Experimental instrumentation and left ventricular pressure-strain relationship

1991 ◽  
Vol 261 (6) ◽  
pp. H1693-H1697 ◽  
Author(s):  
N. W. Scott-Douglas ◽  
M. Traboulsi ◽  
E. R. Smith ◽  
J. V. Tyberg
Keyword(s):  
Confidence Intervals ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Segment Length ◽  
Data Points ◽  
Strain Relationship ◽  
Pressure Volume Relationship ◽  
Pericardial Pressure ◽  
The Individual

Pericardial pressure measurement with a balloon transducer requires opening and reapproximating the pericardium. If this instrumentation significantly compromises pericardial volume, the heart may be constrained, exaggerating the magnitude of pericardial pressure and thus altering the left ventricular end-diastolic pressure-volume relationship. In open-chest dogs, we studied the effects of opening the pericardium, inserting a pericardial balloon transducer and myocardial sonomicrometer crystals, and reapproximating the pericardium on the left ventricular end-diastolic pressure-strain relationship (LVEDPSR). After a thoracotomy, sonomicrometer crystals were inserted through small holes (less than 3 mm) in the pericardium to measure LV segment length. A micromanometer with a reference lumen was used to measure LV pressure. LVEDPSRs were recorded in the following situations: 1) before the pericardium was opened (but after the crystals were inserted); 2) after the pericardium was opened, the heart was instrumented (4 pairs of crystals and 1 balloon), and the pericardium was reapproximated with interrupted sutures; and 3) after the pericardium was removed. For each dog, a cubic regression equation was fitted to the data obtained before opening the pericardium, and the 95% confidence intervals for the individual data points were determined. In each case, the LVEDPSR obtained after instrumentation was similar to the LVEDPSR described before opening the pericardium. Furthermore, data obtained after instrumentation were uniformly located within the confidence intervals of the LVEDPSR obtained before opening the pericardium and instrumenting the heart.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Ventricular interaction and external constraint account for decreased stroke work during volume loading in CHF

2001 ◽  
Vol 281 (6) ◽  
pp. H2385-H2391 ◽  
Author(s):  
Thomas D. Moore ◽  
Michael P. Frenneaux ◽  
Rozsa Sas ◽  
J. J. Atherton ◽  
Jayne A. Morris-Thurgood ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Left Ventricular ◽  
Negative Slope ◽  
Segment Length ◽  
Stroke Work ◽  
Volume Loading ◽  
End Diastolic Volume ◽  
Pulmonary Capillary ◽  
Apparent Decrease ◽  
Pericardial Pressure

The slope of the stroke work (SW)-pulmonary capillary wedge pressure (PCWP) relation may be negative in congestive heart failure (CHF), implying decreased contractility based on the premise that PCWP is simply related to left ventricular (LV) end-diastolic volume. We hypothesized that the negative slope is explained by decreased transmural LV end-diastolic pressure (LVEDP), despite the increased LVEDP, and that contractility remains unchanged. Rapid pacing produced CHF in six dogs. Hemodynamic and dimension changes were then measured under anesthesia during volume manipulation. Volume loading increased pericardial pressure and LVEDP but decreased transmural LVEDP and SW. Right ventricular diameter increased and septum-to-LV free wall diameter decreased. Although the slopes of the SW-LVEDP relations were negative, the SW-transmural LVEDP relations remained positive, indicating unchanged contractility. Similarly, the SW-segment length relations suggested unchanged contractility. Pressure surrounding the LV must be subtracted from LVEDP to calculate transmural LVEDP accurately. When this was done in this model, the apparent decrease in contractility was no longer evident. Despite the increased LVEDP during volume loading, transmural LVEDP and therefore SW decreased and contractility remained unchanged.

Impaired early and intact late diastolic function in stunned myocardium induced by demand ischemia

1993 ◽  
Vol 264 (3) ◽  
pp. H739-H746 ◽  
Author(s):  
S. Miyazaki ◽  
Y. Goto ◽  
H. Nonogi ◽  
Y. Kawase ◽  
K. Haze ◽  
...  
Keyword(s):  
Diastolic Function ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Stunned Myocardium ◽  
Segment Length ◽  
Short Axis ◽  
The Mean

Changes in left ventricular diastolic properties of pacing-induced stunned myocardium were examined in 10 anesthetized dogs instrumented with a micromanometer for left ventricular pressure and sonomicrometers for left ventricular short axis, anterior and posterior segment lengths, and posterior wall thickness. After the creation of a critical stenosis on a carotid-circumflex coronary artery bypass, left ventricular pressure and dimensions were recorded simultaneously during temporary superior and inferior vena caval occlusion to allow for the construction of end-diastolic pressure-segment length curves. After 15 min of high-frequency pacing (190–220 beats/min), measurements were repeated and compared with those before pacing. The mean lengthening rate of each dimension during the first half of diastole was calculated as an index of early diastolic function. Three minutes after the end of pacing, coronary blood flow and perfusion pressure were unchanged, whereas systolic function of the posterior wall was depressed, indicating stunning of the posterior myocardium. The time constant of left ventricular pressure decay was prolonged by 14%. The mean lengthening rate during the first half of diastole decreased by 50% in the left ventricular internal short axis and by 119% in the posterior segment. Despite the significant impairment of early diastolic function, the regional end-diastolic pressure-segment length relation of the posterior wall was unchanged. Thus, in contrast to the results reported for pacing-induced ischemia that were measured immediately after pacing, the distensibility of the left ventricular wall in stunned myocardium induced by pacing was unchanged despite depressed early diastolic function.

Pericardial Pressure and the Left Ventricular Pressure-Volume Relationship

1981 ◽  
Vol 61 (3) ◽  
pp. 34P-35P
Author(s):  
P.J. Oldershaw ◽  
M. St. John Sutton ◽  
P. Kay ◽  
D.G. Gibson
Keyword(s):  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Volume Relationship ◽  
Pressure Volume Relationship ◽  
Pericardial Pressure

scholarly journals Possible mechanism of the cardio-renal protective effects of AVE-0991, a non-peptide Mas-receptor agonist, in diabetic rats

2012 ◽  
Vol 13 (3) ◽  
pp. 334-340 ◽  
Author(s):  
Kulwinder Singh ◽  
Kuldeepak Sharma ◽  
Manjeet Singh ◽  
PL Sharma
Keyword(s):  
Blood Pressure ◽  
Receptor Agonist ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Protective Effects ◽  
Mas Receptor ◽  
Arterial Blood

Hypothesis: This study was designed to investigate the cardio-renal protective effect of AVE-0991, a non-peptide Mas-receptor agonist, and A-779, a Mas-receptor antagonist, in diabetic rats. Materials and methods: Wistar rats treated with streptozotocin (50 mg/kg, i.p., once), developed diabetes mellitus after 1 week. After 8 weeks, myocardial functions were assessed by measuring left ventricular developed pressure (LVDP), rate of left ventricular pressure development (d p/d tmax), rate of left ventricular pressure decay (d p/d tmin) and left ventricular end diastolic pressure (LVEDP) on an isolated Langendorff’s heart preparation. Further, mean arterial blood pressure (MABP) was measured by using the tail-cuff method. Assessment of renal functions and lipid profile was carried out using a spectrophotometer. Results: The administration of streptozotocin to rats produced persistent hyperglycaemia, dyslipidaemia and hypertension which consequently produced cardiac and renal dysfunction in 8 weeks. AVE0991 treatment produced cardio-renal protective effects, as evidenced by a significant increase in LVDP, d p/d tmax, d p/d tmin and a significant decrease in LVEDP, BUN, and protein urea. Further, AVE-0991 treatment for the first time has been shown to reduce dyslipidaemia and produced antihyperglycaemic activity in streptozotocin-treated rats. However, MABP and creatinine clearance remained unaffected with AVE-0991 treatment. Conclusions: AVE-0991 produced cardio-renal protection possibly by improving glucose and lipid metabolism in diabetic rats, independent of its blood pressure lowering action.

Abstract P109: Alteration in Intracellular Calcium During Cardiac Arrest

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Satoshi Takeda ◽  
Hiroshi Yoshida ◽  
Takeki Ogawa
Keyword(s):  
Cardiac Arrest ◽  
Intracellular Calcium ◽  
Cell Injury ◽  
Diastolic Pressure ◽  
Pulseless Electrical Activity ◽  
Left Ventricular Pressure ◽  
Cardiac Metabolism ◽  
Left Ventricular ◽  
Free Calcium ◽  
Developed Pressure

AIM: A cytosolic free calcium is an important regulator of cardiac metabolism and contractility, and an increased [Ca2+]i has been implicated in irreversible cell injury and contractile dysfunction. We investigated intracellular calcium ([Ca2+]i) dynamics during cardiac arrest, especially in pulseless electrical activity (PEA) and asystole. METHODS: Rat hearts (n=18) were perfused with a Langendorff system and loaded with Fura-2/AM, as a [Ca2+]i marker, and BCECF/AM, as a pHi marker. Surface fluorescence of the heart was recorded with an intracellular ion analyzer. A latex balloon was inserted into the left ventricle to monitor left ventricular pressure. Sustained normo-thermic cardiac arrest was induced for 20 min by clamping the aortic cannula. RESULTS: After clamping (cardiac arrest), the left ventricular developed pressure decreased significantly, from 84.3±11 mmHg to 3.88±0.7 mmHg (p<0.01) at 2min. The rhythm was PEA in all cases in this period, followed by asystole. The amplitude of the [Ca2+]i transient (0.30±0.03) was maintained at 2 min, but further significant increases were observed in both systolic (1.14±0.04, p<0.01) and diastolic levels of [Ca2+]i (0.84±0.04, p<0.05), when compared with pre-arrest levels. The [Ca2+]i transient disappeared 4.7±0.6 min. The diastolic [Ca2+]i increased gradually after 5 min to 20 min. This diastolic [Ca2+]i increase was parallel with the increase in left ventricular end diastolic pressure (indicated ischemic contracture). The pHi increased (to 7.6±1.0) immediately after clamping. Thereafter pHi decreased rapidly and remained steady (at pH 6.6±0.6). CONCLUSIONS: The change in the [Ca2+]i-pressure relationship rather than change in the amplitude of the [Ca2+]i transient was the main contributor in the early cardiac arrest phase. The diastolic [Ca2+]i increase might induce irreversible cell injury in the late cardiac arrest phase.

scholarly journals The pericardium substantially affects the left ventricular diastolic pressure-volume relationship in the dog.

1978 ◽  
Vol 42 (3) ◽  
pp. 433-441 ◽  
Author(s):  
S A Glantz ◽  
G A Misbach ◽  
W Y Moores ◽  
D G Mathey ◽  
J Lekven ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Left Ventricular ◽  
Volume Relationship ◽  
Pressure Volume Relationship
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