scholarly journals Hemodynamic Changes during Hepatic Vascular Exclusion: Use of Intraoperative Transesophageal Echocardiography a Case Series

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Franco Marinangeli ◽  
Alessandra Ciccozzi ◽  
Chiara Angeletti ◽  
Cristiana Guetti ◽  
Tommaso Aloisio ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Cardiac Index ◽  
Transesophageal Echocardiography ◽  
Diastolic Pressure ◽  
Case Series ◽  
Left Ventricular ◽  
Vascular Exclusion ◽  
Significant Difference ◽  
Hepatic Vascular Exclusion ◽  
Intraoperative Transesophageal Echocardiography

The aim of this clinical observation was to compare intraoperative transesophageal echocardiography (TEE) and pulmonary artery catheterization (PAC) during hepatic vascular exclusion (HEV). Five non-cirrhotic patients to undergo HVE for major liver resection have been observed. Hemodynamic parameters: pulmonary arterial wedge pressure (PCWP), cardiac index (CI), cardiac output (CO), and systemic vascular resistance (SVR) have been monitored by PAC. Left ventricular end-diastolic area (LVEDA), left ventricular end-systolic area (LVESA), left ventricular end-diastolic pressure (LVEDP), cardiac index (CI), cardiac output (CO), and fractional area changes (FAC) have been monitored by TEE. Hemodynamic variables were assessed before clamping (), at 5 and 30 minutes after clamping (, ) and 15 minutes after unclamping (). No significant difference between PCWP and LVEDP was found. LVEDP significantly decreased at and compared to (); PCWP showed the same trend. A correlation was found between SV and LVEDP (, ) as well as CI (, ). Data confirm that intraoperative TEE may be a reliable method for hemodynamic monitoring during major liver resections.

Dose-dependent effect of ANG II-receptor antagonist on myocyte remodeling in rat cardiac hypertrophy

1997 ◽  
Vol 273 (4) ◽  
pp. H1824-H1831 ◽  
Author(s):  
Masakazu Obayashi ◽  
Masafumi Yano ◽  
Michihiro Kohno ◽  
Shigeki Kobayashi ◽  
Taketo Tanigawa ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Receptor Antagonist ◽  
Pressure Overload ◽  
Wall Stress ◽  
Treated Group ◽  
Left Ventricular ◽  
Abdominal Aortic ◽  
Significant Difference ◽  
And Function ◽  
Vehicle Treated Group

The goal of this study was to examine the effect of an angiotensin II type 1 (AT1)-receptor antagonist (TCV-116) on left ventricular (LV) geometry and function during the development of pressure-overload LV hypertrophy. A low (LD; 0.3 mg ⋅ kg−1 ⋅ day−1) or a high (HD; 3.0 mg ⋅ kg−1 ⋅ day−1) dose of TCV-116 was administered to abdominal aortic-banded rats over 4 wk, and hemodynamics and morphology were then evaluated. In both LD and HD groups, peak LV pressures were decreased to a similar extent compared with the vehicle-treated group but stayed at higher levels than in the sham-operated group. In the LD group, both end-diastolic wall thickness (3.08 ± 0.14 mm) and myocyte width (13.3 ± 0.1 μm) decreased compared with those in the vehicle-treated group (3.67 ± 0.19 mm and 15.3 ± 0.1 μm, respectively; both P < 0.05). In the HD group, myocyte length was further decreased (HD: 82.6 ± 2.6, LD: 94.1 ± 2.9 μm; P < 0.05) in association with a reduction in LV midwall radius (HD: 3.36 ± 0.12, LD: 3.60 ± 0.14 mm; P < 0.05) and peak midwall fiber stress (HD: 69 ± 8, LD: 83 ± 10 × 103dyn/cm2; P < 0.05). There was no significant difference in cardiac output among all groups. The AT1-receptor antagonist TCV-116 induced an inhibition of the development of pressure-overload hypertrophy. Morphologically, not only the width but also the length of myocytes was attenuated with TCV-116, leading to a reduction of midwall radius and hence wall stress, which in turn may contribute to a preservation of cardiac output.

Time course of hemodynamic changes in rats with healed severe myocardial infarction

1989 ◽  
Vol 257 (1) ◽  
pp. H289-H296 ◽  
Author(s):  
A. DeFelice ◽  
R. Frering ◽  
P. Horan
Keyword(s):  
Myocardial Infarction ◽  
Blood Flow ◽  
Cardiac Output ◽  
Diastolic Pressure ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Male Rats ◽  
Coronary Artery Ligation ◽  
Sham Operation ◽  
Functional Changes

Male rats were monitored for 8 mo after severe myocardial infarction (MI) to chronicle hemodynamic and left ventricular (LV) functional changes. Blood pressure (BP), heart rate (HR), cardiac output index (CO), regional blood flow, and systemic vascular resistance (SVR) were measured with catheters and radiolabeled microspheres at 4, 7, 10, 20, and 35 wk after coronary artery ligation (n = 10–16/group) or sham operation (control; n = 9–14/group). At 4 wk, 43 +/- 1% of the LV circumference was scarred, peak LV BP, LV dP/dtmax, mean BP, SVR, and HR were 11–38% less than control (P less than 0.05), and LV end-diastolic pressure (LVEDP) was increased by 313% (P less than 0.05). Mean BP, LVEDP, LVBP, and LV dP/dtmax did not further deviate after 4 wk. However, CO and SVR changed progressively and were 67 and 33%, respectively, of control by 35 wk (P less than 0.05) when blood flow to stomach, small intestine, and kidney was 55, 38, and 27% of control. Lung and heart weights were significantly increased by 148 and 22% at 4 wk, and remained elevated, and lung dry weight-to-wet weight ratio was reduced at 7 and 10 wk. Thus the trajectory of rats with healed severe MI reflects progressive cardiac decompensation, cardiac output redistribution, and terminal heart failure.

Reflex regulation of renal nerve activity in cardiac failure

1994 ◽  
Vol 266 (1) ◽  
pp. R27-R39 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin
Keyword(s):  
Cardiac Index ◽  
Single Unit ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Central Portion ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Afferent Limb ◽  
Pressure Threshold ◽  
Cardiopulmonary Baroreflex

Efferent renal sympathetic nerve activity (ERSNA) is increased in the rat with low-cardiac-output congestive heart failure (CHF; myocardial infarction). Arterial and cardiopulmonary baroreflex control of ERSNA in CHF and control rats was examined. Cardiac index and arterial pressure were lower and total peripheral resistance index, left ventricular end-diastolic pressure, and heart-to-body weight ratio were higher in CHF than in control rats. Increases in left ventricular end diastolic pressure produced by intravenous volume loading failed to increase cardiac index in CHF rats as it did in control rats. Single-unit analysis of aortic baroreceptor nerve activity showed that CHF rats had higher pressure threshold, lower frequency at pressure threshold, and lower gain than control rats. Arterial baroreflex control of ERSNA was attenuated; this was due to diminished gain of the afferent limb while the gain of the central portion of the reflex was normal. Single-unit analysis of vagal nerve activity showed that CHF rats had higher pressure threshold, lower frequency at saturation, and lower gain than control rats. Cardiopulmonary baroreflex control of ERSNA was attenuated; this was due to diminished gain of the afferent limb while the gain of the central portion of the reflex was normal. In the CHF rat, arterial and cardiopulmonary baroreflex control of ERSNA is markedly attenuated because of abnormalities in the periphery at the level of the aortic and cardiopulmonary receptors, respectively, and not in the central nervous system.

Heart functional responses to pressure overload in exercised and sedentary rats

1976 ◽  
Vol 230 (1) ◽  
pp. 199-204 ◽  
Author(s):  
RT Dowell ◽  
AF Cutilletta ◽  
MA Rudnik ◽  
PC Sodt
Keyword(s):  
Cardiac Output ◽  
Diastolic Pressure ◽  
Heart Function ◽  
Pressure Overload ◽  
Normal Growth ◽  
Left Ventricular ◽  
Treadmill Running ◽  
Female Rats ◽  
Heart Weight ◽  
Functional Responses

Female rats that had been subjected to a moderate treadmill running program were compared with sedentary animals on the basis of heart weight, selected biochemical measurements, and heart function. Exercised animals maintained normal growth rate, and cardiac hypertrophy was not present. Left ventricular RNA, DNA, and cytochrome c levels were unchanged. Heart functional measurements obtained in situ were similar in sedentary and exercised animals under control conditions. When subjected to sustained (1-3 days) aortic constriction pressure overload, exercised animals maintained or increased myocardial contractility. Contractility was depressed in sedentary animals. Both sedentary and exercised animals increased left ventricular end diastolic pressure without changing contractility during acute (1-3 min) pressure overload. However, exercised animals were able to fully regain normal cardiac output when the acute overload was relieved. Cardiac output remained approximately 10% below control in sedentary animals. The improved ability of previously exercised animals to withstand pressure overload appears to be due to alterations in adaptation rather than preliminary augmentation of metabolism or function.

Effects of intensive exercise training on myocardial performance and coronary blood flow

1980 ◽  
Vol 49 (3) ◽  
pp. 444-449 ◽  
Author(s):  
R. J. Barnard ◽  
H. W. Duncan ◽  
K. M. Baldwin ◽  
G. Grimditch ◽  
G. D. Buckberg
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Work Capacity ◽  
Left Ventricular ◽  
Maximum Exercise ◽  
Time Index ◽  
Significant Difference ◽  
Tension Time

Five instrumented and eight noninstrumented dogs were progressively trained for 12-18 wk on a motor-driven treadmill. Data were compared with 14 instrumented and 8 noninstrumented control dogs. Gastrocnemius malate dehydrogenase activity was significantly increased in the trained dogs (887 +/- 75 vs. 667 +/- 68 mumol . g-1 . min-1). The trained dogs also showed significant increases in maximum work capacity, cardiac output (7.1 +/- 0.5 vs. 9.1 +/- 0.7 1/min), stroke volume (25.9 +/- 2.0 vs. 32.0 +/- 2.0 ml/beat), and left ventricular (LV) positive dP/dtmax (9,242 +/- 405 vs. 11,125 +/- 550 Torr/s). Negative dP/dtmax was not significantly different. Peak LV systolic pressure increased with exercise, but there was no significant difference between the trained and control dogs. LV end-diastolic pressure did not change with exercise and was the same in both groups. Tension-time index was lower in the trained dogs at rest and submaximum exercise (9.7 km/h, 10%) but was not different at maximum exercise. Diastolic pressure-time index was significantly higher in the trained dogs at rest and during submaximum exercise but was not different at maximum exercise. LV coronary blood flow was significantly reduced at rest (84 +/- 4 vs. 67 +/- 6 mo . min-1 . 100 g-1) and during submaximum exercise (288 +/- 24 vs. 252 +/- 8 ml . min-1 . 100 g-1). During maximum exercise flow was not significantly different (401 +/- 22 vs. 432 +/- 11 ml . min-1 . 100 g-1) between the control and trained groups. The maximum potential for subendocardial flow was unchanged with training despite the development of mild hypertrophy.

Positive end-expiratory pressure shifts left ventricular diastolic pressure-area curves

1980 ◽  
Vol 48 (4) ◽  
pp. 670-676 ◽  
Author(s):  
J. B. Haynes ◽  
S. D. Carson ◽  
W. P. Whitney ◽  
G. O. Zerbe ◽  
T. M. Hyers ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Volume Expansion ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Positive End Expiratory Pressure ◽  
Pressure Area ◽  
Radiopaque Markers ◽  
Peep Ventilation ◽  
Volume Characteristics ◽  
Area Data

Positive end-expiratory pressure (PEEP) ventilation is frequently associated with reduction in cardiac output despite unchanged transmural left ventricular (LV) end-diastolic pressure. These findings have been interpreted to indicate decreased contractility, but could also be explained by altered LV diastolic pressure-volume characteristics. To study this possibility, radiopaque markers were inserted into a plane of the LV in nine dogs. Transmural pressure (LV-pericardial) was synchronized with LV area during ventilation with zero end-expiratory pressure and with 15 cmH2O PEEP. Mean polynomial curves derived from the diastolic pressure-area data demonstrated that PEEP shifted the curves upward so that a given diastolic area was associated with a higher transmural LV pressure (P less than 0.0001). PEEP decreased end-diastolic area and stroke area, both of which were normalized with dextran volume expansion. Restoration of stroke area by normalizing end-diastolic area with volume expansion suggests the initial changes with PEEP were due to a decrease in preload rather than in contractility.

Effects of metoprolol on left ventricular function in rats with myocardial infarction

1994 ◽  
Vol 266 (2) ◽  
pp. H787-H794 ◽  
Author(s):  
W. J. Cherng ◽  
C. S. Liang ◽  
W. B. Hood
Keyword(s):  
Diastolic Pressure ◽  
Pressor Response ◽  
Left Ventricular ◽  
Lv Function ◽  
Sham Operation ◽  
Pressure Function ◽  
Tension Development ◽  
Beta Receptor ◽  
Significant Difference

To study the effect of beta-receptor-blocking agents in an animal model of left ventricular (LV) dysfunction, we measured LV performance in vivo and in vitro in 69 rats with or without metoprolol (M) treatment 3 wk after left coronary arterial ligation or sham operation. Rats were divided into six groups including control (C) and M noninfarct (C-N and M-N), C and M small infarct (C-S and M-S), and C and M large infarct (C-L and M-L). LV function was measured as slope of change in systolic vs. diastolic pressure (pressure-function curve) during pressor response after administration of a bolus of phenylephrine (5 micrograms/kg i.v.). Reduction of LV function was noted in C-L compared with C-N and C-S (slope of pressure-function curve 3.3 +/- 0.3 vs. 11.0 +/- 1.9 and 11.9 +/- 2.3, respectively) and in M-L compared with M-N and M-S rats (slope of 5.5 +/- 1.4 vs. 11.3 +/- 2.0 and 12.1 +/- 1.4, respectively). There was no significant difference between C and M rats, although there was a trend toward partial correction of the pressure-function curves in M-L compared with C-L rats. In muscle bath preparations the uninfarcted LV posterior papillary muscle from shams and rats with small infarcts showed a dose-related increase in peak rate of tension development with isoproterenol stimulation, but this response was lacking in both C-L and M-L. Tissue assays showed no change in beta-receptor number.(ABSTRACT TRUNCATED AT 250 WORDS)

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