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PubMed1992

Cardiovascular simulation using a multiple modeling method on a digital computer--simulation of interaction between the cardiovascular system and angiotensin II.

A cardiovascular system model that simulates interactive responses to drugs has been developed on a small digital computer. The overall model basically consists of three models. The first is a momentum transport model that represents relations between blood pressure and flow in the cardiovascular system. In this model, the cardiovascular system is divided into 14 components and modeled by using equivalent electrical circuits. The second is a mass transport model comprising 14 compartments corresponding to the respective components of the cardiovascular system. This model represents the distribution of the administered drug in the various cardiovascular components. The third is an interaction model that represents the relationships between the momentum and mass transport models. This model causes variations in the resistance and capacitance parameters of the momentum transport model as a function of the current drug concentrations in the appropriate compartments of the mass transport model. The capacitances representing the ventricles are varied in a time-dependent fashion to simulate the beat of the heart. Simulation is performed by using the Euler method to solve a system of 28 ordinary differential equations governing the momentum and mass transport models on a 32-bit microcomputer, a Macintosh II. The model was assessed by performing two demonstrations of the cardiovascular response to the vasopressor angiotensin II (AT II). They first examined the interaction between the cardiovascular system and AT II. The effect of AT II on the cardiovascular system was incorporated into the interaction model. Administration of AT II as a constant infusion (200 micrograms/hr) resulted in an elevation of mean arterial pressure from approximately 100 to 150 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1996

Development of an in-vitro circulatory system with known resistance and capacitance.

An in-vitro (hydrodynamic) model of the circulatory system was developed. The model consisted of a pump, compliant tubing, and valves for resistance. The model is used to simulate aortic pressure and flow. These parameters were measured using a Konigsburg Pressure transducer and a Triton ART2 flow probe. In addition, venous pressure and flow were measured on the downstream side of the resistance. The system has a known compliance and resistance. Steady and pulsatile flow tests were conducted to determine the resistance of the model. A static compliance test was used to determine the compliance of the system. The aortic pressure and flow obtained from the hydrodynamic model will be used to test the accuracy of parameter estimation models such as the 2-element and 4-element Windkessel models and the 3-element Westkessel model. Verifying analytical models used in determining total peripheral resistance (TPR) and systemic arterial compliance (SAC) is important because it provides insight into hemodynamic parameters that indicate baroreceptor responsiveness to situations such as changes in gravitational acceleration.

Animals↗
PubMed1998

Ablation of lung endothelial injury after pacing-induced heart failure is related to alterations in Ca2+ signaling.

We have previously shown that ANG II increases microvascular permeability in normal dog lungs but not after pacing-induced heart failure. This study investigated how ANG II induces permeability in isolated blood-perfused canine lung lobes and what alterations occur during heart failure. In normal lobes, the protein kinase C (PKC) inhibitors staurosporine (500 nM) or chelerythrine (10 microM) did not modify ANG II-induced increases in the capillary filtration coefficient (Kf,c, ml . min-1 . cmH2O-1 . 100 g-1; an index of microvascular permeability), suggesting that PKC is not involved. Thapsigargin (150 nM) was used to stimulate capacitative Ca2+ entry in lobes from control dogs and dogs paced at 245 beats/min for 4 wk to induce heart failure. In control lobes, Kf,c rose after thapsigargin, from 0.06 +/- 0.01 to 0.17 +/- 0.03 ml . min-1 . cmH2O-1 . 100 g-1 (mean +/- SE, P < 0.05) but did not change in the paced group. A Ca2+ ionophore, A-23187, increased Kf,c in both control (10 microM; 0.05 +/- 0.01 to 0.17 +/- 0.05 ml . min-1 . cmH2O-1 . 100 g-1, P < 0.05) and pace (5 microM; 0.06 +/- 0.01 to 0. 21 +/- 0.07 ml . min-1 . cmH2O-1 . 100 g-1, P < 0.05) lobes, indicating that increasing intracellular Ca2+ is sufficient to induce pulmonary microvascular permeability after pacing. We conclude that during heart failure, Ca2+ signaling within the pulmonary microvascular endothelium is altered.

Alkaloids↗
PubMed2006

Dynamics of water transport and storage in conifers studied with deuterium and heat tracing techniques.

The volume and complexity of their vascular systems make the dynamics of long-distance water transport in large trees difficult to study. We used heat and deuterated water (D2)) as tracers to characterize whole-tree water transport and storage properties in individual trees belonging to the coniferous species Pseudotsuga menziesii (Mirb.) Franco and Tsuga heterophylla (Raf.) Sarg. The trees used in this study spanned a broad range of height (13.5-58 m) and diameter (0.14-1.43 m). Sap flow was monitored continuously with heat dissipation probes near the base of the trunk prior to, during and following injection of D2O. The transit time for D2O transport from the base of the trunk to the upper crown and the tracer residence time were determined by measuring hydrogen isotope ratios in water extracted from leaves sampled at regular intervals. Transit times for arrival of D2O in the upper crown ranged from 2.5 to 21 d and residence times ranged from 36 to 79 d. Estimates of maximum sap velocity derived from tracer transit times and path length ranged from 2.4 to 5.4 m d(-1). Tracer residence time and half-life increased as tree diameter increased, independent of species. Species-independent scaling of tracer velocity with sapwood-specific conductivity was also observed. When data from this study were combined with similar data from an earlier study of four tropical angiosperm trees, species-independent scaling of tracer velocity and residence time with sapwood hydraulic capacitance was observed. Sapwood capacitance is an intrinsic tissue-level property that appears to govern whole-tree water transport in a similar manner among both tracheid- and vessel-bearing species.

Biological Transport↗
PubMed1987

Time-dependent coronary blood flow distribution in left ventricular wall.

A mathematical model of the coronary circulation in the left ventricular (LV) wall, which describes the time-dependent local blood perfusion throughout the myocardium and the coronary flow in the epicardial vessels, is presented. The myocardial perfusion is essentially controlled by the intramyocardial resistance and the coronary pressure driving force, whereas the epicardial arterial flow is dominated by the epicardial and intramyocardial arterial capacitance and the local transmural pressure on the vessels. The temporal and spatial intramural pressure [P im(y,t)], calculated based on a nested-shell spheroidal model of the LV, is used to evaluate the local intramural resistance to flow and the corresponding zero flow pressure. The calculation of the instantaneous flow in each layer is based on a local, time-dependent modification of the back-pressure concept. A function representing the local tonus of the small blood vessels [T wf(y)] is used to adjust the average coronary flow rate to the metabolic demand of each layer. The calculated results are compared with experimental data, and the assumptions of the model are examined against a variety of experimental conditions. The model provides a qualitative tool for comprehending the distributed flow phenomenon within the myocardium and its relation to cardiac mechanics and autoregulation.

Blood Pressure↗
PubMed1990

Analysis and prediction of left ventricular performance under load changes during cardiac catheterization.

The applicability of a computer model, which relates the transmural mechanical distribution in the left ventricle (LV) to its global function at different loading conditions, was evaluated in patients with normal to near normal LV function undergoing cardiac catheterization. Left ventriculography and measurements of aortic and LV pressures were performed at baseline conditions and repeated following rapid volume expansion with intravenous infusion of 250 to 300 ml of physiologic saline and also after sublingual isosorbide-dinitrate (ISDN) administration. Twenty patients (18 men and 2 women, average age = 53 years) underwent coronary angiography and left ventriculography. Sixteen patients had coronary artery disease with one- to three-vessel involvement and 4 had normal coronary arteries. The measured input data into the model included the end-diastolic LV volume and wall thickness, aortic pressure, heart rate, and the peripheral resistance. The model parameters of myocardial contractility and arterial system capacitance for the control baseline conditions were estimated so that an accurate match was obtained between the predicted and the measured end-systolic (ES) volume and pressure. Using these parameters, model predictions for the two load perturbations were compared to the measurements. An excellent correlation was found between the predicted and measured LV ES volumes and peak-systolic pressures (PSP) (R2 greater than 0.994). In four patients, who developed ischemic symptoms during saline injection, the prediction of end-systole volumes were lower than the measured values, suggesting an actual reduction in contractility during acute ischemia. Therefore, the model is sensitive to contractility changes. The model predicts global LV performance, under different loading conditions, including stroke work, peak developed wall stress, velocity of fiber shortening, and myocardial oxygen consumption.

Cardiac Catheterization↗
PubMed2001

Gender influences coronary L-type Ca(2+) current and adaptation to exercise training in miniature swine.

Endurance exercise training increases smooth muscle L-type Ca(2+) current density in both resistance and proximal coronary arteries of female miniature swine. The purpose of the present study was to determine 1) whether gender differences exist in coronary smooth muscle (CSM) L-type Ca(2+) current density and 2) whether endurance training in males would demonstrate a similar adaptive response as females. Proximal, conduit (approximately 1.0 mm), and resistance [~200 microm (internal diameter)] coronary arteries were obtained from sedentary and treadmill-trained swine of both sexes. CSM were isolated by enzymatic digestion (collagenase plus elastase), and voltage-gated Ca(2+)-channel current (I(Ca)) was determined by using whole cell voltage clamp during superfusion with 75 mM tetraethylammonium chloride and 10 mM BaCl(2). Current-voltage relationships were obtained at test potentials from -60 to 70 mV from a holding potential of -80 mV, and I(Ca) was normalized to cell capacitance (pA/pF). Endurance treadmill training resulted in similar increases in heart weight-to-body weight ratio, endurance time, and skeletal muscle citrate synthase activity in male and female swine. I(Ca) density was significantly greater in males compared with females in both conduit (-7.57 +/- 0.58 vs. -4.14 +/- 0.47 pA/pF) and resistance arteries (-11.25 +/- 0.74 vs. -6.49 +/- 0.87 pA/pF, respectively). In addition, voltage-dependent activation of I(Ca) in resistance arteries was shifted to more negative membrane potentials in males. Exercise training significantly increased I(Ca) density in both conduit and resistance arteries in females (-7.01 +/- 0.47 and -9.73 +/- 1.13 pA/pF, respectively) but had no effect in males (-8.61 +/- 0.50 and -12.04 +/- 1.07 pA/pF, respectively). Thus gender plays a significant role in determining both the magnitude and voltage dependence of I(Ca) in CSM and the adaptive response of I(Ca) to endurance training.

Adaptation, Physiological↗
PubMedDate not supplied

Model based sensitivity analysis of arterial pressure response to hemodialysis induced hypovolemia.

The role of hemodynamic and regulatory factors in the arterial pressure response to hemodialysis induced hypovolemia was investigated by means of a computer model of the cardiovascular system, including the main short-term pressure regulatory mechanisms. The model mimics the arterial and venous systemic circulation, Starling's law and inotropic heart regulation, arterial and cardiopulmonary baroreflex controls of resistance, and capacitance vessels. All of the model parameters have a clear physiologic meaning: 10 represent the systemic circulation, 4 describe cardiac pump performance, and 3 characterize baroreflex regulation. Sensitivity analysis is performed to determine the effect of each parameter on the pressure response to mild hypovolemia (a 10% blood volume reduction after 4 hours). The results demonstrate that circulatory parameters, such as resistances and compliances, have no relevant effect upon the pressure response. Conversely, regulation of venous capacity seems to play a pivotal role in sustaining arterial pressure during hemodialysis induced hypovolemia. Regulation of systemic peripheral resistance exerts a compensatory action only as long as the blood volume reduction is < 5%, but it is inadequate to compensate for a larger blood volume reduction when venous capacity regulation is absent. A paradoxical arterial pressure increase during hypovolemia can be referred to a prevalence of cardiopulmonary afferences in the regulatory process.

Blood Pressure↗
PubMed1977

Hemodynamic advantage of combined administration of hydralazine orally and nitrates nonparenterally in the vasodilator therapy of chronic heart failure.

Patients with severe left ventricular failure generally have both reduced cardiac output and increased pulmonary and systemic venous pressures. A study was therefore made of the use of combined vasodilator therapy with nonparenterally administered nitrates, which act primarily on venous capacitance vessels and thus reduce preload, and orally administered hydralazine, which acts on arteriolar resistance vessels and thus reduces afterload. Twelve patients with chronic refractory heart failure were given these drugs individually and in combination during continuous hemodynamic monitoring. Heart rate and arterial pressure did not change significantly. Nitrates significantly reduced filling pressures of both ventricles without affecting cardiac index. Hydralazine did not alter filling pressures but dramatically increased cardiac index. The hemodynamic effects of each drug were additive during combined therapy, resulting in a 36 percent (28 to 18 mm Hg) mean decrease in left ventricular filling pressure and a 58 percent (2.1 to 3.3 liters/min per m(2)) mean increase in cardiac index. The seven patients who have continued to receive combined therapy for 3 to 10 months have shown sustained clinical improvement.

Administration, Oral↗
PubMed2005

Contribution of capacitative and non-capacitative Ca2+-entry to M3-receptor-mediated contraction of porcine coronary smooth muscle.

We studied the contribution of store-operated or capacitative Ca2+-entry (SOCE or CCE, respectively) through store-operated Ca2+ channels (SOCCs) and the contribution of Ca2+-entry through receptor-operated, non-selective cation channels (ROCCs or NSCCs, respectively), on the M3-receptor-mediated (270 nM Ach) contractile response of porcine coronary smooth muscle strips by means of the respective inhibitors. In the presence of L-VOCC blockade (1 microM verapamil), LOE 908 (inhibition of NSCCs) decreased the contractile response to 75+/-5% (p<0.01, n=6), 2-APB (inhibition of SOCCs) and SK and F 96365 (inhibition of SOCCs and of NSCCs) decreased the response to 45+/-4% (p<0.001, n=10) and to 23+/-2% (p<0.001, n=5), respectively (control: Ach response in the presence of verapamil alone). In the absence of L-VOCC blockade, LOE 908 reduced the Ach-response to 49+/-7% (p<0.001, n=8) and SK and F 96365 to 3+/-2% (p<0.001, n=4) of control, whereas 2-APB transiently increased the response (peak effect: 130+/-11%; p<0.05, n=8). We conclude: (1) the main source of activator Ca2+ during the M3-receptor-mediated contractile response is the Ca2+ influx through L-VOCCs; (2) however, in the presence of L-VOCC blockade, the contractile response is mainly due to Ca2+-entry through SOCCs; (3) NSCCs may be considerably involved in M3-receptor-mediated contraction as they may serve to depolarize the membrane potential and, thus, to open L-VOCCs; (4) in primary tissue of vascular smooth muscle, both, SOCE and Ca2+-entry through NSCCs are activated during M3-receptor stimulation.

Acetamides↗
PubMed2001

Calcium influx, arachidonic acid,and control of endothelial cell proliferation.

Recent evidences suggest a role for arachidonic acid (AA) in the triggering of store-independent, ornon-capacitative, calcium entry in different cell types. Here, using patch clamp and fluorimetric single-cell calcium measurements, we provide evidence for AA-activated calcium influx in bovine aortic endothelial cells (BAEC). AA-activated calcium entry is independent from intracellular calcium stores depletion at low doses of the fatty acid (< 5 microM) and insensitive to a decrease of pH to 6.7. Single-channel analysis in inside-out configuration reveals the presence of a family of AA-activated calcium-permeable channels, with different conductances and reversal potentials. Treatment with AA or ETYA induces a proliferative effect, significantly affected by external EGTA application during the early period (up to 2h) of stimulation with the agonists. We conclude that low concentrations of arachidonic acid are able to evoke a store-independent calcium influx, exerting a mitogenic role in BAECs.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1997

Nitric oxide induces transient Ca2+ changes in endothelial cells independent of cGMP.

Ca2+ changes induced by nitric oxide (NO.) were investigated in cultured human endothelial cells. Sodium nitroprusside (SNP) (1-100 mumol/L) and S-Nitroso-N-acetylpenicillamine (SNAP) (100 mumol/L) were used as NO. donors. The cytoplasmatic Ca2+ concentration was calculated using ratiometric FURA2 fluorescence measurements. Both NO. donors caused transient oscillatory Ca2+ changes, which were not detectable in the presence of oxyhemoglobin (50 mumol/L). Digital ratio imaging revealed initiation sites within cells where Ca2+ increases started spreading, which indicates that nonuniformly distributed targets might be involved in these reactions. Calcium was released from intracellular stores as indicated by experiments performed in Ca(2+)-free buffer. L-type Ca(2+)-channel blocker diltiazem (100 mumol/L) was not able to block these responses. NO.-induced Ca2+ release from intracellular stores caused capacitative Ca2+ entry. Both thapsigargin (1 mumol/L) and cyclopiazonic acid (10 mumol/L) inhibited the SNP response completely, whereas neither ryanodine (up to 100 mumol/L) nor dantrolene (100 mumol/L) was able to inhibit Ca2+ changes induced by SNP, indicating that primarily inositol 1,4,5-triphosphate (IP3)-dependent stores are released upon stimulation with NO.. A small inhibitory effect of ATP- and SNP-induced peak [Ca2+]i increase was measured in the presence of both caffeine (20 mmol/L) and procaine (1 mmol/L). Evidence is presented that cGMP is not involved in NO.-induced Ca2+ signals, as neither inhibitors of guanylate cyclase (methylene blue and LY 83583) nor cell permeant analogues of cGMP altered or simulated [Ca2+] changes. An inhibitor of cGMP-dependent protein kinase was also ineffective. We therefore propose that endothelial cells have specific targets proximal or at IP3 receptors to induce Ca2+ changes in endothelial cells stimulated with NO..

Adenosine Triphosphate↗
PubMed1987

Basic electrical parameters for safe and effective electro-therapeutics [electro-acupuncture, TES, TENMS (or TEMS), TENS and electro-magnetic field stimulation with or without drug field] for pain, neuromuscular skeletal problems, and circulatory disturbances.

Using voltage-time-dependent negative resistance characteristics of Voltage-Current curves of excitable cell membranes estimated without using artificial voltage clamp method, the author made a quantitative analysis of excitability of cell membranes and different conditions of transmembrane action potentials as a bias voltage to the negative resistance of the excitable cell membrane. The pacemaker cells were classified as "Astable Oscillators" and nonpacemaker excitable cells as "Monostable Oscillators," and application of a rapidly changing electromagnetic field to the cells was analyzed as a means of stimulating the cells. The understanding of the 10 essential electrical parameters is highly desirable for safe and effective electrical stimulation. Among these, emphasis was placed on the often neglected, important electrical parameters of "output impedance" of stimulation pulse wave complexes for + and - polarity components, as well as the importance of capacitive current (Ic = C.dV/dt) which depends on rise time as well as fall time of the stimulation pulse wave, and undesirable side effects of electrolysis phenomena due to excessive D.C. current. The difference and similarity between TENS (Transcutaneous Nerve Stimulation) and TES (Transcutaneous Electrical Stimulation), TENMS (Transcutaneous Electrical Nerve and Muscle Stimulation) or TMS (Transcutaneous Muscle Stimulation) was discussed. The author's clinical study indicated that effective TES (TENMS)--characterized by effective muscle contraction without creating pain with a pulse repetition rate approximately the same as the heart rate of the individual--can often give superior beneficial effects in improvement of micro-circulation and subsequent relief of pain and other symptoms compared with TENS that creates stimulation of large diameter sensory nerve fibers without creating significant muscle contraction. Such improvement is often accompanied by the abolishment of the pain with disappearance of local substance P and increase in local serotonin with disappearance of local L-tryptophan.

Acupuncture Therapy↗
PubMed2004

Targeted ablation of plasma membrane Ca2+-ATPase (PMCA) 1 and 4 indicates a major housekeeping function for PMCA1 and a critical role in hyperactivated sperm motility and male fertility for PMCA4.

The relative importance of plasma membrane Ca2+-ATPase (PMCA) 1 and PMCA4 was assessed in mice carrying null mutations in their genes (Atp2b1 and Atp2b4). Loss of both copies of the gene encoding PMCA1 caused embryolethality, whereas heterozygous mutants had no overt disease phenotype. Despite widespread and abundant expression of PMCA4, PMCA4 null (Pmca4-/-) mutants exhibited no embryolethality and appeared outwardly normal. Loss of PMCA4 impaired phasic contractions and caused apoptosis in portal vein smooth muscle in vitro; however, this phenotype was dependent on the mouse strain being employed. Pmca4-/- mice on a Black Swiss background did not exhibit the phenotype unless they also carried a null mutation in one copy of the Pmca1 gene. Pmca4-/- male mice were infertile but had normal spermatogenesis and mating behavior. Pmca4-/- sperm that had not undergone capacitation exhibited normal motility but could not achieve hyperactivated motility needed to traverse the female genital tract. Ultrastructure of the motility apparatus in Pmca4-/- sperm tails was normal, but an increased incidence of mitochondrial condensation indicated Ca2+ overload. Immunoblotting and immunohistochemistry showed that PMCA4 is the most abundant isoform in testis and sperm and that it is localized to the principle piece of the sperm tail, which is also the location of the major Ca2+ channel (CatSper) required for sperm motility. These results are consistent with an essential housekeeping or developmental function for PMCA1, but not PMCA4, and show that PMCA4 expression in the principle piece of the sperm tail is essential for hyperactivated motility and male fertility.

Alleles↗
PubMedDate not supplied

Pulmonary capillary pressure. A review.

Pulmonary capillary pressure (Pcap) is the predominant force that drives fluid out of the pulmonary capillaries into the interstitium. Increasing hydrostatic capillary pressure is directly proportional to the lung's transvascular filtration rate, and in the extreme leads to pulmonary edema. In the pulmonary circulation, blood flow arises from the transpulmonary pressure gradient, defined as the difference between pulmonary artery (diastolic) pressure and left atrial pressure. The resistance across the pulmonary vasculature consists of arterial and venous components, which interact with the capacitance of the compliant pulmonary capillaries. In pathological states such as acute respiratory distress syndrome, sepsis, and high altitude or neurogenic lung edema, the longitudinal distribution of the precapillary arterial and the postcapillary venous resistance varies. Subsequently, the relationship between Pcap and pulmonary artery occlusion pressure (PAOP) is greatly variable and Pcap can no longer be predicted from PAOP. In clinical practice, PAOP is commonly used to guide fluid therapy, and Pcap as a hemodynamic target is rarely assessed. This approach is potentially misleading. In the presence of a normal PAOP and an increased pressure gradient between Pcap and PAOP, the tendency for fluid leakage in the capillaries and subsequent edema development may substantially be underestimated. Tho-roughly validated methods have been developed to assess Pcap in humans. At the bedside, measurement of Pcap can easily be determined by analyzing a pressure transient after an acute pulmonary artery occlusion with the balloon of a Swan-Ganz catheter.

Algorithms↗
PubMed1985

Isosorbide dinitrate and glyceryl trinitrate: demonstration of cross tolerance in the capacitance vessels.

Cross tolerance to the arterial effects of sublingual glyceryl trinitrate (GTN) has been demonstrated in subjects taking oral isosorbide dinitrate (ISDN). To determine if cross tolerance also develops in the venous system, the effects of 0.6 mg of GTN on venous capacitance were assessed before (stage A) and during (stage B) therapy with ISDN. Venous capacitance was assessed using the radionuclide blood pool method, with relative changes in regional blood volume measured in the forearm in 6 patients and the splanchnic circulation in 4 patients. Heart rate, blood pressure and blood volume were measured before and at 1-minute intervals for 10 minutes after GTN; there was less than 2% variability in regional blood volume during 6 control measurements. During stage A, 5 minutes after GTN, systolic blood pressure (mean +/- standard deviation) decreased by 14% (from 125 +/- 15 to 107 +/- 19 mm Hg, p less than 0.01) and heart rate increased by 17% (from 68 +/- 14 to 80 +/- 17 beats/min, p less than 0.001), while regional blood volume increased to 101 +/- 2% at 1 minute (difference not significant [NS]), 111 +/- 2% at 5 minutes (p less than 0.001) and 107 +/- 3% at 10 minutes (p less than 0.01) relative to baseline measurements.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Effects of a calcium entry blocker on cerebral circulation in essential hypertension.

The acute effects of the calcium entry blocker, nifedipine, on cerebral circulation were studied in 22 patients (56 +/- 5 years) with essential hypertension (EHT, WHO I-II) and 12 age-matched normal subjects. Cerebral effects were reevaluated in sixteen EHT patients after 8 weeks of treatment. The cerebrovascular resistance (Rp), cerebral capacitance (Cp), carotid velocity, and flow volume were measured by a newly developed ultrasonic volume flow meter coupled with a built-in computer which calculates Rp and Cp based on a simulated model. In EHT, acute administration of nifedipine (10 mg orally) decreased Rp from 13.5 +/- 1.8 to 8.0 +/- 0.3 (p less than 0.01) and increased Cp from 22.8 +/- 3.3 to 54.9 +/- 5.2 mFc (p less than 0.01). The carotid blood flow and velocity increased by 25.7% and 22.9%, respectively (p less than 0.05) in the face of lowered arterial pressure. In normal subjects, nifedipine also decreased Rp and increased Cp but to a lesser degree compared with EHT. The acute changes in cerebrovascular circulation in EHT were maintained at 8 weeks of treatment. These results suggest that nifedipine reduces Rp, possibly as the consequence of systemic hypotension and direct vasodilation of the cerebral arteries. This may be beneficial for hypertensive patients.

Adult↗
PubMed2006

Vasodilation and visceral fat in elderly subjects: the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) study.

BACKGROUND: Although obesity has long been recognised as a cardiovascular risk factor, only in recent years has the role of visceral adipose tissue (VAT) been evaluated. In the Prospective Study of the Vasculature in Uppsala Seniors (PIVUS) study, we related VAT and other obesity indices to endothelium-dependent vasodilation in both capacitance and resistance arteries. METHODS AND RESULTS: In this population-based study, 1016 subjects aged 70 were evaluated by the invasive forearm technique with acetylcholine (EDV) and brachial artery ultrasound to assess flow-mediated vasodilation (FMD). Intra-abdominal visceral (VAT) and subcutaneous adipose tissue (SAT) were determined by magnetic resonance imaging in a random sample of 287 subjects. EDV, but not FMD, was inversely related to VAT, SAT, BMI and the waist/hip ratio (r=-0.23, -0.16, -0.21 and -0.11, respectively, p=0.05-0.001 after adjustment for gender). In multiple regression analysis however, only VAT was an independent predictor of EDV. Similar results were obtained for endothelium-independent vasodilation (EIDV, infusion of sodium nitroprusside in the brachial artery). CONCLUSIONS: Both endothelium-dependent and independent vasodilation in the forearm resistance arteries, but not FMD in the brachial artery, was reduced in elderly subjects with increased intra-abdominal adipose tissue mass. This finding suggests deterioration in general vasoreactivity mainly in resistance arteries in elderly subjects with intra-abdominal obesity.

Aged↗