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Biomedical subjects

O A Smiseth

Publications and source records attributed to O A Smiseth.

At least 37 records · Page 2Linked to original sources
PubMed1997

Increased cardiac expression of endothelin-1 mRNA in ischemic heart failure in rats.

OBJECTIVES: Plasma endothelin (ET) concentrations are increased in heart failure. The aims of the present study were to investigate to what extent cardiac ET mRNA expression is induced in ischemic heart failure and whether there may be compensatory downregulation of myocardial mRNA levels for the ETA and ETB receptor subtypes. METHODS: In rats with ischemic heart failure (left ventricular end-diastolic pressure > 15 mmHg) due to left coronary artery ligation. Northern blot analyses were performed on mRNA isolated from cardiac tissues. RESULTS: A substantial upregulation was revealed in all chambers of the failing hearts. Up to 27-fold upregulation (mean 10.6 +/- 4.0, P = 0.002) of left ventricular ET-1 mRNA levels was measured 1 week after myocardial infarction, whereas only a modest upregulation was detected after 6 weeks (mean 2.7 +/- 0.5, P < 0.05). Ribonuclease protection assay revealed 2.8 +/- 0.4-fold higher levels of ET-1 mRNA in the left ventricular area subjected to myocardial infarction compared to the non-infarcted tissue after 1 week. Left ventricular ET-1 mRNA correlated significantly with left ventricular end-diastolic pressure after 1 week (r2 = 0.86, P = 0.007). The ETA and ETB receptor mRNA levels tended to increase 1 week after myocardial infarction although these changes were not statistically significant. CONCLUSIONS: Cardiac ET-1 mRNA levels are increased in ischemic heart failure and correlate significantly with left ventricular end-diastolic pressure 1 week after myocardial infarction. The increase in cardiac ET-1 mRNA is not accompanied by a decrease in ET receptor mRNA.

Animals↗
PubMed1997

Transient, isopeptide-specific induction of myocardial endothelin-1 mRNA in congestive heart failure in rats.

Increased myocardial expression of preproendothelin-1 (ppET-1) mRNA has been associated with congestive heart failure (CHF) in rats. However, the time course and isoform pattern of ppET mRNA induction and the cellular localization of ET in failing hearts are unknown. Thus our aim was to investigate myocardial ppET mRNA expression in CHF rats during the first 6 wk after induction of myocardial infarction. Furthermore, performing immunohistochemical analysis, we also investigated the origin and localization of immunoreactive endothelin (ET) in different regions of the failing heart. Ribonuclease protection assays revealed a marked increase in ppET-1 mRNA levels in rat myocardial tissues during CHF. The induction of ppET-1 mRNA was isopeptide specific and transient. The most substantial upregulation was observed in the infarcted area, where maximal expression of ppET-1 mRNA was observed after 7 days (25-fold increase, P < 0.05). However, a marked and statistically significant induction of ppET-1 mRNA was also observed in the nonischemic myocardium. Immunohistochemical analysis revealed ET-1-like immunoreactivity in cardiomyocytes, vascular endothelial cells, macrophages, and proliferating fibroblasts. Thus immunohistochemistry revealed the structural basis for the dramatic upregulation of the myocardial ET system in the infarcted region, suggesting a role for ET in the healing process after myocardial infarction. However, the global upregulation of ppET-1 mRNA in the heart also suggests an autocrine/paracrine regulatory mechanism in the nonischemic myocardium during CHF.

Animals↗
PubMed1996

[Physicians' view on drug therapy for hypertension. A questionnaire in the county of Hordaland].

A questionnaire survey was conducted in Hordaland county to discover opinions on drug therapy for uncomplicated hypertensives with no other risk factors. The response rate was 66%; 179 general practitioners and 31 hospital doctors. The doctors were well informed about the documentation of the clinical benefit of various drugs. As regards the minimum blood pressure that was considered as warranting drug treatment, the majority of the doctors followed the recently issued national guidelines. For young patients the first choice drugs were beta-blockers (27%), ACE-inhibitors (25%) or calcium-blockers (20%). For older patients 65% of the doctors preferred diuretics or beta-blockers. The majority (80%) based their choice of drug primarily on documentation of clinical value or absence of side effects. The doctors underestimated the cost of the newer antihypertensive drugs.

Adult↗
PubMed1996

[Cardiology education in Norway--does it keep up with the needs?].

Despite an increase in the number of education positions for cardiologists in Norway in the late 1980s, there is felt to be a marked lack of sub-specialists in cardiology in most types of hospitals. A working group under the Norwegian Society of Cardiology has used a questionnaire in 1993, membership data from the Norwegian Society of Cardiology in 1994, a telephone query to all hospitals in the country, and data from the Norwegian Medical Association in 1995 to examine this apparent lack of specialists and the potentials for educating them. We were able to confirm a current lack of approximately 60 cardiologists. In addition, the capacity for education has been reduced and will not compensate for the predicted retirement of specialists from approximately year 2000. The capacity for educating cardiologists must be increased.

Cardiology↗
PubMed1996

A potential clinical method for calculating transmural left ventricular filling pressure during positive end-expiratory pressure ventilation: an intraoperative study in humans.

OBJECTIVES: This study sought to investigate whether right atrial pressure could be used to estimate pericardial pressure during positive end-expiratory pressure (PEEP). BACKGROUND: Because of elevated intrathoracic pressure during PEEP, pulmonary capillary wedge pressure may not accurately reflect left ventricular preload. An estimate of pericardial pressure during PEEP would allow assessment of transmural filling pressure. METHODS: In eight patients, at the start of cardiac surgery, pericardial and pleural pressures were recorded by balloon transducers placed over the anterolateral left ventricular wall. We also recorded intravascular pressures and left ventricular short-axis area by transesophageal echocardiography. RESULTS: A stepwise increase in PEEP from 0 to 15 cm H2O caused a linear increase in pleural pressure from 0.3 +/- 0.6 (mean +/- SEM) to 6.1 +/- 0.8 mm Hg (p < 0.01). Pericardial pressure increased from 2.3 +/- 0.5 to 5.9 +/- 0.6 mm Hg (p < 0.01). The correlation between right atrial (Pra) and pericardial pressure (Pperic) was good: Pra = 0.85 x Pperic + 1.8, r = 0.77. The correlation between changes in right atrial pressure and in pericardial pressure was better: delta Pra = 0.96 x delta Pperic -0.2, r = 0.97. Pulmonary capillary wedge pressure increased with PEEP (p < 0.05), whereas left ventricular area decreased (p < 0.05). However, there was a progressive reduction in transmural pressure, calculated as wedge pressure minus pericardial pressure (p < 0.05), and in transmural pressure, estimated as wedge pressure minus right atrial pressure (p < 0.05). The estimated transmural filling pressure correlated (r = 0.86) with end-diastolic area. CONCLUSIONS: The present observations suggest that right atrial pressure may be used to estimate changes in pericardial pressure with PEEP and that pulmonary capillary wedge pressure minus right atrial pressure is a potentially clinically useful approximation of transmural filling pressure.

Adult↗
PubMed1996

Nitric oxide synthase inhibition reduces venous return in porcine endotoxemia.

Mechanisms of circulatory effects induced by nitric oxide synthase inhibition in endotoxemia were investigated in 36 pigs randomized to 1) endotoxin infusion (1.7 micrograms.kg-1.h-1 iv) for 7 h and bolus NG-nitro-L-arginine methyl ester (L-NAME; 25 mg/kg iv) after 3 h; 2) endotoxin infusion for 7 h; 3) saline infusion for 7 h and L-NAME after 3 h; and 4) saline infusion for 7 h. Fifteen minutes after L-NAME injection during endotoxemia, reductions in cardiac output (41%, P < 0.05), portal venous flow (51%, P < 0.05), and hepatic artery flow (50%, P < 0.05) were observed. Systemic vascular resistance increased by 82% (P < 0.05), and the portocaval vascular resistance increased by 101% (P < 0.05). Despite marked vasoconstriction after L-NAME, left ventricular intracavitary filling pressure, central venous pressure, and arterial pressure remained unchanged. During endotoxemia, hematocrit increased from 38.4 +/- 1.4 to 41.9 +/- 1.2 after L-NAME, and blood volume (n = 3) was reduced by an average of 8.3 ml/kg body wt. These changes probably reflect transcapillary fluid loss as urine output was unchanged. In conclusion, L-NAME decreased intravascular blood volume and increased splanchnic venous resistance. These effects will tend to reduce venous return. Combined with a marked increase in left ventricular after-load, L-NAME may thus compromise cardiovascular function in endotoxemia.

Animals↗
PubMed1996

The NO donor sodium nitroprusside reverses the negative effects on hepatic arterial flow induced by endotoxin and the NO synthase inhibitor L-NAME.

In previous studies we have observed that the nitric oxide synthase inhibitor L-NAME induces a profound deterioration of liver circulation in experimental endotoxemia. Using the same porcine model we now have evaluated the possibility of modulating these effects with the nitric oxide donor sodium nitroprusside. Infusion of endotoxin led to a gradual deterioration of hemodynamic parameters, including liver blood flow. The decreases in portal blood flow paralleled and matched the decreases in cardiac output, and no compensatory increase in hepatic arterial flow occurred. L-NAME had detrimental effects on hemodynamics, including the liver circulation. The latter effects could, however, partially be reversed by sodium nitroprusside. Hepatic arterial flow increased from 1.9 to 7.2 ml/kg/min, with a concomitant decrease in hepatic arterial resistance from 5,364 to 1,746 dyn s/cm5 kg. A control group exhibited no significant change in either flow or resistance. The response to sodium nitroprusside was rapid and vigorous, and probably largely due to relaxation of the hepatic arterioles, and not to abatement of intrahepatic edema or plugging of the sinusoids. Furthermore, we conclude that the endotoxin-induced dysfunction of the hepatic arterial buffer response may be due to a selective inhibition of vascular endothelial function.

Animals↗
PubMed1995

Splanchnic venous pressure-volume relation during experimental acute ischemic heart failure. Differential effects of hydralazine, enalaprilat, and nitroglycerin.

BACKGROUND: Vasodilator drugs have variable effects on veins and arteries. However, direct measurements of their effects on the splanchnic veins, perhaps the most important volume reservoir, have not been reported. We assessed the effect of acute heart failure and the subsequent administration of hydralazine, enalaprilat, and nitroglycerin on the splanchnic venous pressure-volume relation in intact dogs. METHODS AND RESULTS: Experimental acute ischemic heart failure was induced in 19 splenectomized dogs by microsphere embolization of the left main coronary artery. Embolization was repeated until left ventricular end-diastolic pressure (LVEDP) reached 20 mm Hg and cardiac output decreased by 50%. The splanchnic vascular pressure-volume relation was determined by radionuclide plethysmography during the control stage, after acute heart failure had been established, and after administration of a vasodilator (hydralazine, enalaprilat, or nitroglycerin) at a dose sufficient to reduce mean aortic pressure by approximately 20%. Induction of acute heart failure was associated with a decrease in the splanchnic vascular volume from 100% to 86 +/- 2% and an increase in LVEDP from 6 +/- 1 to 21 +/- 1 mm Hg (P < .001). There was a parallel leftward shift of the splanchnic vascular pressure-volume curve. After the administration of hydralazine, enalaprilat, and nitroglycerin, the splanchnic vascular volumes increased from 86% to 88 +/- 3%, 96 +/- 3%, and 113 +/- 3%, respectively (P = NS, P < .01, and P < .001, respectively, versus heart failure). After drug administration, the LVEDPs were 18 +/- 2, 16 +/- 1, and 13 +/- 1 mm Hg (P = NS, P < .05, and P < .001, respectively, versus heart failure). CONCLUSIONS: Acute heart failure was associated with a parallel leftward shift of the splanchnic venous pressure-volume relation (venoconstriction). Splanchnic (systemic) venoconstriction may in part explain the increased LVEDP during acute heart failure by displacement of blood to the central compartment. Subsequently administered enalaprilat and, to a greater degree, nitroglycerin produced splanchnic venodilation, thereby lowering LVEDP. Hydralazine had no significant effect on the splanchnic veins and only a modest effect on LVEDP. In this model, splanchnic capacitance changes appear to modulate change in left ventricular preload.

Animals↗
PubMed1995

Measurement of intestinal vascular capacitance in dogs: an application of blood pool scintigraphy.

To define relative changes in intestinal vascular capacitance, we developed a model that allowed us to construct intestinal vascular pressure-volume relationships (PVR). Thirteen alpha-chloralose-anesthetized and splenectomized dogs were studied using a pneumatic constrictor and a small catheter to change and measure portal venous pressure. A small lead sheet was placed beneath the abdominal wall. Relative changes in intestinal blood volume (IBV) were determined by in vivo blood pool scintigraphy with 99mTc-labeled erythrocytes and were expressed as percentages corrected for specific activity and abdominal wall radioactivity. PVRs were constructed using data recorded during graded inflations of the portal venous constrictor. The abdominal wall contributed 32.4 +/- 7.7% (SD) of the total counts. During a 4-h control period, PVRs varied by no more than 6% (of IBV). In the isolated intestinal circulation, the change in IBV was precisely proportional to the volume of blood added, indicating that this method can detect very small changes in volume (< or = 5 ml). Nitroglycerin (25 micrograms.kg-1.min-1) increased capacitance by 20%. Although it measures only relative changes, the model is stable and sensitive, provides reproducible measurement of intestinal PVRs, and, with adaptation, may prove useful in patient studies.

Abdomen↗
PubMed1994

Juxtacardiac pleural pressure during positive end-expiratory pressure ventilation: an intraoperative study in patients with open pericardium.

OBJECTIVES: This study was conducted to measure the cardiac constraining effect of the lungs during positive end-expiratory pressure and relate extracardiac pleural pressure (radial stress) to airway pressure, right atrial pressure and left ventricular filling. BACKGROUND: During positive end-expiratory pressure ventilation, the extracardiac pressure is elevated, and therefore intracavitary filling pressure does not reflect ventricular preload. Estimates of this pressure might be useful clinically to assess left ventricular preload. METHODS: In eight patients who had undergone coronary or valvular surgery and whose pericardium was left widely open, a flat pleural balloon transducer was placed over the anterolateral left ventricular wall. We recorded pulmonary capillary wedge pressure, right atrial pressure and left ventricular short-axis end-diastolic area by transesophageal echocardiography. Incremental positive end-expiratory pressure was applied. RESULTS: Extracardiac pleural pressure increased (p < 0.01) from 0.6 +/- 1.8 (+/- SD) to 2.4 +/- 1.8, 5.3 +/- 1.5 and 8.2 +/- 1.5 mm Hg at a positive end-expiratory pressure of 5, 10 and 15 cm H2O, respectively. The slope relating extracardiac pleural pressure to positive end-expiratory pressure (in mm Hg) was 0.70 +/- 0.10, and the intercept was zero. Increasing extracardiac pleural pressure was associated with a progressive increase in pulmonary capillary wedge pressure and a decrease in left ventricular end-diastolic area. Consequently, although pulmonary capillary wedge pressure and left ventricular area changed in opposite directions, the value of pulmonary capillary wedge pressure minus extracardiac pleural pressure correlated positively with left ventricular area (r = 0.95, p < 0.001). Changes in right atrial pressure (Pra) correlated with changes in extracardiac pleural pressure (Ppleural): delta Pra = -0.3 + 0.56. delta Ppleural (r = 0.89, p < 0.001). CONCLUSIONS: In postoperative patients with open pericardium, pulmonary capillary wedge pressure minus extracardiac pleural pressure predicts left ventricular end-diastolic area during positive end-expiratory pressure. Further studies should be done to determine whether the observed relations between airway pressure and extracardiac pleural pressure and between right atrial pressure and extracardiac pleural pressure may give clinically useful estimates of left ventricular preload during positive end-expiratory pressure.

Aged↗
PubMed1994

Visual assessment of intra ventricular flow from colour M-mode Doppler images.

Left intra ventricular filling was studied by colour M-mode Doppler ultrasound to determine whether the flow pattern can be assessed visually, and explore its relation to left ventricular (LV) function. Patients with coronary artery disease (CAD) or dilated cardiomyopathy (DCM) were divided into three groups according to angiographically evaluated LV function. The groups were compared with a control group of 54 healthy volunteers. The mitral to apical delay of early diastolic flow was qualitatively assessed from printed colour M-mode images, twice by four independent observers blinded to the subject's status. The repeatability of the assessments as determined by the kappa statistic was good intra observer (kappa = 0.75) and moderate inter observer (kappa = 0.53). The CAD-group with angiographically normal LV function (n = 25) had flow patterns resembling those observed in the control group. The group with ejection fraction (EF) < 50% (n = 19) had flow patterns clearly different from the control group. Patients with regional wall motion abnormality (RWMA) but EF > 50% (n = 16) exhibited flow patterns intermediate between the control and the low EF group. Among the 50 CAD patients there was a negative correlation between EF and the presence of delay of apical peak velocity (Spearman's rs = -0.62, p < 0.0001). A visible delay of apical peak velocity had a sensitivity towards DCM of 83% and specificity of 75%. The sensitivity towards CAD with either RWMA or low EF was 55% and the specificity 75%. In conclusion, visual assessment of intra ventricular flow patterns was feasible and allowed discrimination between normal and diseased ventricles.

Adult↗
PubMed1994

Repeatability of colour M-mode Doppler measurements of left ventricular filling.

We investigated the repeatability of two recently reported colour M-mode Doppler measures of left ventricular diastolic function. 'Delay of peak velocity' is the time interval from peak velocity of early filling at the mitral tip level to peak velocity in the apical region. The 'velocity of flow propagation' is the speed of the mitral to apical spread of the early diastolic filling. Two examiners independently and blindly made measurements by both methods on 32 digital recordings twice, using custom software. Inter- and intra-observer repeatability were given in terms of limits of agreement, where 1 denotes perfect agreement. Limits of intra-observer agreement were 0.72-1.43 for measurements of 'delay of peak velocity', and 0.39-2.28 for 'velocity of flow propagation'. Limits of inter-observer agreement were 0.68-1.42 and 0.19-2.04 respectively. The correlation between the methods was weak (r = 0.45), suggesting that they may detect different properties of early diastole. We suggest that the reliability of the methods may be improved by replicate measurements performed blindly. There are reasons to express the velocity of flow propagation on a logarithmic scale.

Echocardiography, Doppler↗
PubMed1994

Intracavitary filling pattern in the failing left ventricle assessed by color M-mode Doppler echocardiography.

OBJECTIVES: The present study aimed to investigate the mechanism of intracavitary changes in filling pattern during acute ischemic left ventricular failure and during beta-adrenergic blockade. BACKGROUND: Recent clinical studies with color M-mode Doppler imaging have shown abnormal intracavitary filling patterns in the diseased ventricle. METHODS: In open chest anesthetized dogs with intracardiac micromanometers and myocardial segment-length crystals, global ischemic left ventricular failure was induced (n = 8) by coronary microembolization. In nonischemic ventricles inotropy was decreased (n = 6) by intravenous propranolol and increased (n = 6) by intravenous isoproterenol. From color M-mode Doppler images we calculated the time difference between peak early diastolic filling velocity at the mitral tip and apex using computer analysis. The time difference of peak velocity was used as an index of the timing of apical filling. RESULTS: There was marked retardation of apical filling with microembolization and propranolol. Time difference of peak velocity increased from 20 +/- 6 (mean +/- SEM) to 101 +/- 17 ms (p < 0.05) and from 21 +/- 8 to 80 +/- 18 ms (p < 0.05), respectively. Time constant of isovolumic relaxation increased from 34 +/- 3 to 43 +/- 5 ms (p < 0.05) and from 31 +/- 1 to 39 +/- 3 ms (p < 0.05) during microembolization and beta-blockade, respectively. Isoproterenol tended to cause the opposite changes. Time difference of peak velocity showed a positive correlation with time constant of isovolumic relaxation (r = 0.89, p < 0.01) and a negative correlation with peak early transmitral pressure gradient (r = 0.88, p < 0.01). In the intact left ventricle, peak apical filling velocity coincided with peak early transmitral pressure gradient. During ischemic failure however, peak apical filling velocity occurred 53 +/- 14 ms after peak early transmitral pressure gradient had decreased to zero and at a time when transmitral flow had ceased, suggesting a change in intraventricular flow distribution. CONCLUSIONS: Color M-mode Doppler imaging revealed retarded apical filling during depression of myocardial function by global myocardial ischemia or beta-blockade. The abnormal filling pattern may be a sign of impaired left ventricular relaxation.

Animals↗
PubMed1994

Selective positive end-expiratory pressure and right ventricular function in dogs.

Differential ventilation with selective positive end-expiratory pressure (PEEP) has been shown to reduce cardiac output less than general PEEP. In previous studies we have demonstrated that during selective PEEP left ventricular preload is better maintained than during general PEEP. The present study was designed to determine whether the different haemodynamic responses to selective and general PEEP also might be due to different effects on RV preload. The study was performed on nine acutely instrumented dogs, in which extraventricular pressure was measured by pericardial balloon transducers. Measures of RV preload were obtained by the use of ultrasonic segment length transducers as well as end-diastolic transmural pressure (RVEDP). The study showed reductions in RVEDP during general and selective right (R) PEEP, accompanied by moderate reductions in RV inflow tract segment lengths. These changes were most marked with general PEEP. Selective LPEEP did not change RV preload significantly. Therefore, better maintained cardiac output with selective PEEP than with general PEEP is partly due to less impairment of right ventricular filling.

Animals↗
PubMed1994

Effect of carotid sinus baroreceptor reflex on hepatic and splenic vascular capacitance in vagotomized dogs.

Mechanisms of how baroreflex activation changes splanchnic vascular volumes were studied in eight vagotomized dogs, anesthetized by chloralose/urethan. Hepatic and splenic vascular volume changes were determined from organ dimensions by sonomicrometry. Pulsatile carotid sinus pressure (CSP) in isolated and separately perfused carotid sinuses was changed among 200, 120, and 40 mmHg. Lowering CSP from 120 to 40 mmHg significantly decreased both hepatic and splenic vascular volume (at similar portal pressure) by 1.9 +/- 0.5 and 1.8 +/- 0.6 ml/kg body wt, respectively. Increasing CSP from 120 to 200 mmHg tended to increase regional vascular volumes (P = NS). The combined volume change of liver and spleen between CSP 40 and 200 mmHg was 4.2 +/- 0.6 ml/kg body wt (P < 0.001). Pressure-volume (dimension) curves at high, low, and baseline CSP were determined to separate active and passive mechanisms of vascular volume changes. Changes in CSP did not change regional vascular compliance. Low CSP significantly decreased unstressed liver and unstressed splenic volume by 3.3 +/- 0.9 and 1.9 +/- 0.5 ml/kg body wt, respectively. These results indicate that liver and spleen both contribute to blood volume mobilization by vasoconstriction during low CSP and that the carotid sinus baroreceptor reflex modulates hepatic and splenic vascular capacitance by changing unstressed volume rather than by changing vascular compliance.

Animals↗
PubMed1994

Effect of enalaprilat on splanchnic vascular capacitance during acute ischemic heart failure in dogs.

This study investigates the effect of angiotensin-converting-enzyme inhibition by intravenous enalaprilat (100 micrograms/kg) on splanchnic vascular capacitance during acute left ventricular failure induced by coronary microembolization in alpha-chloralose/urethan anesthetized dogs. Changes in hepatic and splenic vascular volumes were determined from organ diameters (sonomicrometry) at 15, 30, and 45 min after enalaprilat injection. Changes in vascular capacitance were assessed from organ pressure-diameter curves obtained during transient hepatic outflow occlusion. Thirty minutes after enalaprilat, hepatic volume was increased by 52 +/- 14 ml (P < 0.01), and portal and hepatic vein pressures were decreased from 10.2 +/- 0.9 to 8.7 +/- 0.8 mmHg (P < 0.01) and from 3.9 +/- 1.6 to 3.1 +/- 0.7 mmHg (P < 0.05), respectively. Splenic volume did not change. Enalaprilat shifted the hepatic pressure-diameter curve upward, resulting in a larger hepatic volume at any given pressure. Curve intercept was increased, suggesting an increase in unstressed vascular volume. Curve slope was unchanged. In conclusion, enalaprilat increased hepatic vascular volume during acute left ventricular failure in dogs. The pressure-diameter curve shift suggests a reduction in the smooth muscle tone of hepatic capacitance vessels.

Acute Disease↗
PubMed1994

Influence of heart rate and left atrial pressure on pulmonary venous flow pattern in dogs.

In six open-chest anesthetized dogs we investigated the effect of heart rate (HR) on the relationship between left atrial pressure (LAP) and pulmonary venous flow (QPV). QPV was measured by ultrasonic transit time during volume loading and right atrial pacing. Consistent with previous studies, we found a negative correlation between LAP and mean flow rate during atrial systole divided by mean flow rate in the R-R interval. However, this relationship was shifted upward by tachycardia. The QPV maximum amplitude divided by mean flow rate in the R-R interval increased with loading but decreased with tachycardia. mean flow rate during ventricular systole divided by mean flow rate during the R-R interval increased with both loading and tachycardia. Regression coefficients for HR and LAP as predictors of these indexes were all significantly different from zero (P = 0.0001). We conclude that HR significantly influences the relationship between the QPV pattern and LAP. This could be a limitation of the pulmonary venous flow pattern as an indicator of left ventricular diastolic function.

Animals↗