to stabilize the availability of nitric oxide (NO) at levels compatible with normal systemic haemodynamics to provide a model for studies of complex regulations in the absence of changes in NO levels. Methods:, Normal volunteers (23,28 years) were infused i.v. with the nitric oxide synthase (NOS) inhibitor NG -nitro- l -arginine methyl ester (l -NAME) at 0.5 mg kg,1 h,1. One hour later, the NO donor sodium nitroprusside (SNP) was co-infused in doses eliminating the haemodynamic effects of l -NAME. Haemodynamic measurements included blood pressure (MABP) and cardiac output (CO) by impedance cardiography. Results:,l -NAME increased MABP and total peripheral resistance (TPR, 1.02 ± 0.05 to 1.36 ± 0.07 mmHg s mL,1, mean ± SEM, P < 0.001). With SNP, TPR fell to a stable value slightly below control (0.92 ± 0.05 mmHg s mL,1, P < 0.05). CO decreased with l -NAME (5.8 ± 0.3 to 4.7 ± 0.3 L min,1, P < 0.01) and returned to control when SNP was added (6.0 ± 0.3 L min,1). A decrease in plasma noradrenaline (42%, P < 0.01) during l -NAME administration was completely reversed by SNP. Plasma renin activity decreased during l -NAME administration and returned towards normal after addition of SNP. In contrast, plasma aldosterone was increased by l -NAME and remained elevated. Conclusions:, Concomitant NOS inhibition and NO donor administration can be adjusted to maintain TPR at control level for hours. This approach may be useful in protocols in which stabilization of the peripheral supply of NO is required. However, the dissociation between renin and aldosterone secretion needs further investigation. [source]

    Stroke volume decreases during mild dynamic and static exercise in supine humans

    ACTA PHYSIOLOGICA, Issue 2 2009
    M. Elstad
    Abstract Aim:, The contributions of cardiac output (CO) and total peripheral resistance to changes in arterial blood pressure are debated and differ between dynamic and static exercise. We studied the role stroke volume (SV) has in mild supine exercise. Methods:, We investigated 10 healthy, supine volunteers by continuous measurement of heart rate (HR), mean arterial blood pressure, SV (ultrasound Doppler) and femoral beat volume (ultrasound Doppler) during both dynamic mild leg exercise and static forearm exercise. This made it possible to study CO, femoral flow (FF) and both total and femoral peripheral resistance beat-by-beat. Results:, During a countdown period immediately prior to exercise, HR and mean arterial pressure increased, while SV decreased. During mild supine exercise, SV decreased by 5,8%, and most of this was explained by increased mean arterial pressure. Dynamic leg exercise doubled femoral beat volume, while static hand grip decreased femoral beat volume by 18%. FF is tightly regulated according to metabolic demand during both dynamic leg exercise and static forearm exercise. Conclusion:, Our three major findings are, firstly, that SV decreases during both dynamic and static mild supine exercise due to an increase in mean arterial pressure. Secondly, femoral beat volume decreases during static hand grip, but FF is unchanged due to the increase in HR. Finally, anticipatory responses to exercise are apparent prior to both dynamic and static exercise. SV changes contribute to CO changes and should be included in studies of central haemodynamics during exercise. [source]

    Twenty-four-hour non-invasive monitoring of systemic haemodynamics and cerebral blood flow velocity in healthy humans

    ACTA PHYSIOLOGICA, Issue 1 2002
    M. DIAMANT
    ABSTRACT Acute short-term changes in blood pressure (BP) and cardiac output (CO) affect cerebral blood flow (CBF) in healthy subjects. As yet, however, we do not know how spontaneous fluctuations in BP and CO influence cerebral circulation throughout 24 h. We performed simultaneous monitoring of BP, systemic haemodynamic parameters and blood flow velocity in the middle cerebral artery (MCAV) in seven healthy subjects during a 24-h period. Finger BP was recorded continuously during 24 h by Portapres and bilateral MCAV was measured by transcranial Doppler (TCD) during the first 15 min of every hour. The subjects remained supine during TCD recordings and during the night, otherwise they were seated upright in bed. Stroke volume (SV), CO and total peripheral resistance (TPR) were determined by Modelflow analysis. The 15 min mean value of each parameter was assumed to represent the mean of the corresponding hour. There were no significant differences between right vs. left, nor between mean daytime vs. night time MCAV. Intrasubject comparison of the twenty-four 15-min MCAV recordings showed marked variations (P < 0.001). Within each single 15-min recording period, however, MCAV was stable whereas BP showed significant short-term variations (P < 0.01). A day,night difference in BP was only observed when daytime BP was evaluated from recordings in the seated position (P < 0.02), not in supine recordings. Throughout 24 h, MCAV was associated with SV and CO (P < 0.001), to a lesser extent with mean arterial pressure (MAP; P < 0.005), not with heart rate (HR) or TPR. These results indicate that in healthy subjects MCAV remains stable when measured under constant supine conditions but shows significant variations throughout 24 h because of activity. Moreover, changes in SV and CO, and to a lesser extent BP variations, affect MCAV throughout 24 h. [source]

    Arterial stiffening and cardiac hypertrophy in a new rat model of type 2 diabetes

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2006
    K.-C. Chang
    Abstract Background, We determined the effects of NIDDM on haemodynamic parameters describing arterial wall elasticity and cardiac hypertrophy in rats administered streptozotocin (STZ) and nicotinamide (NA), using the aortic impedance analysis. Methods, Male Wistar rats at 2 months were administered intraperitoneally 180 mg kg,1 of NA, 30 min before an intravenous injection of 50 mg kg,1 STZ, to induce type 2 diabetes. The STZ-NA rats were divided into two groups, 4 weeks and 8 weeks after induction of diabetes, and compared with untreated age-matched controls. Pulsatile aortic pressure and flow signals were measured by a high-fidelity pressure sensor and electromagnetic flow probe, respectively, and were then subjected to Fourier transformation for the analysis of aortic input impedance. Results, In each diabetic group, the experimental syndrome was characterized by a moderate and stable hyperglycaemia and a relative deficiency of insulin secretion. However, the 8-week but not the 4-week STZ-NA diabetic rats showed a decrease in cardiac output in the absence of any significant changes in mean aortic pressure, having increased total peripheral resistance. The diabetic syndrome at 8 weeks also contributed to an increase in aortic characteristic impedance, from 1·49 ± 0·33 (mean ± SD) to 1·95 ± 0·28 mmHg s mL,1 (P < 0·05), suggesting a detriment to the aortic distensibility in NIDDM. Meanwhile, the STZ-NA diabetic animals after 8 weeks had an increased wave reflection factor (0·46 ± 0·09 vs. 0·61 ± 0·13, P < 0·05) and decreased wave transit time (25·8 ± 3·8 vs. 20·6 ± 2·8 ms, P < 0·05). Ratio of the left ventricular weight to body weight was also enhanced in the 8-week STZ-NA diabetic rats. Conclusion, The heavy intensity with early return of the pulse wave reflection may augment systolic load of the left ventricle coupled to the arterial system, leading to cardiac hypertrophy in the rats at 8 weeks after following STZ and NA administration. [source]

    Effect of deep brain stimulation of the posterior hypothalamic area on the cardiovascular system in chronic cluster headache patients

    EUROPEAN JOURNAL OF NEUROLOGY, Issue 9 2007
    P. Cortelli
    The objective of this study was to determine the cardiovascular effects of chronic stimulation of the posterior hypothalamic area (PHA) in cluster headache (CH) patients. Systolic and diastolic blood pressure (SBP, DBP), cardiac output, total peripheral resistance (TPR), heart rate (HR) and breathing were monitored at supine rest and during head-up tilt test (HUTT), Valsalva manoeuvre, deep breathing, cold face test and isometric handgrip in eight drug-resistant chronic CH patients who underwent monolateral electrode implantation in the PHA for therapeutic purposes. Autoregressive power spectral analysis (PSA) of HR variability (HRV) was calculated at rest and during HUTT. Each subject was studied before surgery (condition A) and after chronic deep brain stimulation (DBS) of PHA (condition B). Baseline SBP, DBP, HR and cardiovascular reflexes were normal and similar in both conditions. With respect to condition A, DBP, TPR and the LF/HF obtained from the PSA of HRV were significantly (P < 0.05) increased during HUTT in condition B. In conclusion, chronic DBS of the PHA in chronic CH patients is associated with an enhanced sympathoexcitatory drive on the cardiovascular system during HUTT. [source]

    Modelflow estimates of cardiac output compared with Doppler ultrasound during acute changes in vascular resistance in women

    EXPERIMENTAL PHYSIOLOGY, Issue 4 2010
    Kenneth S. Dyson
    We compared Modelflow (MF) estimates of cardiac stroke volume (SV) from the finger pressure-pulse waveform (Finometer®) with pulsed Doppler ultrasound (DU) of the ascending aorta during acute changes in total peripheral resistance (TPR) in the supine and head-up-tilt (HUT) postures. Twenty-four women were tested during intravenous infusion of 0.005 or 0.01 ,g kg,1 min,1 isoprenaline, 10 or 50 ng kg,1 min,1 noradrenaline and 0.3 mg sublingual nitroglycerine. Responses to static hand-grip exercise (SHG), graded lower body negative pressure (LBNP, from ,20 to ,45 mmHg) and 45 deg HUT were evaluated on separate days. Bland,Altman analysis indicated that SVMF yielded lower estimates than SVDU during infusion of 0.01 ,g kg,1 min,1 isoprenaline (SVMF 92.7 ± 15.5 versus SVDU 104.3 ± 22.9 ml, P= 0.03) and SHG (SVMF 78.8 ± 12.0 versus SVDU 106.1 ± 28.5 ml, P < 0.01), while larger estimates were recorded with SVMF during ,45 mmHg LBNP (SVMF 52.6 ± 10.7 versus SVDU 46.2 ± 14.5 ml, P= 0.04) and HUT (SVMF 59.3 ± 13.6 versus SVDU 45.2 ± 11.3 ml, P < 0.01). Linear regression analysis revealed a relationship (r2= 0.41, P < 0.01) between the change in TPR from baseline and the between-methods discrepancy in SV measurements. This relationship held up under all of the experimental protocols (regression for fixed effects, P= 0.46). These results revealed a discrepancy in MF estimates of SV, in comparison with those measured by DU, during acute changes in TPR. [source]

    Region-specific changes in sympathetic nerve activity in angiotensin II,salt hypertension in the rat

    EXPERIMENTAL PHYSIOLOGY, Issue 1 2010
    John W. Osborn
    It is now well accepted that many forms of experimental hypertension and human essential hypertension are caused by increased activity of the sympathetic nervous system. However, the role of region-specific changes in sympathetic nerve activity (SNA) in the pathogenesis of hypertension has been difficult to determine because methods for chronic measurement of SNA in conscious animals have not been available. We have recently combined indirect, and continuous and chronic direct, assessment of region-specific SNA to characterize hypertension produced by administration of angiotensin II (Ang II) to rats consuming a high-salt diet (Ang II,salt hypertension). Angiotensin II increases whole-body noradrenaline (NA) spillover and depressor responses to ganglionic blockade in rats consuming a high-salt diet, but not in rats on a normal-salt diet. Despite this evidence for increased ,whole-body SNA' in Ang II,salt hypertensive rats, renal SNA is decreased in this model and renal denervation does not attenuate the steady-state level of arterial pressure. In addition, neither lumbar SNA, which largely targets skeletal muscle, nor hindlimb NA spillover is changed from control levels in Ang II,salt hypertensive rats. However, surgical denervation of the splanchnic vascular bed attenuates/abolishes the increase in arterial pressure and total peripheral resistance, as well as the decrease in vascular capacitance, observed in Ang II,salt hypertensive rats. We hypothesize that the ,sympathetic signature' of Ang II,salt hypertension is characterized by increased splanchnic SNA, no change in skeletal muscle SNA and decreased renal SNA, and this sympathetic signature creates unique haemodynamic changes capable of producing sustained hypertension. [source]

    The baroreflex is counteracted by autoregulation, thereby preventing circulatory instability

    EXPERIMENTAL PHYSIOLOGY, Issue 4 2004
    Roberto Burattini
    The aims of this study were (a) to apply in the animal with intact baroreflex a two-point method for estimation of overall, effective open-loop gain, G0e, which results from the combined action of baroregulation and total systemic autoregulation on peripheral resistance; (b) to predict specific baroreflex gain by correcting the effective gain for the autoregulation gain; and (c) to discuss why the effective gain is usually as low as 1,2 units. G0e was estimated from two measurements of both cardiac output, Q, and mean systemic arterial pressure, P: one in the reference state (set-point) and the other in a steady-state reached 1,3 min after a small cardiac output perturbation. In anaesthetized cats and dogs a cardiac output perturbation was accomplished by partial occlusion of the inferior vena cava and by cardiac pacing, respectively. Average (±s.e.m.) estimates of G0e were 1.4 ± 0.2 (n= 8) in the cat and 1.5 ± 0.4 (n= 5) in the dog. The specific baroreflex open-loop gain, G0b, found after correction for total systemic autoregulation, was 3.3 ± 0.4 in the cat and 2.8 ± 0.8 in the dog. A model-based analysis showed that, with G0e as low as 1.4, the closed-loop response of P to a stepwise perturbation in Q results in damped oscillations that disappear in about 1 min. The amplitude and duration of these oscillations, which have a frequency of about 0.1 Hz, increase with increasing G0e and cause instability when G0e is about 3. We conclude that autoregulation reduces the effectiveness of baroreflex gain by about 55%, thereby preventing instability of blood pressure response. [source]

    Arterial Myogenic Properties of the Spontaneously Hypertensive Rat

    EXPERIMENTAL PHYSIOLOGY, Issue 5 2002
    Jennifer M. Hughes
    When subject to a transmural pressure gradient resistance arteries develop a spontaneous, intrinsically initiated contraction which varies according to the pressure stimulus and occurs in the absence of vasoconstrictor agonists. Such pressure-dependent active changes in vascular tone are indicative of the vascular myogenic response and contribute to autoregulation and the setting of total peripheral resistance and hence blood pressure regulation. The myogenic behaviour of blood vessels provides the background tone upon which other vasomotor influences act. Hypertension is associated with a raised vascular resistance and in this article the evidence for increased myogenic activity contributing to the raised vascular resistance is reviewed. Although there are some cases that provide evidence for exaggerated myogenic responsiveness in resistance arteries taken from hypertensive animals it is not possible to conclude that enhanced myogenic contractile responses within normal pressure ranges contribute to the raised total peripheral resistance. However, the myogenic tone of the resistance arteries of the various vascular beds is subject to differing modulatory influences in hypertensive animals and their normotensive controls which may contribute to the aetiology of hypertension. [source]

    Cool dialysate reduces asymptomatic intradialytic hypotension and increases baroreflex variability

    HEMODIALYSIS INTERNATIONAL, Issue 2 2009
    Lindsay J. CHESTERTON
    Abstract Intradialytic hypotension (IDH) remains an important cause of morbidity and mortality in chronic hemodialysis (HD) patients and can be ameliorated by cool temperature HD. The baroreflex arc is under autonomic control and is essential in the short-term regulation of blood pressure (BP). This study aimed to investigate if the baroreflex sensitivity (BRS) response to HD differed between standard and cool-temperature dialysate. Ten patients (mean age 67±2 years) prone to IDH were recruited into a randomized, crossover study to compare BRS variation at dialysate temperatures of 37 °C (HD37) and 35 °C (HD35). Each patient underwent continuous beat-to-beat BP monitoring during a dialysis session of HD37 and HD35. During HD37 2 patients developed symptomatic IDH, as opposed to 1 with HD35. However, asymptomatic IDH occurred with a frequency of 0.4 episodes per session with HD35 and 6.2 episodes per session during HD37 (odds ratio15.5; 95%CI 5.6,14.2). Although absolute BRS measurements did not differ between the 2 modalities, BRS variability increased during HD35. Our study has demonstrated that in IDH-prone patients, cool HD resulted in a reduction in heart rate and a greater reduction in cardiac output and stroke volume. Mean arterial pressure was maintained through a significantly greater increase in total peripheral resistance. Furthermore, although absolute BRS values during HD were not significantly altered by a reduction in dialysate temperature, there was a greater percentage increase in BRS values during cool HD. Understanding the varied causes of, and categorizing impaired hemodynamic responses to HD will enable further individualization of HD prescriptions according to patient need. [source]

    Temperature and Thermal Balance Monitoring and Control in Dialysis

    HEMODIALYSIS INTERNATIONAL, Issue 2 2003
    Franti, ek Lopot
    Temperature and thermal balance have been studied in an effort to explain better tolerance of ultrafiltration during isolated ultrafiltration and other convective techniques as compared to conventional hemodialysis. The large number of published studies has led to the conclusion that negative thermal balance of the extracorporeal circuit ameliorates hemodynamic stability by increased vasoreactivity and increased peripheral resistance. On the other hand, measurement of dialysis efficiency (urea removal) did not unequivocally confirm the theoretically predicted decrease in efficiency of "cool" dialysis. Another suggested application of temperature and thermal balance for assessing bioincompatibility is currently hampered by the ability of existing technology to evaluate thermal parameters of the extracorporeal circuit only. Publications on impact of negative thermal balance of the extracorporeal circuit on ultrafiltration-induced changes in blood volume give contradictory results. Further studies are needed for elucidation of the impact of thermal balance on overall biological response to dialysis. [source]

    Left ventricular hypertrophy in rats with biliary cirrhosis

    HEPATOLOGY, Issue 3 2003
    Javier Inserte
    Portal hypertension induces neuroendocrine activation and a hyperkinetic circulation state. This study investigated the consequences of portal hypertension on heart structure and function. Intrahepatic portal hypertension was induced in male Sprague-Dawley rats by chronic bile duct ligation (CBDL). Six weeks later, CBDL rats showed higher plasma angiotensin-II and endothelin-1 (P < .01), 56% reduction in peripheral resistance and 73% reduction in pulmonary resistance (P < .01), 87% increase in cardiac index and 30% increase in heart weight (P < .01), and increased myocardial nitric oxide (NO) synthesis. In CBDL rats, macroscopic analysis demonstrated a 30% (P < .01) increase in cross-sectional area of the left ventricular (LV) wall without changes in the LV cavity or in the right ventricle (RV). Histomorphometric analysis revealed increased cell width (12%, P < .01) of cardiomyocytes from the LV of CBDL rats, but no differences in myocardial collagen content. Myocytes isolated from the LV were wider (12%) and longer (8%) than right ventricular myocytes (P < .01) in CBDL rats but not in controls. CBDL rats showed an increased expression of ANF and CK-B genes (P < .01). Isolated perfused CBDL hearts showed pressure/end-diastolic pressure curves and response to isoproterenol identical to sham hearts, although generated wall tension was reduced because of the increased wall thickness. Coronary resistance was markedly reduced. This reduction was abolished by inhibition of NO synthesis with N -nitro-L-arginine. Expression of eNOS was increased in CBDL hearts. In conclusion, portal hypertension associated to biliary cirrhosis induces marked LV hypertrophy and increased myocardial NO synthesis without detectable fibrosis or functional impairment. This observation could be relevant to patients with cirrhosis. [source]

    Albumin infusion fails to restore circulatory function following paracentesis of tense ascites as assessed by beat-to-beat haemodynamic measurements

    INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 12 2008
    D. Schneditz
    Summary Aims:, To study whether circulatory changes during large volume paracentesis (LVP) in patients with liver cirrhosis and tense ascites as assessed by novel non-invasive haemodynamic measuring technology are reversed by subsequent albumin infusion. Materials and methods:, Eleven patients with portal hypertensive ascites secondary to liver cirrhosis of Child's class B or C were studied during LVP (10.7 ± 4.4 l) and subsequent infusion of albumin. Digital arterial pulse waves were continuously measured by vascular unloading technique providing data for beat-to-beat values of systolic (Ps), diastolic (Pd) and mean arterial pressures (Pm), respectively, as well as for heart rate (Fh), stroke volume (Vs), cardiac output (Qco) and peripheral resistance (R). Data extrapolated to the end of paracentesis, albumin infusion and follow-up phases were compared with the end of the equilibration phase. Results:, At the end of paracentesis, Ps, Pm and Pd changed by ,14 ± 15% (p < 0.05), ,16 ± 11% (p < 0.01) and ,17 ± 11% (p < 0.001), respectively, whereas Qco and Fh did not change substantially. There was a highly significant increase in Vs by +21 ± 25% (p < 0.01). The largest change was seen in R which significantly decreased by ,29 ± 24% (p < 0.01). This change was not reversed by infusion of albumin and persisted up to the end of follow-up. Conclusion:, The haemodynamic changes following LVP appear to be first and foremost controlled by changes in peripheral resistance with insufficient cardiac compensation. Further studies combining albumin with vasopressors for prevention of paracentesis-induced circulatory changes are needed. [source]

    Facilitation of Myocardial PI3K/Akt/nNOS Signaling Contributes to Ethanol-Evoked Hypotension in Female Rats

    ALCOHOLISM, Issue 7 2009
    Mahmoud M. El-Mas
    Background:, The mechanism by which ethanol reduces cardiac output (CO) and blood pressure (BP) in female rats remains unclear. We tested the hypothesis that enhancement of myocardial phosphatidylinositol 3-kinase (PI3K)/Akt signaling and related neuronal nitric oxide synthase (nNOS) and/or endothelial nitric oxide synthase (eNOS) activity constitutes a cellular mechanism for the hemodynamic effects of ethanol. Methods:, We measured the level of phosphorylated eNOS (p-eNOS) and p-nNOS in the myocardium of ethanol (1 g/kg intragastric, i.g.) treated female rats along with hemodynamic responses [BP, CO, stroke volume, (SV), total peripheral resistance, (TPR)], and myocardial nitrate/nitrite levels (NOx) levels. Further, we investigated the effect of selective pharmacological inhibition of nNOS with N, -propyl- l -arginine (NPLA) or eNOS with N5 -(1-iminoethyl)- l -ornithine (l -NIO) on cellular, hemodynamic, and biochemical effects of ethanol. The effects of PI3K inhibition by wortmannin on the cardiovascular actions of ethanol and myocardial Akt phosphorylation were also investigated. Results:, The hemodynamic effects of ethanol (reductions in BP, CO, and SV) were associated with significant increases in myocardial NOx and myocardial p-nNOS and p-Akt expressions while myocardial p-eNOS remained unchanged. Prior nNOS inhibition by NPLA (2.5 or 12.5 ,g/kg) attenuated hemodynamic effects of ethanol and abrogated associated increases in myocardial NOx and cardiac p-nNOS contents. The hemodynamic effects of ethanol and increases in myocardial p-Akt phosphorylation were reduced by wortmannin (15 ,g/kg). On the other hand, although eNOS inhibition by l -NIO (4 or 20 mg/kg) in a dose-dependent manner attenuated ethanol-evoked hypotension, the concomitant reductions in CO and SV remained unaltered. Also, selective eNOS inhibition uncovered dramatic increases in TPR in response to ethanol, which appeared to have offset the reduction in CO. Neither NPLA nor l -NIO altered plasma ethanol levels. Conclusions:, These findings implicate the myocardial PI3K/Akt/nNOS signaling in the reductions in BP and CO produced by ethanol in female rats. [source]

    Microvascular Structure and Function in Salt-Sensitive Hypertension

    MICROCIRCULATION, Issue 4 2002
    Dr. Matthew A. Boegehold
    In many individuals with essential hypertension, dietary salt can further increase blood pressure by augmentation of an already elevated total peripheral resistance. There is little information on the microvascular changes that contribute to salt-sensitive hypertension in humans, but studies in the Dahl salt-sensitive rat have provided some knowledge of the microcirculation in this form of hypertension. These studies, most of which have used intravital microscopy or isolated vessel technology, are the focus of this review. The salt-induced exacerbation of hypertension in Dahl rats is due to a uniform increase in hemodynamic resistance throughout most of the peripheral vasculature. In the spinotrapezius muscle, this resistance increase is largely due to the intense constriction of proximal arterioles. The mechanisms responsible for this increased arteriolar tone include increased responsiveness to oxygen and a loss of tonic nitric oxide (NO) availability caused by reduced endothelial NO production and/or accelerated NO degradation by reactive oxygen species. Within the last decade, it has become increasingly clear that high salt intake can also lead to changes in microvascular structure and function in the absence of increased arterial pressure. This effect must also be considered when evaluating microvascular changes and their functional consequences in salt-sensitive hypertension. [source]

    Cardiovascular measures independently predict performance in a university course

    PSYCHOPHYSIOLOGY, Issue 3 2010
    Mark D. Seery
    Abstract The factors that predict academic performance are of substantial importance yet are not understood fully. This study examined the relationship between cardiovascular markers of challenge/threat motivation and university course performance. Before the first course exam, participants gave speeches on academics-relevant topics while their cardiovascular responses were recorded. Participants who exhibited cardiovascular markers of relative challenge (lower total peripheral resistance and higher cardiac output) while discussing academic interests performed better in the subsequent course than those who exhibited cardiovascular markers of relative threat. This relationship remained significant after controlling for two other important predictors of performance (college entrance exam score and academic self-efficacy). These results have implications for the challenge/threat model and for understanding academic goal pursuit. [source]

    Socioeconomic status and hemodynamic recovery from mental stress

    PSYCHOPHYSIOLOGY, Issue 2 2003
    Andrew Steptoe
    Abstract We assessed the changes in cardiac index and total peripheral resistance underlying blood pressure reactions and recovery from acute mental stress, in relation to socioeconomic status. A sample of 200 men and women aged 47,59 years was divided on the basis of occupation into higher, intermediate, and lower socioeconomic status groups. Blood pressure was monitored using the Portapres, and hemodynamic measures were derived by Modelflow processing of the arterial pressure waveform. Blood pressure increases during two stressful behavioral tasks were sustained by increases in cardiac index and total peripheral resistance. During the 45-min posttask recovery period, cardiac index fell below baseline levels, whereas peripheral resistance remained elevated. Peripheral resistance changes during recovery varied with socioeconomic status and blood pressure stress reactivity, with particularly high levels in reactive low status participants. Results are consistent with the hypothesis that disturbances of stress-related autonomic processes are relevant to the social gradient in cardiovascular disease risk. [source]

    Cardiovascular patterns associated with threat and challenge appraisals: A within-subjects analysis

    PSYCHOPHYSIOLOGY, Issue 3 2002
    Karen S. Quigley
    Previous studies demonstrated distinct cardiovascular patterns associated with threat and challenge appraisals for groups of participants. We extend these results by assessing whether appraisals continue to be associated with these cardiovascular response patterns within an individual as appraisals change. Participants completed four verbal mental arithmetic tasks for which they made appraisals before and after each task. Cardiac reactivity and total peripheral resistance (TPR) were calculated for the first and last minutes of each task, and the number of responses and percent correct were measured for each task. In line with our prediction, pretask appraisals were related to some task-related cardiac responses across the four tasks. In addition, task-related cardiovascular reactivity and behaviors both influenced appraisals following the task. Our findings suggest that an idiographic analysis of appraisals, cardiovascular physiology, and task-related behaviors provides a richer understanding of the appraisal process and reveals sex differences deserving further assessment. [source]

    Comparison of hemodynamic responses to social and nonsocial stress: Evaluation of an anger interview

    PSYCHOPHYSIOLOGY, Issue 6 2001
    Kenneth M. Prkachin
    Hemodynamic responses to an anger interview and cognitive and physical stressors were compared, and the stability of associated hemodynamic reactions examined. Participants experienced control, handgrip, counting, and mental arithmetic tests and an anger interview on two occasions. Systolic and diastolic blood pressure, heart rate, stroke volume, and cardiac output were measured. Total peripheral resistance was also derived. The anger interview produced larger, more sustained changes in blood pressure in both sessions than the other stressors. These changes were largely a consequence of increased peripheral resistance. Consistent with previous findings, handgrip was associated with a resistance-type reaction whereas arithmetic was associated with a cardiac output-type reaction. There was low-to-modest stability of hemodynamic reactions to the interview. Further research is necessary to optimize its utility in studies of cardiovascular function. Nevertheless, the findings underscore the ability of ecologically relevant stressors to provoke unique configurations of cardiovascular activity. [source]

    De novo expression of Kv6.3 contributes to changes in vascular smooth muscle cell excitability in a hypertensive mice strain

    THE JOURNAL OF PHYSIOLOGY, Issue 3 2009
    Alejandro Moreno-Domínguez
    Essential hypertension involves a gradual and sustained increase in total peripheral resistance, reflecting an increased vascular tone. This change associates with a depolarization of vascular myocytes, and relies on a change in the expression profile of voltage-dependent ion channels (mainly Ca2+ and K+ channels) that promotes arterial contraction. However, changes in expression and/or modulation of voltage-dependent K+ channels (Kv channels) are poorly defined, due to their large molecular diversity and their vascular bed-specific expression. Here we endeavor to characterize the molecular and functional expression of Kv channels in vascular smooth muscle cells (VSMCs) and their regulation in essential hypertension, by using VSMCs from resistance (mesenteric) or conduit (aortic) arteries obtained from a hypertensive inbred mice strain, BPH, and the corresponding normotensive strain, BPN. Real-time PCR reveals a differential distribution of Kv channel subunits in the different vascular beds as well as arterial bed-specific changes under hypertension. In mesenteric arteries, the most conspicuous change was the de novo expression of Kv6.3 (Kcng3) mRNA in hypertensive animals. The functional relevance of this change was studied by using patch-clamp techniques. VSMCs from BPH arteries were more depolarized than BPN ones, and showed significantly larger capacitance values. Moreover, Kv current density in BPH VSMCs is decreased mainly due to the diminished contribution of the Kv2 component. The kinetic and pharmacological profile of Kv2 currents suggests that the expression of Kv6.3 could contribute to the natural development of hypertension. [source]

    Vasomotor sympathetic neural control is maintained during sustained upright posture in humans

    THE JOURNAL OF PHYSIOLOGY, Issue 2 2006
    Qi Fu
    Vasomotor sympathetic activity plays an important role in arterial pressure maintenance via the baroreflex during acute orthostasis in humans. If orthostasis is prolonged, blood pressure may be supported additionally by humoral factors with a possible reduction in sympathetic baroreflex sensitivity. We tested the hypothesis that baroreflex control of muscle sympathetic nerve activity (MSNA) decreases during prolonged upright posture. MSNA and haemodynamics were measured supine and during 45 min 60 deg upright tilt in 13 healthy individuals. Sympathetic baroreflex sensitivity was quantified using the slope of the linear correlation between MSNA and diastolic pressure during spontaneous breathing. It was further assessed as the relationship between MSNA and stroke volume, with stroke volume derived from cardiac output (C2H2 rebreathing) and heart rate. Total peripheral resistance was calculated from mean arterial pressure and cardiac output. We found that MSNA increased from supine to upright (17 ± 8 (s.d.) versus 38 ± 12 bursts min,1; P < 0.01), and continued to increase to a smaller degree during sustained tilt (39 ± 11, 41 ± 12, 43 ± 13 and 46 ± 15 bursts min,1 after 10, 20, 30 and 45 min of tilt; between treatments P < 0.01). Sympathetic baroreflex sensitivity increased from supine to upright (,292 ± 180 versus,718 ± 362 units beat,1 mmHg,1; P < 0.01), but remained unchanged as tilting continued (,611 ± 342 and ,521 ± 221 units beat,1 mmHg,1 after 20 and 45 min of tilt; P= 0.49). For each subject, changes in MSNA were associated with changes in stroke volume (r= 0.88 ± 0.13, P < 0.05), while total peripheral resistance was related to MSNA during 45 min upright tilt (r= 0.82 ± 0.15, P < 0.05). These results suggest that the vasoconstriction initiated by sympathetic adrenergic nerves is maintained by ongoing sympathetic activation during sustained (i.e. 45 min) orthostasis without obvious changes in vasomotor sympathetic neural control. [source]

    The obligatory role of the kidney in long-term arterial blood pressure control: extending Guyton's model of the circulation

    ANAESTHESIA, Issue 11 2009
    K. L. Dorrington
    Summary We describe a model for the essential role of the kidney in long-term blood pressure regulation. We begin with a simple hydraulic model for the circulation, with a constant circulating volume. We show, with the help of a modification of Guyton's classic diagram, that cardiac output and mean arterial pressure are functions of circulating volume, peripheral resistance, venous and arterial compliances, and the cardiac Starling curve. This approach models only acute changes in a ,closed' circulation , one where there is no intake or excretion of fluid. The model is then adapted to ,open' the circulation, include a role for the kidney, and represent more chronic changes. Arterial pressure is then a sole function of renal behaviour and daily sodium (and liquid) intake, and becomes independent of other cardiovascular variables. As well as generating specific hypotheses for further investigation, these models can be used for the purpose of education in cardiovascular control and the treatment of hypertension. [source]

    On-Line Parameter Identification of Systemic Circulation Using the Delta Operator

    ARTIFICIAL ORGANS, Issue 8 2002
    Ryo Kosaka
    Abstract: To develop effective medical care with the artificial heart, we propose a new method, on-line parameter identification of the systemic circulation using the delta operator which can calculate the time-varying and unmeasured hemodynamics of the internal human body from some measured data: aortic pressure and total flow in real time. This method consists of first, a dynamic physiological model which is configured with the physiological parameters Ca (aortic compliance) and Rp (total peripheral resistance); and second, a system identification method using the delta operator. In the computer simulation study, we could confirm the effectiveness to identify the physiological parameters. In animal experiments with a left ventricular assist system, the physiological parameters, Ca = 1.8 (ml/mm Hg) and Rp = 0.8 (mm Hg s/ml), could be identified on-line. [source]

    Study of peripheral circulation in non-pregnant, pregnant and pre-eclamptic women using applied potential tomography

    AUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 4 2004
    Badreldeen AHMED
    Abstract Background:, Profound changes are known to occur in the cardiovascular system during pregnancy, involving an increase in cardiac output and a fall in peripheral resistance. In some women these adaptations may be inappropriate and this may result in pregnancy-induced hypertension and pre-eclampsia. Aims and methods:, The aims of the study were to evaluate the relatively new, non-invasive technique of applied potential tomography (APT) in measurements of peripheral blood flow, to study peripheral blood flow in a sample of non-pregnant, pregnant and pre-eclamptic women, and to investigate whether the adaptive changes in the peripheral circulation are different in pre-eclampsia compared with normal pregnancy. Applied potential tomography was used to assess peripheral vascular reactivity, by monitoring fluid distribution in calf muscles during postural change Results:, The APT technique was able to detect peripheral vasoconstriction in response to an increase in intramural pressure brought about by passive lowering of the leg (peripheral mechanisms). The peripheral vasoconstriction response was found to be more prominent in woman with pre-eclampsia. Conclusions:, The presence of a local reflex in the lower limb had been postulated and the effect of this reflex on the peripheral circulation could be detected using APT, regardless of how it was initiated. In normal pregnant women this reflex was diminished when compared to non-pregnant women, which might contribute to the reduction in peripheral vascular resistance seen in normal pregnancy. This reflex was defective in pre-eclampsia and this lack of adaptation may be a local reflex contributing to the raised peripheral resistance, which in turn may be a factor in high blood pressure in pre-eclampsia. [source]

    Oral treatment and in vitro incubation with fructose modify vascular prostanoid production in the rat

    AUTONOMIC & AUTACOID PHARMACOLOGY, Issue 1 2006
    H. A. Peredo
    Summary 1 In the rat, a fructose-enriched diet induces hyperglycaemia, hypertriglyceridaemia, insulin resistance and hypertension; a model which resembles the human metabolic syndrome. 2 Prostanoids, metabolites of arachidonic acid, include vasoactive substances synthesized and released from the vascular wall that have been implicated in the increase of peripheral resistance, one of the mechanisms involved in the fructose-induced hypertension. 3 The aim of the present study was to: (i) analyse the effects of the in vitro incubation with fructose on the production and release of prostanoids in rat thoracic aorta and in rat mesenteric bed and (ii) compare the effects of incubation with those of the in vivo acute and chronic treatment of rats with fructose and with the combination of both in vivo and in vitro procedures. 4 Blood pressure, glycaemia and triglyceridaemia were significantly elevated in both 4- and 22-week fructose-treated groups. Meanwhile, body and heart weight as well as insulinaemia were similar between experimental animals and controls. 5 In aortae, 4 weeks of Fructose treatment did not modify the prostanoid pattern release, but in vitro incubation decreased prostacyclin (PGI2) production. However, after 22 weeks, fructose treatment and incubation exerted the same effect. 6 In mesenteric bed, after 4 weeks, the incubation and the combination of both procedures reduced the release of the vasodilators PGI2 and PGE2, while fructose treatment only diminished the PGE2 release. On the contrary, the production of the vasoconstrictor thromboxane A2 (TXA2) was enhanced by incubation and both the procedures. After 22 weeks, fructose treatment increased PGI2 release, while it was reduced by incubation. The combination of both did not modify this peripheral resistance when compared with controls. Finally, incubation of tissues from treated rats increased the release of the vasoconstrictors, PGF2, and TXA2. 7 In conclusion, the mesenteric bed, a resistance vascular bed, seems to be more sensitive than the aorta, a conductance vessel, to the effects of fructose on prostanoid production. This difference could be related to a more relevant role of resistance vessels in the regulation of peripheral resistance and consequently of blood pressure. The observed effects should contribute to a shift in the balance of the release of prostanoid in favour of vasoconstrictor metabolites. This phenomenon could be related to an increase in the peripheral resistance and the mild hypertension observed in the fructose-treated rats. [source]

    Maternal cardiac function and uterine artery Doppler at 11,14 weeks in the prediction of pre-eclampsia in nulliparous women

    BJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 3 2008
    A Khaw
    Objective, To assess maternal cardiac function in nulliparous women in the first trimester of pregnancy and evaluate its potential role for predicting pre-eclampsia and small for gestational age (SGA). Design, Prospective, observational, cross-sectional study. Setting, Maternity unit of a teaching hospital. Population, Nulliparous women with singleton pregnancies presenting consecutively for routine antenatal care (n= 534). Methods, Two-dimensional and M-mode echocardiography and uterine artery Dopplers were carried out at 11-14 weeks. Main outcome measures, Cardiac output (CO), stroke volume (SV), mean arterial pressure (MAP), total vascular resistance and uterine artery pulsatility index (UAPI) were compared in four outcome groups according to the development of pre-eclampsia and/or SGA. Results, Compared with the normal outcome group (n= 457), in those with pre-eclampsia but not SGA (n = 8), CO and MAP were increased; in the group with pre-eclampsia and SGA (n= 19) MAP, TRP and UAPI were increased and in the group with SGA but no pre-eclampsia (n= 50) total peripheral resistance and UAPI were increased. Independent predictors of pre-eclampsia were MAP, SV and UAPI and of SGA SV and UAPI. Conclusions, Alterations in maternal cardiac function and UAPI are observed in the first trimester of pregnancy in nulliparous women that subsequently develop pre-eclampsia and/or SGA. [source]

    Pharmacokinetics and pharmacodynamic effects of ABT-627, an oral ETA selective endothelin antagonist, in humans

    BRITISH JOURNAL OF CLINICAL PHARMACOLOGY, Issue 6 2000
    Marianne C. Verhaar
    Aims, Endothelins (ETs) may play a role in the pathogenesis of a variety of cardiovascular diseases. The present study was designed to investigate the pharmacokinetic and pharmacodynamic effects of the orally active ETA selective receptor antagonist ABT-627 in healthy humans. Methods, Healthy volunteers were included in two studies with cross-over design. Subjects received single or multiple dose (an 8 day period) administration of oralABT-627 or matched placebo, in a dose range of 0.2,40 mg. The pharmacokinetics of ABT-627 were described and its effects on systemic haemodynamics under resting conditions and on forearm vasoconstriction in response to ET-1 were assessed. Results, ABT-627 was generally well tolerated in both studies, with transient headache being the most reported adverse event (in 62%vs 4% during placebo, P < 0.05, for Study 1 and in 42%vs 60%, P = 0.2, for Study 2). ABT-627 was rapidly absorbed, reaching maximum plasma levels at ,,1 h post dose. Single dose ABT-627, at a dose of 20 and 40 mg, inhibited ET-1 induced forearm vasoconstriction at 8 h post dose. Eight days ABT-627 treatment, at a dose level of 5 mg and above, also effectively blocked forearm vasoconstriction to ET-1. ABT-627 caused a significant reduction in peripheral resistance as compared with placebo (16 ± 1 vs 19 ± 1, 18 ± 2 vs 23 ± 3, 15 ± 1 vs 17 ± 1 AU at 1, 5, 20 mg in Study 2) with only a mild decrease in blood pressure (79 ± 2 vs 84 ± 3, 80 ± 4 vs 90 ± 5, 75 ± 3 vs 79 ± 1 at 1, 5, 20 mg in Study 2). ABT-627 caused a moderate dose-dependent increase in circulating immunoreactive ET levels (a maximal increase of 50% over baseline at the 20 mg dose level). Conclusions, The oral ETA receptor blocker ABT-627 is well tolerated, rapidly absorbed, effectively blocks ET-1 induced vasoconstriction and causes a decrease in total peripheral resistance and mean arterial pressure. Our data suggest that ABT-627 may be a valuable tool in treatment of cardiovascular disease. [source]

    Redox-dependent signalling by angiotensin II and vascular remodelling in hypertension

    CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2003
    Rhian M Touyz
    Summary 1.,Hypertension is associated with structural alterations of resistance arteries, a process known as remodelling (increased media-to-lumen ratio). 2.,At the cellular level, vascular remodelling involves changes in vascular smooth muscle cell (VSMC) growth, cell migration, inflammation and fibrosis. These processes are mediated via multiple factors, of which angiotensin (Ang) II appears to be one of the most important in hypertension. 3.,Angiotensin II signalling, via AT1 receptors, is upregulated in VSMC from resistance arteries of hypertensive patients and rats. This is associated with hyperactivation of vascular NADPH oxidase, leading to increased generation of reactive oxygen species (ROS), particularly O2, and H2O2. 4.,Reactive oxygen species function as important intracellular second messengers to activate many downstream signalling molecules, such as mitogen-activated protein kinase, protein tyrosine phosphatases, protein tyrosine kinases and transcription factors. Activation of these signalling cascades leads to VSMC growth and migration, modulation of endothelial function, expression of pro-inflammatory mediators and modification of extracellular matrix. 5.,Furthermore, ROS increase intracellular free Ca2+ concentration ([Ca2+]i), a major determinant of vascular reactivity. 6.,All these processes play major roles in vascular injury associated with hypertension. Accordingly, ROS and the signalling pathways that they modulate provide new targets to regress vascular remodelling, reduce peripheral resistance and prevent hypertensive end-organ damage. 7.,In the present review, we discuss the role of ROS as second messengers in AngII signalling and focus on the implications of these events in the processes underlying vascular remodelling in hypertension. [source]

    Circadian systemic haemodynamics in borderline and mild hypertension

    CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2000
    R. Takalo
    Circadian variations in blood pressure (BP), stroke volume (SV), heart rate (HR), cardiac output (CO) and total peripheral resistance (TPR) were determined by a pulse contour method from the intra-arterial pulse wave in 32 normotensive (NT), 32 borderline hypertensive (BHT) and 31 hypertensive (HT) middle-aged men. Daytime averages were used as the reference levels. The nocturnal decrease in BP and HR were similar in the three groups. In the night, SV did not change in the NT group, but was increased in the BHT and HT groups. The nocturnal increase in SV may reflect reduced venous capacity causing increased cardiac filling. As a consequence of the difference in SV, the nocturnal CO fall was diminished in the HT group as compared with the NT group. Moreover, TPR had a tendency to decrease in the HT group, which may be considered as a baroreflex response to buffer the expected rise in BP. Five years later, 25 NT, 24 BHT and 19 HT subjects were reassessed using casual BP measurements. In the NT and BHT groups, six and 17 subjects, respectively, had progressed to hypertension. In a logistic regression model for those who became HT, the nocturnal increase in SV was a significant predictor for future hypertension. In conclusion, the results suggest that circadian systemic haemodynamics may be altered before BP is markedly elevated, and that haemodynamic studies might be useful in predicting the development of sustained hypertension. [source]