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PubMed1993

Effects of spiraprilat, an angiotensin-converting enzyme inhibitor, on anesthetized dogs in a new model of acute left ventricular failure.

Spiraprilat, a new angiotensin-converting enzyme (ACE) inhibitor, was compared with enalaprilat for its ability to improve left ventricular (LV) function and metabolism in anesthetized open-chest dogs with a new model of acute LV failure (ALVF) induced by embolization of the left coronary artery with 50 microns plastic microspheres followed by intravenous (i.v.) infusion of methoxamine. With this procedure, LV end-diastolic pressure (LVEDP) increased from 4.2 +/- 0.7 to 12.8 +/- 1.3 mm Hg and remained at approximately 12 mm Hg throughout the experiment. Cardiac output (CO) decreased from 1.25 +/- 0.12 to 0.79 +/- 0.06 and 0.55 +/- 0.02 L/min at 30 and 90 min after methoxamine infusion, respectively. LVdP/dtmax and dP/dt/P decreased, while total peripheral resistance (TPR) increased. These hemodynamic changes indicated establishment of stable ALVF of a moderate degree. Moreover, decreases in myocardial lactate consumption and contents of creatine phosphate in the myocardium indicated the existence of moderate ischemia. The new ACE inhibitor, spiraprilat, as well as enalaprilat (30 micrograms/kg i.v.) effectively decreased mean aortic pressure (30%), LVEDP (20%), and TPR (30%) and increased stroke volume (SV) CO, and dP/dt/P. Both agents decreased myocardial oxygen consumption (20%) and caused a significant increase in myocardial creatine phosphate contents. These data indicate that the beneficial effects of both inhibitors extended not only to LV function but also to myocardial energy metabolism in ALVF.

Adenosine Triphosphate↗

PubMed1993

Potent hemodynamic effects of bimakalim, a new potassium channel opener, in humans.

The cardiac hemodynamic effects of bimakalim, a new potassium channel opener, were evaluated in 12 normal volunteers by echocardiography (ECHO)/Doppler in a placebo-controlled, randomized double-blind, cross-over, dose-ranging study. A single oral dose (0.25-1 mg) was given at weekly intervals. Hemodynamic measurements were made at 0, 90, 120, and 240 min after drug intake and ECHO/Doppler was performed at 0 and 90 min. Reproducibility of the ECHO/Doppler study was assessed by comparing predose baseline values of the four different phases of treatment (placebo and 0.25, 0.5, and 1 mg) by analysis of variance (ANOVA), which showed no significant differences for left ventricular ejection fraction (LVEF). Doppler-derived stroke volume (SV), total peripheral resistance (TPR), and peak mitral early to late velocity ratio (PEV/PAV). ANOVA showed significant increases in LVEF (p = 0.0003) and SV (p = 0.03), however, and decreases in TPR (p = 0.002) and PEV/PAV (p = 0.005) after bimakalim treatment. Heart rate (HR) showed a dose-dependent increase, but systolic and diastolic blood pressure (SBP, DBP) did not change with bimakalim. Despite vasodilatory headaches, none of the volunteers discontinued the study. Bimakalim appears to be a potent vasodilating drug that may have an important role in management of patients with compromised LV function.

Administration, Oral↗

PubMed1994

Endothelin-1 causes a biphasic response in systemic vasculature and increases myocardial contractility in conscious rabbits.

We studied the effects of an intravenous (i.v.) bolus of endothelin-1 (ET-1, 0.2 nmol/kg) in conscious rabbits, measuring arterial blood pressure (BP), heart rate (HR), myocardial contractility, and cardiac output and evaluating direct and indirect effects of ET-1 with pacing and pharmacologic antagonists. ET-1 caused a brief initial decrease in BP of 18 +/- 1 mm Hg, followed by a sustained increase of 26 +/- 3 mm Hg (n = 16, p < 0.001). HR increased initially by 60 +/- 11 beats/min and then decreased by 68 +/- 6 beats/min (n = 16, p < 0.001). Left ventricular (LV) dP/dt increased by 2,120 +/- 380 mm Hg/s (n = 5, p < 0.01). LV end-diastolic pressure (LVEDP) increased by 4 +/- 1 mm Hg (n = 5, p < 0.05). Cardiac output (CO) increased initially by 34 +/- 4% and then decreased by 28 +/- 3% (n = 16, p < 0.001). Total peripheral resistance (TPR) decreased initially by 34 +/- 3% and then increased by 72 +/- 13% (n = 16, p < 0.001). Pacing did not alter the effect of ET-1 on arterial BP, LVdP/dt, or LVEDP. The combination of propranolol and scopolamine significantly reduced the increase and decrease in HR and the increase in LVdP/dt. None of the antagonists significantly altered the effect of ET-1 on TPR. ET-1 causes brief initial vasodilation and increased myocardial contractility, followed by sustained vasoconstriction. The vascular effects appear to be of greater significance than the cardiac effects at the dose used.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Effect of various angiotensin receptor antagonists on cardiovascular responses to angiotensin II in pithed rats.

The effects of four nonpeptide angiotensin receptor antagonists, i.e., losartan (AT1) PD123177 (AT2), and 4'-[(2-n-butyl-6-cyclohexylaminocarbonylamino-benzimidazole-1-yl)- methyl]biphenyl-carboxylic acid (BIBS 39; AT1 and AT2), and 2-n-butyl-1-[4-(6-carboxy-2,5-di-chlorbenzoylamino)-benzyl]-6-N- (methylaminocarbonyl)-n-pentylamino-benzimidazole (BIBS 222; AT1 and AT2) on cardiovascular responses to angiotensin II (AII) were investigated in propranolol-pretreated pithed rats. AII (0.01-10 nmol/kg intravenously, i.v.) induced a dose-dependent increase in diastolic blood pressure (DBP), the rate of increase in left ventricular pressure (LVdP/dtmax), cardiac output (CO), and total peripheral resistance (TPR) without changing LV end-diastolic pressure (LVEDP) or heart rate (HR). Losartan 3 and 10 mg/kg i.v. caused dose-dependent parallel rightward shifts of the dose-response curves (DBP and LVdP/dtmax) without altering the maximal responses to AII. PD123177 (100 mg/kg i.v.) did not influence the dose-response curves for AII significantly. BIBS 39 (1, 3, and 10 mg/kg i.v.) and BIBS 222 (1, 3, and 10 mg/kg, i.v.) shifted the dose-response curves (DBP and LVdP/dtmax) for AII to the right. Although these two compounds (BIBS 39 1, 3, and 10 mg/kg and BIBS 222 1 and 3 mg/kg) did not alter the maximal increase in DBP to angiotensin AII, they decreased the maximal increase in LVdP/dtmax by approximately 35%. BIBS 39 (3 and 10 mg/kg) significantly reduced the increase in CO caused by AII and therefore mean arterial pressure (MAP), whereas the AII-induced increase in TPR remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1995

Cardiovascular effects of the novel potassium channel opener UR-8225.

We compared the hemodynamic and electrophysiological effects of UR-8225, a new potassium channel opener with those of levcromakalim. UR-8225 and levcromakalim (0.03-1 mg/kg) dose-dependently decreased mean arterial pressure (MAP) in conscious spontaneously hypertensive rats (SHR) and deoxycorticosterone-salt (DOCA) hypertensive rats and in conscious and anesthetized normotensive rats. The decrease in MAP was accompanied by a dose-dependent increase in heart rate (HR). Levcromakalim was about twice as potent as an antihypertensive agent, and its hypotensive and tachycardic effects were of longer duration than those of UR-8225. In conscious normotensive rats, the hypotensive response to UR-8225 (1 mg/kg) did not diminish with repeated dosing for 16 days. In conscious SHR, propranolol antagonized the tachycardic response of UR-8225 without affecting its hypotensive response. In anesthetized rats, glibenclamide (3, 10, and 20 mg/kg) dose-dependently reduced the hypotensive effect of the drug. In anesthetized dogs, UR-8225 and levcromakalim (0.01-30 micrograms/kg) dose-dependently decreased MAP and total peripheral resistance (TPR): UR-8225 was approximately 10 times less potent than potent than levcromakalim. UR-8225 had no effect on HR, left ventricular end-diastolic pressure (LVEDP), stroke volume (SV), or cardiac output (CO) but decreased rate-pressure product (RPP) and cardiac work (CW). In contrast, levcromakalim decreased HR, RPP, and CW and increased SV and LVEDP, whereas CO remained unaltered. UR-8225 and levcromakalim (0.1-10 microM) had no effect on the ventricular action potentials (APs), whereas at higher concentrations they shortened the AP duration (APD), an effect that was antagonized by glibenclamide. UR-8225 and levcromakalim decreased the Vmax and shortened the APD of the slow ventricular APs elicited by isoprenaline in K(+)-depolarized ventricular muscle fibers. These results indicated that UR-8225 decreases blood pressure (BP) by reducing TPR. Its electrophysiological and hemodynamic effects were blocked by glibenclamide, which suggests that they may be mediated largely through the activation of ATP-sensitive K+ channels.

Action Potentials↗

PubMed1995

Effects of ketanserin on heart rate and blood pressure variability: implications for the effect on the baroreflex mechanisms.

Ketanserin is an antihypertensive drug with affinity to both serotonin S2- and alpha 1-adrenoceptors. The specific effects of ketanserin on the baroreflex are not fully understood. We, therefore, studied baroreflex regulation based on blood pressure (BP) and heart rate (HR) responses to several maneuvers before and after the administration of 2 x 5 mg of ketanserin i.v. both in supine and in standing posture. Seven young healthy volunteers were investigated. We measured spontaneous variability in HR and BP (Finapres), and performed deep inspiration, Valsalva, and lying-to-standing tests. We also used a modified Valsalva maneuver that consist of Deep Inspiration Breath-holding with closed glottis and EXpiration: DIBEX maneuver. From the BP recordings, peripheral resistance (TPR) and stroke volume (SV) were estimated by the Modelflow method. Thirty minutes after the administration of ketanserin, there was no significant change in mean HR, BP, spectral power of HR and BP variability, baroreflex sensitivity, or Valsalva ratio. Thus ketanserin did not affect the cardiac baroreflex mechanism. However, in standing position, SV increased and TPR decreased under the influence of ketanserin, and BP overshoot after the Valsalva and DIBEX maneuver was significantly decreased as well. There was also no reflex recovery of BP during the DIBEX maneuver in three volunteers, who felt faint. These observations indicate that there is a lack of vasoconstriction. We conclude that ketanserin is not a vasodilator but seems to inhibit vasoconstriction.

Adult↗

PubMed1999

Protective effects of endothelin receptor antagonists in dogs with aortic cross-clamping.

Endothelin (ET) may play an important role in the pathogenesis of vasoconstriction and acute renal failure after aortic cross-clamping (ACC). However, the relative contribution of the ET(A) and ET(B) receptors to the physiopathology of ischemic acute renal failure is poorly understood. This study was carried out to evaluate the potential protective effect of a selective ET(A) antagonist versus combined ET(A)/ET(B) antagonist on altered systemic, pulmonary, and renal hemodynamics induced by cross-clamping the suprarenal aorta for 1 h, followed by 2-h reperfusion. Studies were performed in three groups of anesthetized mongrel dogs. After baseline measurements, treatment (3 mg/kg i.v. bolus + 3 mg/kg/h infusion) with either a selective ET(A) antagonist, Ro 61-1790 (n = 5), or a combined ET(A)/ET(B) antagonist, bosentan (n = 5) or vehicle (n = 8) was initiated 5 min before ACC. There were marked increases in total peripheral (TPR), pulmonary (PVR), and renal (RVR) vascular resistances, and significant decreases in cardiac output (CO) and glomerular filtration rate (GFR) and tubular sodium reabsorption after ACC in the vehicle group. Both Ro 61-1790 and bosentan prevented the marked increases in TPR, PRV, and RVR, and attenuated the declines in CO, GFR, and tubular sodium reabsorption. We concluded that the profound systemic, pulmonary, and renal vasoconstriction, as well as the impairments in glomerular and tubular functions associated with ACC, is mostly ET mediated and that the ET(A) receptor activation makes a major contribution to the ET-mediated impairments of hemodynamics and renal function after ACC.

Acute Kidney Injury↗

PubMed2002

Use of A-192621 and IRL-2500 to unmask the mesenteric and renal vasodilator role of endothelin ET(B) receptors.

Endothelin-1 (ET-1) is known to cause a transient (<1 min) depressor followed by a sustained (>1 h) pressor response. The former through the activation of ET(B) receptors, and the latter through the activation of ET(A) and ET(B) receptors. This study examines if ET(B) receptors mediate sustained mesenteric and renal dilation in anesthetized rats. Intravenous bolus ET-1 (0.8, 1.4, and 2 nmol/kg) and IRL-1620 (ET(B) agonist, 2, 5, and 10 nmol/kg) caused transient decrease followed by sustained increases in mean arterial pressure (MAP) that were accompanied by increases in total peripheral resistance (TPR), reductions in cardiac output (CO), and mesenteric and renal vasoconstriction. Pretreatment with FR-139317 (ET(A) antagonist, 1 mg/kg) attenuated the pressor and constrictor effects of ET-1 but did not alter responses to IRL-1620. IRL-2500 (ET(B) antagonist, 5 mg/kg) slightly inhibited the renal constrictor effect of IRL-1620, whereas A-192621 (ET(B) antagonist, 5 mg/kg) abolished all hemodynamic responses to IRL-1620. Both IRL-2500 and A-192621 markedly enhanced MAP, TPR, and mesenteric, and the renal constrictor effects of ET-1. Therefore, A-192621 was more effective than IRL-2500 in blocking IRL-1620-induced vasoconstriction, but both augmented constrictor responses to ET-1. The potentiation of ET-1-induced vasoconstriction by ET(B) receptor antagonists revealed a sustained vasodilator role of ET(B) receptors.

Animals↗

PubMed2003

Effect of extracellular volume expansion and surgical stress on splanchnic blood flow and cardiac output in anesthetized rats: role of nitric oxide.

In a normal volume state, surgical stress decreases rather than increases nitric oxide (NO) production in the vascular system. In our studies, the effect of minor and major surgical stress and three different degrees of volume expansion on systemic and splanchnic circulatory parameters and on the NO dependence of the circulation have been investigated. When the degree of volume expansion was increased, cardiac output and organ blood flow increased without significant change in vascular resistances. Major surgical stress reduced the increase in cardiac output and organ blood flow elicited by the volume expansion. NO synthase (NOS) inhibition significantly increased blood pressure and total peripheral resistance (TPR) and decreased cardiac output in all groups of animals. As the degree of volume expansion was increased, the NO dependence of the circulation in the surgically less- and more-stressed animals was inversely influenced in some cases. With the three degrees of volume expansion (20, 40, and 60 ml/kg), the NOS inhibition increased the TPR from 30.7 R/kg +/- 1.90 to 73.6 R/kg +/- 5.00, from 20.7 R/kg +/- 1.43 to 66.7 R/kg +/- 3.88, and from 19.9 R/kg +/- 1.25 to 49.1 R/kg +/- 3.84 in the surgically less-stressed animals and from 38.6 R/kg +/- 2.14 to 59.8 R/kg +/- 5.62, from 31.9 R/kg +/- 2.70 to 81.7 R/kg +/- 9.89, and from 29.1 R/kg +/- 2.49 to 91.1 R/kg +/- 6.36 in the surgically more-stressed animals. Volume expansion increases the NO dependence of the vascular resistance in the surgically more-stressed animals but decreases it in the surgically less-stressed animals.

Abdominal Cavity↗

PubMed1996

Hemodynamic patterns and duration of post-dynamic exercise hypotension in hypertensive humans.

We investigated: 1) the mechanism of the hypotensive effect of a single bout of dynamic exercise in hypertensive subjects by measuring hemodynamic parameters before and for 2 h after treadmill exercise, and 2) the duration of the effect using ambulatory blood pressure (BP) monitoring once the subjects left the test site. Ten minutes after exercise there was a significant decrease from baseline systolic pressure (SP; -14 +/- 3 mm Hg), mean arterial pressure (MAP; -7 +/- 2 mm Hg), total peripheral resistance (TPR; -3.7 +/- 1.2 units), calf vascular resistance (CVR; -25.4 +/- 4.1 units), and an increase in HR (19 +/- 2 bpm). The changes in SP, DP, MAP, and HR were maintained during the 2 h of post-exercise monitoring; CVR remained decreased for 1 h; TPR returned to baseline within 20 min and then tended to be slightly elevated. CO was significantly decreased at 50, 60, and 120 min after exercise. We conclude that the early decline in BP after dynamic exercise in hypertensive subjects follows a biphasic pattern: 1) an initial decrease in total and regional vascular resistance with maintained CO, 2) followed by increasing resistance and decrease CO. Pre-exercise hypertensive BP values returned during subsequent ambulatory monitoring.

Blood Pressure↗

PubMed2001

Is there a disassociation of maximal oxygen consumption and maximal cardiac output?

PURPOSE: The purpose of the present study was to determine whether maximal cardiac output (Q) is affected by the duration of the maximal exercise test. METHODS: Nine healthy men (N = 6) and women (N = 3) performed three separate maximal treadmill exercise tests, separated by at least 24 h, and underwent a body composition assessment by hydrostatic weighing, all within a 2-wk period. A baseline maximal exercise test was performed to establish VO(2max). The second and third tests, assigned randomly, were designed to elicit the subjects' predetermined VO(2max) in either 6 or 12 min. Heart rate (HR), blood pressure (BP), minutes of ventilation, and oxygen consumption (VO(2)) were measured during all tests. At the end of the 6- and 12-min tests, Q was measured using an acetylene rebreathing technique. Stroke volume (SV), mean arterial pressure (MAP), total peripheral resistance (TPR), and arteriovenous O(2) difference were calculated using standard equations. RESULTS: Repeated-measures ANOVA indicated that there were no significant differences in HR and VO(2max) between the baseline, 6-min, and 12-min tests. Paired t-tests revealed significantly greater Q (25.1 +/- 5.6 vs 23.7 +/- 5.2 L.min-1) and SV (138.3 +/- 31.5 vs 130.5 +/- 31.2 mL) in the 6- versus 12-min tests, respectively. There were no significant differences in systolic BP, diastolic BP, MAP, TPR, or arteriovenous O(2) difference. CONCLUSIONS: Despite there being no difference in VO(2max) between the two tests, the 6-min maximal exercise test resulted in a significantly greater Q than the 12-min test, because of a significantly greater SV. Thus, there was a disassociation between VO(2) and Q during maximal exercise.

Adult↗

PubMedDate not supplied

Smoking status and nicotine administration differentially modify hemodynamic stress reactivity in men and women.

OBJECTIVES: To investigate the impact of cigarette smoking and oral contraceptive (OC) use on hemodynamic stress responses of women. Also, to examine gender differences in stress reactivity as a function of smoking status and acute nicotine administration. METHODS: Thirty men and 46 women, differing in smoking status and OC use, were tested for cardiovascular stress responses to a variety of behavioral and physical stressors. Each was tested twice, once under a transdermal nicotine patch condition and once under a placebo patch condition. Impedance cardiography was used to estimate hemodynamic reactivity noninvasively. RESULTS: In response to behavioral stressors, women smokers, irrespective of OC use or nicotine vs placebo, demonstrated significantly blunted cardiac output and heart rate reactivity to stressors, and showed significantly greater estimated total peripheral resistance (TPR) under stress relative to women nonsmokers. There were no differences in hemodynamic stress reactivity between men smokers and nonsmokers. The only significant effect involving nicotine administration on stress reactivity was seen in men where, regardless of smoking status, nicotine increased heart rate reactivity to all stressors relative to placebo responses. CONCLUSIONS: Results suggest that cigarette smoking may act differently in men and women to increase risk for cardiovascular disease (CVD). For men, nicotine may exert pathogenic influences via increasing the magnitude of heart rate reactivity to stressors. For women, however, smoking seems to have deleterious effects on hemodynamic stress reactivity patterns, reducing myocardial but increasing TPR contributions to blood pressure responses.

Administration, Cutaneous↗

PubMed1998

Molecular subtyping of Treponema pallidum subspecies pallidum.

BACKGROUND AND OBJECTIVES: Epidemiologic studies on syphilis have been hampered by the fact that strains of Treponema pallidum subspecies pallidum (T. pallidum), the causative agent of this disease, cannot be differentiated by either protein-based or deoxyribonucleic acid-based methods. Syphilis is endemic in many developing countries and is common in some industrialized nations. In addition, the disease has been shown to increase the risk of infection with the human immunodeficiency virus. GOAL: To develop a molecular subtyping method for T. pallidum. STUDY DESIGN: Two genes exhibiting intrastrain variability were identified as potential targets for strain differentiation: the acidic repeat protein (arp) gene, which contains a variable number of 60 base pair repeats, and a member of the treponema pallidum repeat (tpr) gene family. Polymerase chain reaction amplification and restriction endonuclease digestion of polymerase chain reaction products from laboratory strains and clinical specimens were used to develop a molecular subtyping scheme for T. pallidum. RESULTS: Determining the number of repeats in the arp gene by polymerase chain reaction resulted in 12 different subtypes among the 63 isolates that were studied. Among those, most (54.2%) had arp genes with 14 repeats. The other 11 subtypes had arp genes with 7 to 21 repeats, each accounting for 2% to 14% of the isolates. Polymerase chain reaction amplification of a member of the tpr gene family from a subset of 46 isolates followed by digestion of the polymerase chain reaction product with MseI resulted in seven restriction fragment length polymorphism patterns designated a to g. Strains with 14 repeats could be grouped into five restriction fragment length polymorphism subtypes. By combining the two systems we observed 16 subtypes among 46 isolates examined. This typing system is stable, reproducible, and easy to perform. In addition, the use of the ABI Genetic Analyzer for the determination of fragment size and banding patterns makes the results unbiased. CONCLUSION: This is the first molecular subtyping system that distinguishes among clinical isolates of T. pallidum.

Animals↗

PubMed1999

Haemodynamic effects of chronic tetramethylpyrazine administration on portal hypertensive rats.

OBJECTIVE: The purpose of this study was to investigate the therapeutic effects of tetramethylpyrazine, an alkaloid isolated from a Chinese herb Ligusticum wallichii Franch, on portal hypertensive rats. METHODS: There were three groups of animals: partial portal vein ligated (PVL) rats, bile duct ligated (BDL) rats and sham-operated (Sham) rats. Each rat in every group was given only one of three treatment regimens: tetramethylpyrazine 30 or 50 mg/kg/12 h, or vehicle (0.2 N HCl, 0.7 ml/12 h). There were seven rats allocated to each regimen, with a total of 63 rats studied. Tetramethylpyrazine or vehicle was given via gastric gavage every 12 h for 8 days, starting just after PVL or 3 weeks after BDL, and haemodynamic parameters were measured thereafter. RESULTS: Both PVL and BDL rats exhibited portal hypertensive and hyperdynamic state as compared with Sham rats. Eight-day tetramethylpyrazine treatment induced dose-dependent reductions of portal venous pressure (PVP), mean arterial pressure (MAP), and total peripheral resistance (TPR) in both PVL and BDL rats. Tetramethylpyrazine at 30 and 50 mg/kg/12 h induced PVP reduction by 10.2 and 16.1% in PVL rats, and 10.5 and 14.8% in BDL rats, respectively, as compared with the vehicle group. There were no significant changes of cardiac index or heart rate (HR) after tetramethylpyrazine treatment in either PVL or BDL rats. In the Sham rats, tetramethylpyrazine did not significantly change PVP, MAP, HR or TPR, despite a tendency of reduction. CONCLUSION: Our results showed that 8-day treatment of tetramethylpyrazine induced reductions of both portal venous and systemic arterial pressure in portal hypertensive rats with and without cirrhosis. Overall, the therapeutic effects are neither outstandingly efficacious nor altogether beneficial.

Animals↗

PubMed2004

Temporal stability of twenty-four-hour ambulatory hemodynamic bioimpedance measures in African American adolescents.

BACKGROUND: The reliability of ambulatory impedance cardiography has not been evaluated. OBJECTIVE: The purpose of this study was to determine the reproducibility of daytime and night-time ambulatory bioimpedance-derived measures of hemodynamic function in youth. METHODS: Thirty-five African American adolescents (ages 16.2+/-1.4 years, 14 girls, 21 boys) with high normal systolic resting blood pressure (BP) were evaluated twice, separated by a 2-month interval. Measures were collected using the AIM-8-V3 Wearable Cardiac Performance Monitor (Bio-impedance Technology, Inc., Chapel Hill, North Carolina, USA) and the Spacelabs ambulatory BP monitor 90207 (Spacelabs Inc., Redmond, Washington, USA) from 0600 h to midnight every 20 min and from midnight to 0600 h every 30 min in the natural environment. RESULTS: There were no significantly different means (P>0.15) between the two visits for daytime ambulatory heart rate (HR, r = 0.81), stroke volume (SV, r = 0.54), cardiac output (CO, r = 0.56), pre-ejection period (PEP, r = 0.59), left ventricular ejection time (LVET, r = 0.74), Heather Index (HI, r = 0.79), systolic BP (SBP, r = 0.79), diastolic BP (DBP, r = 0.66), mean arterial pressure (MAP, r = 0.65) and total peripheral resistance (TPR, r = 0.47). Overall means for night-time ambulatory HR (r = 0.76), SV (r = 0.49), CO (r = 0.45), LVET (r = 0.43), HI (r = 0.82), SBP (r = 0.65), DBP (r = 0.62), MAP (r = 0.63) and TPR (r = 0.20) were not significantly different between visits (P > 0.06). Mean differences (P < 0.01) were observed for PEP (r = 0.57). CONCLUSIONS: The findings demonstrate that across 2 months in youth daytime and night-time ambulatory bioimpedance-derived measures of HR, HI, SBP, DBP and MAP are highly repeatable and SV, CO, PEP and LVET are moderately repeatable. This methodology should prove useful in cardiovascular research and clinical care.

Adolescent↗

PubMed2006

Effect of nos inhibition on retinal arterial and capillary circulation in early arterial hypertension.

BACKGROUND: Arterial hypertension is involved in the pathogenesis of end organ damage by influencing the ability of the vascular endothelium to produce nitric oxide (NO). This study analyzes changes of retinal and systemic NO-dependent circulation parameters by inhibiting nitric oxide synthase (NOS) in both hypertensive and normotensive individuals. METHODS: In a double-blind crossover trial, 19 hypertensive patients (H, age 28.2 +/- 0.9 years) and 19 normotensive controls (N, age 26.9 +/- 0.9 years) were randomized treated either with candesartan or placebo. Both retinal capillary flow (RCF) and mean blood flow velocity of the central retinal artery (VCRA) were registered before and after NOS inhibition with N-monomethyl-L-arginine (L-NMMA, 3 mg/kg). In a subpopulation mean arterial pressure (MAP), cardiac output (CO), and the total peripheral resistance (TPR) were determined simultaneously. RESULTS: Changes from baseline: In normotensive and hypertensive subjects infusion of L-NMMA led to an increase of MAP (N, +13.3 +/- 1.8%, P < 0.01; H, +14.3 +/- 2.4%, P < 0.01) and TPR (N, +36.9 +/- 3.8%, P < 0.01; H, +45.0 +/- 4.5%, P < 0.01), and to a decrease of CO (N, -21.1 +/- 1.5%, P < 0.01; H, -24.6 +/- 2.3%, P < 0.01). The L-NMMA effect on VCRA and RCF differed between controls and hypertensives. VCRA changed by + 17.3 +/- 6.2% (P < 0.05) and RCF by -7.3 +/- 3.0% (P < 0.05) in controls. In hypertensive subjects corresponding results were + 9.5 +/- 5.2% (P = NS) and + 2.7 +/- 3.8% (P = NS), respectively. The decrease of RCF due to L-NMMA was reduced in hypertension as compared to controls (P < 0.05). The calculated cross-sectional area of CRA was reduced by -58.7% in controls and increased by + 31.1% in hypertensive subjects. There was no significant correlation between the flow in the systemic and retinal circulation. CONCLUSION: Only normotensives L-NMMA induces an acceleration of VCRA due to a probable vasoconstriction of the central retinal artery and despite of a reduced RCF. Already in early hypertension the NOS-dependent vascular tone in retinal arteries and capillaries is impaired. The regulation of the retinal capillary flow appeared to be independent from systemic circulation.

Adult↗

PubMedDate not supplied

Anger suppression and adiposity modulate association between ADRB2 haplotype and cardiovascular stress reactivity.

OBJECTIVES: The purpose of this study was to examine how variation in the beta-2 adrenergic receptor gene (ADRB2), in combination with the moderating influences of race, body mass index (BMI), and anger expression style (anger-in, anger-out), affects blood pressure (BP) at rest and in response to acute laboratory stress. METHODS: Four hundred fifty adolescents (mean age = 18.5 +/- 2.7 years; 228 [124 males] whites and 222 [110 males] blacks completed two stressors (video game challenge, forehead cold pressor). Hemodynamic measures were taken before, during, and after each stressor. Stressors were separated by a 20-minute rest period. RESULTS: Frequency of detrimental haplotype (Gly16/Glu27) carrier status was greater among whites than blacks (p < .05). A significant three-way interaction among haplotype, BMI, and race for resting systolic blood pressure (SBP) found the highest BP level to be among high BMI carriers, but only for whites. A separate three-way interaction was found to be significant for haplotype, anger-in and race such that high anger-in carriers showed the highest level of resting SBP (p < .05) and total peripheral resistance (TPR) (p < .05) and the greatest TPR reactivity to the cold pressor task (p < .01). Post hoc analyses revealed these interactions with anger-in were only present among blacks. No significant interactions with anger-out for either ethnic group were observed. CONCLUSIONS: This study demonstrates modulating influences of BMI and anger expression styles on ADRB2 gene associations with hemodynamic function at rest and in response to laboratory stress. These findings support the hypothesis that consideration of gene-environment interactions may better characterize the role of ADRB2 variation in the development of stress-induced essential hypertension.

Adaptation, Psychological↗

PubMed2006

Effect of DHEA on the hemodynamic response to resuscitation in a porcine model of hemorrhagic shock.

BACKGROUND: Hemorrhagic shock is a major cause of death from trauma. Pharmacologic treatment has not been satisfactory. The objective of this study was to use a porcine model of hemorrhagic shock and resuscitation to access the hemodynamic effects of dehydroepiandrosterone (DHEA), an adrenal steroid hormone reported to improve cardiac function in patients. METHODS: Hemorrhagic shock was produced in 20- to 30-kg male Yorkshire pigs anesthetized with 2% isoflurane by withdrawing blood through a carotid cannula to a mean arterial pressure (MAP) of 40 to 45 mm Hg and maintaining that level for 60 minutes by further removals of blood. Resuscitation was with 21 mL/kg Ringer's lactate (LR), with (n = 6) or without (n = 6) DHEA (4 mg/kg) dissolved in propylene glycol. The animals were killed after 7 days. Continuous cardiac output (CCO) was recorded using a modified Swan-Ganz catheter system. MAP, heart rate (HR), central venous pressure (CVP), and pulmonary arterial pressure (PAP) were measured every 5 minutes until 60 minutes postresuscitation. From MAP, CCO, HR, and CVP, we calculated total peripheral resistance (TPR), stroke volume (SV), and left ventricular stroke work (SW). RESULTS: The MAP, CCO, SV, and SW decreased significantly during hemorrhagic shock, and then gradually increased to baseline levels during and 1 hour after resuscitation. The TPR was increased during hemorrhagic shock, and then gradually decreased to baseline levels during and after resuscitation. DHEA administration was associated with no significant improvement. CONCLUSION: DHEA when added to standard fluid resuscitation showed no added benefit as resumed by the hemodynamic response.

Adjuvants, Immunologic↗