Microvascular response to metabolic and pressure challenge in the human coronary circulation

2011 ◽  
Vol 301 (2) ◽  
pp. H434-H441 ◽  
Author(s):  
Stefano F. de Marchi ◽  
Steffen Gloekler ◽  
Stefano F. Rimoldi ◽  
Patrizia Rölli ◽  
Hélène Steck ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Contrast Echocardiography ◽  
Resistance Index ◽  
Applanation Tonometry ◽  
Myocardial Oxygen Demand ◽  
Coronary Vascular Resistance ◽  
Bicycle Exercise ◽  
Capillary Recruitment

In vivo observations of microcirculatory behavior during autoregulation and adaptation to varying myocardial oxygen demand are scarce in the human coronary system. This study assessed microvascular reactions to controlled metabolic and pressure provocation [bicycle exercise and external counterpulsation (ECP)]. In 20 healthy subjects, quantitative myocardial contrast echocardiography and arterial applanation tonometry were performed during increasing ECP levels, as well as before and during bicycle exercise. Myocardial blood flow (MBF; ml·min−1·g−1), the relative blood volume (rBV; ml/ml), the coronary vascular resistance index (CVRI; dyn·s·cm−5/g), the pressure-work index (PWI), and the pressure-rate product (mmHg/min) were assessed. MBF remained unchanged during ECP (1.08 ± 0.44 at baseline to 0.92 ± 0.38 at high-level ECP). Bicycle exercise led to an increase in MBF from 1.03 ± 0.39 to 3.42 ± 1.11 ( P < 0.001). The rBV remained unchanged during ECP, whereas it increased under exercise from 0.13 ± 0.033 to 0.22 ± 0.07 ( P < 0.001). The CVRI showed a marked increase under ECP from 7.40 ± 3.38 to 11.05 ± 5.43 and significantly dropped under exercise from 7.40 ± 2.78 to 2.21 ± 0.87 (both P < 0.001). There was a significant correlation between PWI and MBF in the pooled exercise data (slope: +0.162). During ECP, the relationship remained similar (slope: +0.153). Whereas physical exercise decreases coronary vascular resistance and induces considerable functional capillary recruitment, diastolic pressure transients up to 140 mmHg trigger arteriolar vasoconstriction, keeping MBF and functional capillary density constant. Demand-supply matching was maintained over the entire ECP pressure range.

Effect of acute edema on left ventricular function and coronary vascular resistance in the isolated rat heart

1994 ◽  
Vol 267 (3) ◽  
pp. H1054-H1061 ◽  
Author(s):  
A. Rubboli ◽  
P. A. Sobotka ◽  
D. E. Euler
Keyword(s):  
Linear Relationship ◽  
Water Content ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Myocardial Edema ◽  
Left Ventricular ◽  
Coronary Vascular Resistance ◽  
Ventricular Performance ◽  
Developed Pressure ◽  
The Impact

The impact of acute myocardial edema on coronary flow and left ventricular performance was studied in isolated isovolumic rat hearts. After 15 min of aortic perfusion with Krebs-Henseleit buffer, hearts (10/group) were either removed for determination of water content or perfused for another 90 min. Three groups were perfused at a constant pressure of 60, 100, or 140 mmHg, and two groups were perfused at 60 or 140 mmHg with adenosine added. Compared with the 15-min group, there was a significant increase in water content in all groups except the 60-mmHg group (P < 0.005). There was a direct linear relationship between increases in coronary vascular resistance over time and water content (P < 0.0001). A decrease in developed pressure and peak +dP/dt was observed only in those groups that accumulated water. An inverse linear relationship was found between changes in developed pressure and water content (P = 0.0001). Water content had no effect on end-diastolic pressure below 5 ml/g; above 5 ml/g, a direct linear relationship was evident (P = 0.009). The results suggest that myocardial edema increases vascular resistance and decreases systolic performance. End-diastolic pressure is less influenced by edema than either systolic or coronary vascular function.

Coronary blood flow in senescent rats with late-onset hypertension

1993 ◽  
Vol 264 (6) ◽  
pp. H1854-H1860
Author(s):  
R. J. Tomanek ◽  
M. R. Aydelotte ◽  
K. E. Anderson ◽  
R. J. Torry
Keyword(s):  
Vascular Resistance ◽  
Late Onset ◽  
Diastolic Pressure ◽  
Age Groups ◽  
Left Ventricular ◽  
Relative Reduction ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
Fischer 344 Rats ◽  
Fischer 344

We tested the hypothesis that the imposition of hypertension late in life would markedly limit maximal myocardial perfusion (MP). Young adult (8 mo) and senescent (24 mo) Fischer 344 rats were studied 3 mo after one-kidney, figure-8 renal wrap hypertension (RH) was induced. Sham-operated rats served as controls (Con). Regional MP was determined with radioactive microspheres in conscious rats before and during maximal coronary vasodilation with infusion of dipyridamole. Systolic arterial pressure (SAP) was significantly elevated in both RH age groups during weeks 2-6 following surgery and then fell to normotensive levels. After 3 mo SAP (mmHg) was significantly lower in the senescent RH rats (125 +/- 5) compared with their controls (147 +/- 3). In senescent RH rats left ventricular (LV) end-diastolic pressure increased fivefold. LV mass increased with age but not with treatment. LV minimal coronary vascular resistance (MCVR, mmHg.ml-1.min-100 g) increased significantly both with age and treatment (8 mo: Con = 0.07 +/- 0.01, RH = 0.14 +/- 0.01; 24 mo: Con = 0.11 +/- 0.01, RH 0.17 +/- 0.02). Treatment affected similar changes in the right ventricular MCVR. LV endocardial-to-epicardial perfusion ratio during rest was lower in the senescent groups but was not altered by hypertension. These data indicate that 1) both aging and this model of hypertension compromise maximal coronary perfusion and reserve in Fischer 344 rats, and 2) aging is associated with an increase in coronary vascular resistance in both ventricles at rest and in a relative reduction in maximal endocardial perfusion in the left ventricle.

Abstract 2085: Increased Regional Coronary Vascular Resistance During Hyperemia in Hypertrophic Cardiomyopathy Is Associated with Reduced Myocardial Blood Volume

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Hiroshi Komatsu ◽  
Satoshi Yamada ◽  
Masanao Naya ◽  
Hisao Onozuka ◽  
Taisei Mikami ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Contrast Echocardiography ◽  
Interventricular Septum ◽  
Power Doppler ◽  
Doppler Imaging ◽  
Coronary Vascular Resistance ◽  
Coronary Resistance ◽  
Myocardial Blood Volume

Introduction: In patients with hypertrophic cardiomyopathy ( HCM ), myocardial blood flow ( MBF ) is decreased during hyperemia because of high coronary vascular resistance. Recently myocardial blood volume ( MBV ) can be estimated in vivo using myocardial contrast echocardiography ( MCE ) with the compensation for acoustic field inhomogeneity. The relationship between MBV and coronary resistance, however, has not been investigated. We thus assessed the hypothesis that increased regional coronary vascular resistance during hyperemia in HCM is associated with reduced MBV. Methods: In 13 patients with HCM ( H , 53±16 years) with asymmetric septal hypertrophy and 9 normal volunteers ( N , 54±11 years), MCE was performed under infusion of Levovist at rest and during hyperemia induced by ATP. Apical 4-chamber views of intermittent harmonic power Doppler imaging were acquired at end-diastole of every sixth beat. MBV was calculated as 10 X/10 ×100%, where X was myocardial contrast intensity minus contrast intensity of the adjacent intracavity blood pool in dB. 15 O-water PET was performed to measure regional MBF. These parameters were measured in the interventricular septum ( IVS ) and LV posterolateral ( PL ) wall. Regional coronary vascular resistance was calculated as (mean blood pressure)/MBF. Results: Wall thickness was significantly greater in H than in N (IVS: 19±4 vs 10±1 mm, p<0.0001; PL: 10±1 vs 9±1 mm, p<0.05). MBV of IVS was lower in H than in N (rest: 2.1±0.7 vs 3.5±1.1%, p<0.01; hyperemia: 2.1±1.3 vs 4.3±1.7%, p<0.01), whereas MBV of PL wall did not differ between groups. Coronary resistance at rest did not differ between groups, but the resistance during hyperemia was significantly greater in H than in N (IVS: 59±16 vs 31±14 mmHg·min·g·ml −1 , p<0.001; PL: 40±10 vs 30±11 mmHg·min·g·ml −1 , p<0.05). Coronary resistance at rest did not correlate with MBV, whereas that during hyperemia inversely correlated with MBV during hyperemia (r=−0.77, p<0.0001) as well as MBV at rest (r=−0.65, p<0.0001). Conclusions: Increased coronary vascular resistance during hyperemia in HCM was significantly associated with reduced MBV. MCE is useful for assessing the dynamic function of coronary circulation in the clinical setting.

Methylprednisolone on circulating eicosanoids and vasomotor tone after endotoxin

1986 ◽  
Vol 61 (1) ◽  
pp. 185-191 ◽  
Author(s):  
C. A. Hales ◽  
R. D. Brandstetter ◽  
C. F. Neely ◽  
M. B. Peterson ◽  
D. Kong ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Physiological Effect ◽  
High Dose ◽  
Systemic Blood ◽  
Eicosanoid Production ◽  
Circulating Levels

Acute pulmonary and systemic vasomotor changes induced by endotoxin in dogs have been related, at least in part, to the production of eicosanoids such as the vasoconstrictor thromboxane and the vasodilator prostacyclin. Steroids in high doses, in vitro, inhibit activation of phospholipase A2 and prevent fatty acid release from cell membranes to enter the arachidonic acid cascade. We, therefore, administered methylprednisolone (40 mg/kg) to dogs to see if eicosanoid production and the ensuing vasomotor changes could be prevented after administration of 150 micrograms/kg of endotoxin. The stable metabolites of thromboxane B2 (TxB2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) were measured by radioimmunoassay. Methylprednisolone by itself did not alter circulating eicosanoids but when given 2.5 h before endotoxin not only failed to inhibit endotoxin-induced eicosanoid production but actually resulted in higher circulating levels of 6-keto-PGF1 alpha (P less than 0.05) compared with animals receiving endotoxin alone. Indomethacin prevented the steroid-enhanced concentrations of 6-keto-PGF1 alpha after endotoxin and prevented the greater fall (P less than 0.05) in systemic blood pressure and systemic vascular resistance with steroid plus endotoxin than occurred with endotoxin alone. Administration of methylprednisolone immediately before endotoxin resulted in enhanced levels (P less than 0.05) of both TxB2 and 6-keto-PGF1 alpha but with a fall in systemic blood pressure and vascular resistance similar to the animals pretreated by 2.5 h. In contrast to the early steroid group in which all of the hypotensive effect was due to eicosanoids, in the latter group steroids had an additional nonspecific effect. Thus, in vivo, high-dose steroids did not prevent endotoxin-induced increases in eicosanoids but actually increased circulating levels of TxB2 and 6-keto-PGF1 alpha with a physiological effect favoring vasodilation.

An experimental method for evaluating constitutive models of myocardium in in vivo hearts

1994 ◽  
Vol 267 (2) ◽  
pp. H853-H863 ◽  
Author(s):  
L. L. Creswell ◽  
M. J. Moulton ◽  
S. G. Wyers ◽  
J. S. Pirolo ◽  
D. S. Fishman ◽  
...  
Keyword(s):  
Experimental Method ◽  
Diastolic Pressure ◽  
Constitutive Models ◽  
Fe Analysis ◽  
Small Displacement ◽  
Ventricular Wall ◽  
Canine Heart ◽  
Unknown Parameters ◽  
Tissue Tagging

A new experimental method for the evaluation of myocardial constitutive models combines magnetic resonance (MR) radiofrequency (RF) tissue-tagging techniques with iterative two-dimensional (2-D) nonlinear finite element (FE) analysis. For demonstration, a nonlinear isotropic constitutive model for passive diastolic expansion in the in vivo canine heart is evaluated. A 2-D early diastolic FE mesh was constructed with loading parameters for the ventricular chambers taken from mean early diastolic-to-late diastolic pressure changes measured during MR imaging. FE solution was performed for regional, intramyocardial ventricular wall strains using small-strain, small-displacement theory. Corresponding regional ventricular wall strains were computed independently using MR images that incorporated RF tissue tagging. Two unknown parameters were determined for an exponential strain energy function that maximized agreement between observed (from MR) and predicted (from FE analysis) regional wall strains. Extension of this methodology will provide a framework in which to evaluate the quality of myocardial constitutive models of arbitrary complexity on a regional basis.

scholarly journals Physiologic and hemodynamic changes in patients undergoing open abdominal cytoreductive surgery with hyperthermic intraperitoneal chemotherapy

2021 ◽  
Vol 49 (1) ◽  
pp. 030006052098326
Author(s):  
Myoung Hwa Kim ◽  
Young Chul Yoo ◽  
Sun Joon Bai ◽  
Kang-Young Lee ◽  
Nayeon Kim ◽  
...  
Keyword(s):  
Body Temperature ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Intraperitoneal Chemotherapy ◽  
Cytoreductive Surgery ◽  
Hyperthermic Intraperitoneal Chemotherapy ◽  
Resistance Index ◽  
Volume Index ◽  
Hemodynamic Changes ◽  
Arterial Blood

Objective We aimed to determine the physiological and hemodynamic changes in patients who were undergoing hyperthermic intraperitoneal chemotherapy (HIPEC) cytoreductive surgeries. Methods This prospective, observational study enrolled 21 patients who were undergoing elective cytoreductive surgery with HIPEC at our hospital over 2 years. We collected vital signs, hemodynamic parameters including global end-diastolic volume index (GEVI) and extravascular lung water index (ELWI) using the VolumeView™ system, and arterial blood gas analysis from all patients. Data were recorded before skin incision (T1); 30 minutes before HIPEC initiation (T2); 30 (T3), 60 (T4), and 90 (T5) minutes after HIPEC initiation; 30 minutes after HIPEC completion (T6); and 10 minutes before surgery completion (T7). Results Patients showed an increase in body temperature and cardiac index and a decrease in the systemic vascular resistance index. GEDI was 715.4 (T1) to 809.7 (T6), and ELWI was 6.9 (T1) to 7.3 (T5). Conclusions HIPEC increased patients’ body temperature and cardiac output and decreased systemic vascular resistance. Although parameters that were extracted from the VolumeView™ system were within their normal ranges, transpulmonary thermodilution approach is helpful in intraoperative hemodynamic management during open abdominal cytoreductive surgery with HIPEC. Trial registry name: ClinicalTrials.gov Trial registration number: NCT02325648 URL: https://clinicaltrials.gov/ct2/results?cond=NCT02325648&term

scholarly journals Empagliflozin does not change cardiac index nor systemic vascular resistance but rapidly improves left ventricular filling pressure in patients with type 2 diabetes: a randomized controlled study

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Matthias Rau ◽  
Kirsten Thiele ◽  
Niels-Ulrik Korbinian Hartmann ◽  
Alexander Schuh ◽  
Ertunc Altiok ◽  
...  
Keyword(s):  
Cardiac Index ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Resistance Index ◽  
Stroke Volume Index ◽  
Left Ventricular ◽  
Volume Index ◽  
Hemodynamic Parameters ◽  
Mitral Inflow ◽  
Ventricular Filling Pressure

Abstract Background In the EMPA-REG OUTCOME trial (Empagliflozin Cardiovascular Outcome Event Trial) treatment with the sodium-glucose cotransporter-2 (SGLT2) inhibitor empagliflozin significantly reduced heart failure hospitalization (HHF) in patients with type 2 diabetes mellitus (T2D) and established cardiovascular disease. The early separation of the HHF event curves within the first 3 months of the trial suggest that immediate hemodynamic effects may play a role. However, hitherto no data exist on early effects of SGLT2 inhibitors on hemodynamic parameters and cardiac function. Thus, this study examined early and delayed effects of empagliflozin treatment on hemodynamic parameters including systemic vascular resistance index, cardiac index, and stroke volume index, as well as echocardiographic measures of cardiac function. Methods In this placebo-controlled, randomized, double blind, exploratory study patients with T2D were randomized to empagliflozin 10 mg or placebo for a period of 3 months. Hemodynamic and echocardiographic parameters were assessed after 1 day, 3 days and 3 months of treatment. Results Baseline characteristics were not different in the empagliflozin (n = 22) and placebo (n = 20) group. Empagliflozin led to a significant increase in urinary glucose excretion (baseline: 7.3 ± 22.7 g/24 h; day 1: 48.4 ± 34.7 g/24 h; p < 0.001) as well as urinary volume (1740 ± 601 mL/24 h to 2112 ± 837 mL/24 h; p = 0.011) already after one day compared to placebo. Treatment with empagliflozin had no effect on the primary endpoint of systemic vascular resistance index, nor on cardiac index, stroke volume index or pulse rate at any time point. In addition, echocardiography showed no difference in left ventricular systolic function as assessed by left ventricular ejections fraction and strain analysis. However, empagliflozin significantly improved left ventricular filling pressure as assessed by a reduction of early mitral inflow velocity relative to early diastolic left ventricular relaxation (E/eʹ) which became significant at day 1 of treatment (baseline: 9.2 ± 2.6; day 1: 8.5 ± 2.2; p = 0.005) and remained apparent throughout the study. This was primarily attributable to reduced early mitral inflow velocity E (baseline: 0.8 ± 0.2 m/s; day 1: 0.73 ± 0.2 m/sec; p = 0.003). Conclusions Empagliflozin treatment of patients with T2D has no significant effect on hemodynamic parameters after 1 or 3 days, nor after 3 months, but leads to rapid and sustained significant improvement of diastolic function. Trial registration EudraCT Number: 2016-000172-19; date of registration: 2017-02-20 (clinicaltrialregister.eu)

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