Cerebral nitric oxide concentration and microcirculation during hypercapnia, hypoxia, and high intracranial pressure in pigs.

Intracerebral nitric oxide (NO) concentration was measured to establish the technique and to investigate the response of the NO concentration to CO(2)variations, hypoxia, and reduced cerebral perfusion pressure. An intracerebral nitric oxide sensor was used in 10 pigs. Cerebral microcirculation was measured by laser Doppler flowmetry. Five pigs received 40 mg/kg nitro-1-arginine methyl ester (L-NAME). Baseline NO concentration was 246 +/- 42 nM. Hypercapnia increased cerebral microcirculation (P< 0.05) and NO concentration (P< 0.05). Hypoxia decreased NO concentration (P< 0.05). During high intracranial pressure, cerebral microcirculation decreased (P< 0.05) before the NO concentration decreased (P< 0.05), and after normalisation of the intracranial pressure the NO concentration increased, but more slowly than the cerebral microcirculation. L-NAME caused a decrease in cerebral microcirculation (P< 0.05) and NO concentration (P< 0.05) to a new steady state, and L-NAME attenuated the changes in NO concentration after hypoxia (P< 0.05) and high intracranial pressure (P< 0.05). In conclusion, the electrochemical sensor appears to reliably detect changes in localised intracerebral NO concentration and seems to be a promising tool for direct measurement of this chemically unstable substance.

Methods for assessing hepatic distending pressure and changes in hepatic capacitance in pigs.

The equilibrium pressure obtained during simultaneous occlusion of hepatic vascular inflow and outflow was taken as the reference estimate of hepatic vascular distending pressure (P(hd)). P(hd) at baseline was 1.1 +/- 0.2 (mean +/- SE) mmHg higher than hepatic vein pressure (P(hv)) and 0.7 +/- 0.3 mmHg lower than portal vein pressure (P(pv)). Norepinephrine (NE) infusion increased P(hd) by 1. 5 +/- 0.5 mmHg and P(pv) by 3.7 +/- 0.6 mmHg but did not significantly increase P(hv). Hepatic lobar vein pressure (P(hlv)) measured by a micromanometer tipped 2-Fr catheter closely resembled P(hd) both at baseline and during NE-infusion. Dynamic pressure-volume (PV) curves were constructed from continuous measurements of P(hv) and hepatic blood volume increases (estimated by sonomicrometry) during brief occlusions of hepatic vascular outflow and compared with static PV curves constructed from P(hd) determinations at five different hepatic volumes. Estimates of hepatic vascular compliance and changes in unstressed blood volume from the two methods were in close agreement with hepatic compliance averaging 32 +/- 2 ml. mmHg(-1). kg liver(-1). NE infusion reduced unstressed blood volume by 110 +/- 38 ml/kg liver but did not alter compliance. In conclusion, P(hlv) reflects hepatic distending pressure, and the construction of dynamic PV curves is a fast and valid method for assessing hepatic compliance and changes in unstressed blood volume.

Cerebrovascular effects of high intracranial pressure after moderate hemorrhage.

Patients with head injuries often develop increased intracranial pressure after hemorrhage. The authors studied the effect of moderate hemorrhage followed by elevated intracranial pressure on cerebrovascular variables. Cerebral blood flow in 13 pigs was measured with laser Doppler flowmetry, and cerebral venous blood gases were taken from the sagittal sinus. High intracranial pressure (80% of mean arterial pressure) was induced by infusion of artificial cerebrospinal fluid into the cisterna magna, and blood pressure was reduced by bleeding to a mean of 78% of the prebleeding values in eight pigs. Five pigs served as secondary controls. High intracranial pressure before hemorrhage caused a decrease in cerebral blood flow to 34% of the baseline values, a decrease in sagittal sinus oxygen saturation to 46%, and a decrease in cerebral perfusion pressure to 36%, but did not change cerebrovascular resistance. High intracranial pressure after hemorrhage decreased cerebral blood flow to 14% of baseline values. Sagittal sinus oxygen saturation decreased to 22%, cerebral perfusion pressure decreased to 30%, and the cerebrovascular resistance increased by 355%. The moderate hypotension after hemorrhage caused a considerable enhancement of the effects of high intracranial pressure on cerebral hemodynamics.

Effect of hemorrhage on cerebral microcirculation during normal and high cerebrospinal fluid pressure in pigs.

Studies on cerebral blood flow during hypotension and high intracranial pressure are scarce. Accordingly, this study examines the effects of increased cerebrospinal fluid (CSF) pressure on the cerebral circulatory response to hemorrhage. Measurements of cerebral microcirculation with laser Doppler flowmetry was performed in 12 pentobarbital-anesthetized pigs during hemorrhage, with and without high CSF pressure. Arterial and CSF pressures were monitored. Laser Doppler microprobes were positioned on the brain surface and in the gray and white matter. High CSF pressure (80% of mean arterial pressure) was induced by infusion of artificial CSF into the cisterna magna in eight pigs, whereas four animals served as controls. The response to rapid arterial bleeding at normal and high CSF pressure was recorded. When CSF pressure was normal, bleeding of 15% and 25% of the total blood volume caused a drop of cerebral perfusion pressure to 73 and 71 mmHg, respectively, causing a decrease in the laser Doppler signal to 90+/-8% of the baseline value. During high CSF pressure, the cerebral perfusion pressure was 23 mmHg and the laser Doppler signal was 52+/-29% of baseline. Bleeding of 15% of blood volume reduced the laser Doppler signal to 0 (equal to postmortem values) in three pigs, and bleeding of 25% of the blood volume reduced the laser Doppler signal to 0 in seven of eight pigs. Consequently, a blood loss that is of minor importance for the cerebral microcirculation in the normal state may be deleterious to the circulation when combined with high CSF pressure.

Local variations in the cerebral microcirculatory response to hypercapnia and haemorrhage.

This study evaluates local variations of the cerebral vasomotor responses to hypercapnia and haemorrhagic hypotension in a pig model. Four laser Doppler flow probes were used in each pig. There was considerable variation in laser Doppler signals between the four probes in baseline recordings. The increases in flow after CO2 administration in 7 pigs had a mean coefficient of variation of 0.43 +/- 0.31, and the flow changes after blood loss in another 7 pigs had a mean coefficient of variation of 0.45 +/- 0.34. The range of flow changes within each animal was large; the probe with the highest CO2 response showed on the average a 273% +/- 157% larger CO2 response than the probe with the lowest CO2 response. Correspondingly, the probe with the best preserved blood flow after blood loss had on the average a flow value of 93% +/- 12% of the baseline value, while the probe that changed most with haemorrhage had a flow value of 44% +/- 24% of the baseline value. Single laser Doppler recordings have been used for the monitoring of cerebral blood flow in neurosurgical critical care, but our results suggest that a single laser Doppler flow probe is not an adequate method to monitor vasoreactivity in neurosurgical patients because flow signals from one probe may be unrepresentative for other sites in the brain.

Regulation of hepatic vascular volume: contributions from active and passive mechanisms during catecholamine and sodium nitroprusside infusion.

BACKGROUND: It is unclear how the liver contributes to regulation of cardiac filling. The aims of this study were to establish an animal model to quantify hepatic vascular capacitance and to determine the mechanisms whereby catecholamines and sodium nitroprusside modify hepatic blood volume. METHODS AND RESULTS: In 8 anesthetized pigs we measured hepatic and systemic pressures and flows. Liver vascular volume was measured by sonomicrometry calibrated against integrated hepatic inflow during outflow occlusion. Pressure-volume (P-V) curves were constructed during outflow occlusion. Sonomicrometry accurately reflected hepatic blood volume (r=.99+/-.001), and hepatic P-V curves were highly reproducible. Norepinephrine (0.3 and 0.7 microg x kg body weight (bwt)(-1) min(-1) intraportally) significantly reduced hepatic blood volume by 3.3+/-1 and 4.3+/-1 mL x kg bwt(-1), respectively. Nitroprusside (8 and 18 microg x kg bwt(-1) x min(-1) intraportally) increased hepatic blood volume by 1.1+/-0.2 and 1.9+/-0.3 mL x kg bwt(-1), respectively. Norepinephrine and nitroprusside parallel shifted the hepatic P-V curves, indicating reduced and increased unstressed blood volume, respectively. These curve shifts accounted for more than 90% of the respective blood volume changes. Compliance was unchanged. Phenylephrine but not isoprenaline yielded similar results as norepinephrine. CONCLUSIONS: The pig model used in this study, accurately quantified hepatic capacitance. Alpha-adrenergic stimulation decreased and nitroprusside increased capacitance by changing unstressed blood volume. These changes in capacitance correspond to expulsion of 300 mL and pooling of 130 mL of blood, respectively, in a 70-kg individual, reflecting that the liver is not only a passive blood reservoir but can respond actively and vigorously to pharmacological interventions.

Cardiovascular response to blood loss during high intracranial pressure.

The authors hypothesized that the combination of hemorrhage and increased intracranial pressure (ICP) has deleterious effects on cardiovascular function. The effect of blood loss during normal and increased ICP was studied in eight pigs. The mean arterial pressure (MAP), pulmonary arterial pressure, pulmonary capillary wedge pressure, cardiac output, and cerebrospinal fluid (CSF) pressure were measured. The regional tissue blood flow was determined with radioactive microspheres labeled with four different nuclides. High ICP (80% of MAP) was induced by infusion of artificial CSF into the cisterna magna. The response to rapid arterial bleeding of 25% of blood volume was measured. The decrease in blood flow to the intestine, skeletal muscle, and the kidneys after blood loss was significantly greater during high ICP. The decrease in blood flow to the spleen and pancreas tended to be greater during high ICP, whereas the changes in blood flow to the liver, adrenal glands, and heart muscle showed no such tendency. The fall in cardiac output and heart stroke volume after blood loss were more pronounced when the ICP was high, and the increase in systemic vascular resistance was considerably greater. These observations suggest that during high ICP the physiological protective mechanisms against blood loss are impaired in the systemic circulation, and a loss of 25% of the blood volume, normally well compensated for, may induce a state of shock.

Cerebral blood flow measured with intracerebral laser-Dopplerflow probes and radioactive microspheres.

We have measured cerebral blood flow with intracerebral laser-Doppler microprobes in pentobarbital-anesthetized pigs. We compared the results with measurements from laser-Doppler probes placed on the surface of the brain and with blood flow estimation by the radioactive microsphere method. The cerebral blood flow was varied by alterations in inspired carbon dioxide, hemorrhagic hypotension, and high cerebrospinal fluid pressure. The intracerebral probes and the surface probes showed parallel responses to variations in cerebral blood flow. The correlation was closest between surface probes and the intracerebral probes measuring from the cerebral cortex (r = 0.46; P < 0.005). The r value between laser-Doppler flowmetry and radioactive microspheres was 0.41 (P < 0.0005) for all measurements. The correlation to microspheres was best for the probes located 3 or 10 mm into the brain and poorest for the surface probe. In conclusion, intracerebral laser-Doppler flow measurements reflect changes in blood flow, and the technique appears useful for continuous estimates of cerebral blood flow.

Rhythmical fluctuations of the intracerebral microcirculation studied in pigs.

Rhythmic variations in blood flow have been observed in various vascular beds, including brain. We have characterized fluctuations of the microcirculation in different locations in the brain, and studied the response to changes in arterial carbon dioxide tension, arterial pressure, and cerebrospinal fluid pressure. Laser Doppler flowmetry was performed in 20 pentobarbital-anesthetized pigs. Flow probes were positioned on the brain surface and 3, 10, and 20 mm into the cerebral tissue. The protocol included carbon dioxide breath- ing, hemorrhagic hypotension, and infusion into the cisterna magna. Twenty-five periods of low-frequency oscillations (4.5/min) were found in 10 pigs with superimposed spindle-shaped rhythmic variations (0.5/min) of the amplitude in 7. There were no rhythmic changes in arterial pressure or intracranial pressure. Rhythmic activity was most often seen in the probe positioned 20 mm into the brain and was often seen in several probes at the same time. Animals with rhythmic oscillations before interventions had lower cerebral perfusion pressure and arterial pressure, lower heart rate, and higher laser Doppler signal than the others. Blood loss often initiatied oscillations. High intracranial pressure tended to abolish preexisting oscillations. Hypercapnia always abolished preexisting oscillations. Oscillations were more frequent if the cerebral perfusion pressure was in the low range of cerebral autoregulation, occurred more often in the cerebral locations with relatively high local flow, were most likely to be localized, and therefore probably caused by local metabolic or myogenic variations.

Intraventricular early diastolic velocity profile during acute myocardial ischemia: a color M-mode Doppler echocardiographic study.

The aim of the study was to investigate the effect of acute myocardial ischemia on the early diastolic mitral-to-apical velocity profile. Intraventricular filling velocities were measured by color M-mode Doppler echocardiography, which allows simultaneous measurements of velocities at multiple sites. Twenty patients were examined during angioplasty and eight dogs during transient coronary artery occlusion. Velocities at each 0.46 cm level from the mitral tip toward the apex were determined at the time of peak early transmitral velocity. Before angioplasty, early diastolic flow velocities decreased progressively from the mitral tip toward the apex. During angioplasty, intraventricular velocities showed a more abrupt decrease from the middle region toward the apex (p < 0.05). A similar change in the mitral-to-apical profile was found during myocardial ischemia in dogs (p < 0.05). Also, there was a decrease in peak early transmitral velocity (p < 0.01) and peak early transmitral pressure gradient (p = 0.06). Volume loading and constriction of the caval veins performed in the nonischemic ventricle did not appear to change the mitral-to-apical velocity profile. Regional myocardial ischemia was associated with a change in the mitral-to-apical velocity profile as measured by color M-mode Doppler echocardiography. The altered filling pattern could not be explained by changes in loading conditions and may reflect impaired relaxation of the ischemic ventricle.

A new color M-mode index of diastolic filling compared with radionuclide ventriculography.

We correlated the new diastolic index 'delay of apical peak velocity', as measured by colour M-mode Doppler, with radionuclide ventriculographic indices of ventricular function. Thirty-seven patients with coronary artery disease participated in the prospective and blinded study, which included repeated acquisitions to determine the effect of realigning the Doppler sample beam. In multiple regression, neither peak filling rate, left ventricular phase histogram width nor ejection fraction were statistically significantly related to delay of apical peak velocity. The standard deviation of the differences between duplicate colour M-mode acquisitions corresponded to half the reference range of the index. We conclude that in this blinded investigation, the new Doppler index did not provide information about ventricular function equivalent to radionuclide ventriculography. The index may be significantly influenced by sample beam position.

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.

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.

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.

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.

Intraventricular early diastolic filling during acute myocardial ischemia, assessment by multigated color m-mode Doppler echocardiography.

BACKGROUND: Color M-mode Doppler echocardiography has been suggested as a new noninvasive technique for assessing left ventricular diastolic function. The present study investigated intraventricular filling pattern by color M-mode Doppler in patients during percutaneous transluminal coronary angioplasty (PTCA). In a dog model of myocardial ischemia, the color M-mode flow pattern was related to indices of global and regional myocardial function. METHODS AND RESULTS: From color M-mode images, the time difference (TD) between occurrence of peak velocity in the apical region and at the mitral tip was determined in 20 patients and eight anesthetized dogs during coronary occlusions. During PTCA, the timing of peak velocity was progressively delayed from mitral valve to apex. Consistent with this, the dog model showed delayed apical filling during coronary occlusion; TD increased from 18 +/- 4 to 71 +/- 9 milliseconds (P < .01). In the ischemic region, systolic shortening (sonomicrometry) decreased from 20 +/- 3% to -5 +/- 2% (p < .01). The one-third filling fraction decreased from 59 +/- 5% to 31 +/- 6% (P < .01) and correlated with TD (r = .85, P < .01). The time constant of isovolumic relaxation (tau) increased slightly and correlated with TD (r = .81, P < .01). Pacing tachycardia, caval constriction, and volume loading were performed to mimic the ischemia-induced changes in heart rate, stroke volume, and intracavitary filling pressure, respectively. There were no significant changes in TD or tau during these interventions. CONCLUSIONS: Color M-mode Doppler echocardiography showed a marked delay of apical peak filling velocity during PTCA. The experimental data suggest that this reflects retarded filling of the ischemic ventricle. Thus, color M-mode Doppler may provide a useful method for assessing diastolic dysfunction.

Effect of nifedipine on splanchnic and pulmonary vascular capacitance.

This study examines the hypothesis that nifedipine may increase splanchnic vascular capacitance and thus change the distribution of blood between the splanchnic and pulmonary circulation in heart failure patients. Relative regional blood volumes were determined by equilibrium blood pool scintigraphy during a 10 min baseline period and for 30 min after nifedipine 20 mg sublingually, with simultaneous recordings of systemic and pulmonary arterial pressures, hepatic venous wedge pressure, and cardiac output. Eight patients with ischaemic heart failure received nifedipine. Four patients served as controls. Nifedipine reduced mean arterial pressure and systemic vascular resistance in every patient. There were no significant changes in the relative blood volumes of the intestinal, hepatic, or splenic regions or in hepatic venous wedge pressure (reflecting portal venous pressure), suggesting unchanged splanchnic vascular pressure-volume relationship. Nifedipine caused a 6.3 +/- 1.0% increase in relative pulmonary blood volume and a slight increase in pulmonary vascular distending pressure from 16.1 +/- 2.9 mmHg to 17.5 +/- 2.8 mmHg (P < 0.05), suggesting that the increase in pulmonary blood volume was passively mediated. In conclusion, nifedipine did not change splanchnic vascular capacitance, but caused a small increase in pulmonary blood volume, which probably was a passive response to increased distending pressure.

Is there a pericardial restriction to the cardiac secretion of atrial natriuretic factor?

Atrial natriuretic factor (ANF) is secreted from atrial myocytes in response to increased atrial wall stress caused by increased transmural pressure. This study investigates whether the presence of an intact pericardium restricts the ANF secretory response to an increment in left atrial pressure caused by acute aortic constriction in anaesthetized open-chest pigs. The rise in ANF plasma concentration secondary to constriction was higher when the pericardium had been surgically opened than when it was left intact. Furthermore, an opened pericardium led to a larger increase during constriction in left atrial diameter as measured by sonomicrometry. The results suggest that the intact pericardium restricts the cardiac release of ANF secondary to aortic constriction, probably by restricting left atrial dilatation.

Endothelin-1 and endotoxemia.

Sepsis leads to changes in blood volume and distribution. In the experiments reported here we monitored circulatory changes during endotoxemia and their relation to portal and systemic levels of endothelin-1 (ET-1). Piglets were monitored cardiovascularly under ketamine anesthesia for 6 h after an endotoxin infusion (saline controls). ET-1 levels in plasma were analyzed by RIA. In both portal and systemic blood a twofold increase in ET-1 levels was found after 1 h. This level remained significantly elevated for a further 3 h. This increase was concurrent with a drop in cardiac output, systemic vascular resistance, and blood pressure. In the portal circulation there was increased portal pressure and vascular resistance. There was no significant difference between the systemic and portal levels of ET-1.

Selective positive end-expiratory pressure and intracardiac dimensions in dogs.

Effects of differential ventilation with general vs. selective right (R) and left (L) positive end-expiratory pressure (PEEP) on left (LV) and right ventricular (RV) end-diastolic dimensions were compared in seven pentobarbital-anesthetized dogs. All three modes of PEEP reduced LV cross-sectional area: general PEEP more than RPEEP and RPEEP more than LPEEP. General PEEP and, to a lesser degree, RPEEP decreased both the LV anteroposterior diameter and LV septum-free wall diameter, whereas LPEEP reduced the LV septum-free wall diameter only. Cardiac output was unaffected by LPEEP, whereas general PEEP (20 cmH2O) reduced cardiac output by 48%, and RPEEP (20 cmH2O) reduced it by 23%. RV septum-free wall diameter was not changed by any mode of PEEP. In conclusion, cardiac output was better maintained with selective PEEP than with general PEEP because LV filling was less impeded with selective PEEP. During LPEEP LV assumed a different configuration than during RPEEP and general PEEP, probably reflecting a different pattern of heart-lung interaction.