Hemodynamic response to norepinephrine with and without inhibition of nitric oxide synthase in porcine endotoxemia

The objective of this study was to determine the circuit and cardiac effects of norepinephrine (NE) with and without endotoxin, and how these responses are modified by the inhibition of nitric oxide synthase (NOS). We anesthetized eight pigs and instrumented them for measurements of cardiac output (Q), arterial pressure (Part), and mean pulmonary arterial pressure (Ppa). We also placed a 40-ml balloon in the right atrium for transient obstruction of flow and measurement of the mean circulatory filling pressure (MCFP) and resistance to venous return (RVR). After baseline measurements, animals were treated with 10 microg/kg/h of Escherichia coli endotoxin. At 105 min the measurements were repeated. We then infused 12.5 mg/kg of N(G)-nitro-L-arginine methyl ester (L-NAME) for 10 min and repeated the measurements. At baseline, at the end of endotoxin infusion, and after L-NAME infusion we infused 3, 9, and 27 microg/min of NE for 10 min each, and recorded hemodynamic measurements at each dose. NE shifted the venous return curve (i.e., increased MCFP) to the right without changing RVR, and increased cardiac output (CO) both at baseline and after endotoxin. Endotoxemia markedly flattened the dose-response curves for the change in Part, Ppa, CO, and heart rate with NE. The peak response of Part to NE after endotoxemia was restored with L-NAME, but the other dose-response curves were not affected. NE also did not shift the venous return curve after L-NAME. Furthermore, the increase in Part with NE was of shorter duration after L-NAME than in the baseline condition. In conclusion, NE shifts the venous return curve to the right and improves CO in endotoxic and nonendotoxic conditions. Endotoxemia decreases the arterial responsiveness to NE. L-NAME partly restored this loss of responsiveness in arteries but not in the venous circulation.     

Coronary sinus catheter placement: assessment of placement criteria and cardiac complications

STUDY OBJECTIVES: To evaluate the placement and complications of a coronary sinus (CS) catheter in human subjects. DESIGN: Sixty-two CS catheters inserted in patients scheduled for coronary artery bypass graft surgery (CABG). SETTING: University hospital, anesthesia and cardiothoracic surgery departments. PATIENTS: Sixty-two patients without valvular or concomitant diseases undergoing CABG. INTERVENTIONS: CS fluoroscopy, measurements of CS flow, CS oxygen saturation, and CS distal tip pressure before incision, after incision, 20 min after aortic cross-clamp release (X-off), 50 min after X-off, 2 h after X-off, 4 h after X-off, and 6 h after X-off. RESULTS: In 57 patients (92%), we achieved successful CS catheter placement. In five patients (8%), CS catheter positioning was not possible. Of the 57 CS catheters placed, dislocation occurred during the operation in six patients (11%) and postoperatively in three patients (6%). Cardiac complications of CS catheter placement occurred in nine patients (15%). Four patients (6%) acquired hemopericardium. Three of these patients had a small hematoma in the right ventricle. In two other patients, contrast medium appeared in the right ventricular wall during catheterization. No hemodynamic signs of these complications were detected clinically. Irregular heart rhythm was observed in only three patients. CS blood oxygen saturation ranged from 40 to 60%. CS flow amounted to 3% of cardiac output. Variations in CS flow paralleled changes in cardiac output. CONCLUSIONS: A CS catheter is a useful tool for clinical human cardiac research; however, the placement of a CS catheter can cause minor myocardial damage in > 10% of patients. Importantly, this damage may not be clinically evident, but only observed after thoracotomy. CS oxygen saturation, CS flow, distal tip pressure, and fluoroscopy are reliable tools to assess a safe and correct positioning of the CS catheter.     

Time course of resolution of pulmonary hypertension and right ventricular remodeling after orthotopic cardiac transplantation

Most patients with severe congestive heart failure have secondary pulmonary hypertension (PHT). Elevation of pulmonary vascular resistance (PVR) to greater than 480 dynes.sec.cm-5 (6 Wood units) is currently the principle hemodynamic contraindication to orthotopic cardiac transplantation. We performed serial two-dimensional Doppler echocardiographic examinations and right heart catheterizations in 24 recipients (21 men, 14-58 years old) of orthotopic cardiac transplants to determine the time course of resolution of PHT and the concomitant remodeling of the donor right ventricle. Right and left heart filling pressures declined in parallel and reached the upper normal range at 2 weeks after the transplant procedure and remained unchanged at 1 year follow-up. Mean pulmonary arterial pressure (mm Hg) decreased from 38 +/- 9 preoperatively to 22 +/- 5 at 2 weeks and was 19 +/- 5 at 1 year after the transplantation procedure. At 1 year after surgery, PVR had decreased from 202 +/- 89 dynes.sec.cm-5 preoperatively to 99 +/- 36 dynes.sec.cm-5 (p less than .001), while cardiac output increased from 3.7 +/- 1.2 to 6.3 +/- 1.5 liters/min (p less than .001). Echocardiographic analysis showed that transplant recipients had an enlarged right ventricle on day 1 after surgery, and a volume overload contraction pattern and tricuspid regurgitation was present in the majority. This increase in right ventricular size was maintained at 1 year follow-up while the incidence of tricuspid regurgitation decreased. We conclude that there is rapid resolution of moderately elevated pulmonary arterial pressures after cardiac transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamics and gas exchange during angioscopy in the dog

We have previously developed a technique for the in vivo visualization of the pulmonary arteries in the experimental animal with a fiberoptic instrument (angioscope). To assess the potential hemodynamic and gas exchange effects of angioscopy, we studied five dogs before and after pulmonary embolization. Sequential observations were made of arterial blood gases, mean arterial pressure, pulmonary artery pressure, heart rate, cardiac output, and the electrocardiogram. The most common arrhythmias were ventricular premature contractions which were comparable to those seen with right heart catheterization. Statistically significant, but clinically minor, effects were found on cardiac output, mean arterial pressure, and heart rate in dogs when angioscopy was performed after pulmonary embolization. We conclude that fiberoptic angioscopy does not induce deleterious effects on hemodynamics or gas exchange in the experimental animal, prior to or after embolization.     

Regional changes in hemodynamics and cardiac myocyte size in rats with aortocaval fistulas. 2. Long-term effects

Regional changes in hemodynamics and cardiac myocyte size were examined in adult rats 5 months after creating a large aortocaval fistula. At that time, cardiac output, left and right ventricular pressures, and left and right ventricular dP/dtmax were measured. Subsequently, isolated cardiac myocytes were collected from the left ventricle, right ventricle, and septum for cell size measurements. Compared with sham-operated controls, percent dry weight was reduced in the liver and kidney but was unchanged in the lung. Heart rate, left ventricular systolic pressure, left ventricular dP/dtmax, and systolic aortic pressure were not changed in rats with fistulas. However, cardiac output, stroke volume, left ventricular end-diastolic pressure, and all measured parameters in the right ventricle were significantly increased. Mean cell volume and the ratio of heart weight to body weight were both elevated 92%. Cell volume, cell length, and cross-sectional area increased significantly in each heart region examined. Hypertrophy was more pronounced in cells from the right ventricle and the endomyocardium of the left ventricle. The percentage of cells with mononucleation or binucleation was not changed in any heart region of rats with fistulas. In summary, despite evidence of renal and hepatic congestion, most indexes of cardiac function were normal or elevated 5 months after creation of a large volume-overload-induced hypertrophy. Data from isolated cardiac myocytes suggested that cellular hypertrophy, rather than hyperplasia, was responsible for the increased cardiac mass.     

Clinical conference: Rupture of right ventricle complicating closed chest cardiac massage.

Two cases of rupture of the right ventricle following closed chest cardiac massage are presented. This is believed to result from trapping of blood in the right ventricle at levels of systemic arterial pressure. In one case there was massive pulmonary embolism which interfered with egress of blood from the right ventricle. In the other case, application of pressure during a closed chest resuscitative attempt might have closed the right ventricular outflow tract.     

Optimal right ventricular filling pressures and the role of pericardial constraint in right ventricular infarction in dogs.

BACKGROUND. Previous studies have reported an important role for right ventricular function in the pathophysiology of the low cardiac output state that can accompany right ventricular infarction. Some studies have suggested that right ventricular distensibility impairs right ventricular filling and stroke output; others have demonstrated that the pericardium can mediate depressed left ventricular filling and stroke output. METHODS AND RESULTS. To determine the role of pericardial constraint and optimal volume loading in an experimental model of right ventricular wall infarction, six mongrel dogs were studied before and after right ventricular wall infarction and after volume loading. The pericardium was then opened in two phases. In the first phase, the pericardium was opened partially to allow the atria to distend freely, and in the second phase, the pericardium was opened completely. The animals were preinstrumented with two sets of piezoelectric crystals attached to the right ventricular free wall, one in the infarct and the other in the noninfarct territory. Left ventricular size was estimated by left ventricular crystals on the anterior wall of the left ventricle. Right ventricular and left ventricular Millar catheters were used to assess intracavitary pressure, and a flat balloon was used to assess intrapericardial pressure. Right ventricular infarction reduced cardiac output by 23% and stroke volume by 30%. End-diastolic segment length and transmural pressure of the left ventricle decreased. Volume loading restored cardiac output to baseline values and was mediated by a significant increase in end-diastolic length in the noninfarct territory. This was achieved by increasing right ventricular end-diastolic pressure from 9 +/- 2 to 16 +/- 3 mm Hg (p less than 0.01). Partial opening of the pericardium mediated significant increases in both end-diastolic segment lengths of the left ventricle and the noninfarct territory. Left ventricular end-diastolic pressure decreased slightly by 3 mm Hg (p = NS). Complete opening of the pericardium increased cardiac output and stroke volume and mediated a significant decrease in right and left ventricular end-diastolic pressures. Left ventricular transmural pressure and end-diastolic segment lengths of the left ventricle and the noninfarct territory increased. Left ventricular diastolic pressure-segment length relations were shifted upward by right ventricular infarction. A partial opening of the pericardium shifted this relation downward in all animals, and complete opening of the pericardium shifted the relation rightward and further downward. CONCLUSIONS. Cardiac output is restored to baseline values by volume loading sufficient to increase the right ventricular diastolic pressure to 16 +/- 3 mm Hg. Evidence of pericardial constraint was observed and appears to be mediated by an atrioventricular interaction in addition to the direct ventricular interaction.     

Delayed presentation of pericardial pseudocyst following blunt chest trauma

An unusual presentation of blunt chest trauma is reported. A 21-year-old man presented with symptoms and signs of congestive cardiac failure. 2D echocardiogram showed a thickened pericardium with a mass compressing the right ventricle. CT scan revealed a large mass anterior and to the right of the heart with evidence of pericardial thickening and calcification. However, its delineation from the pericardium and its exact tissue characterization were not possible. Cardiac catheterization showed elevation and equalization of diastolic pressures in all cardiac chambers with characteristic waveforms suggestive of pericardial constriction. The precise definition and characterization of the mass was obtained only on Magnetic Resonance Imaging (MRI) of the chest which showed it to be a solid, well encapsulated, partially calcified mass between the heart and the diaphragm extending anteriorly and to the right of the right ventricle. These findings were confirmed at the time of thoracotomy. Histopathology revealed blood clots and hyalinised fibrous tissue without any evidence of granuloma or malignancy. This report highlights an insiduous, late presentation of blunt chest trauma. It also demonstrates the superiority of MRI over computed X-ray tomography for mediastinal paracardiac masses.     

Comparison of open-chest cardiac massage techniques in dogs

Manual compression of the heart during open-chest cardiac massage (OCPR) has been shown to be superior to closed-chest compression. Our study sought to determine, in a canine model, the optimal hand position for manual compression of the heart. Twelve dogs were anesthetized with ketamine, an orotracheal tube was placed, and anesthesia was maintained with halothane and nitrous oxide. Cannulae were placed to monitor diastolic (DBP) and systolic (SBP) blood pressures, intracranial pressure (ICP), and common carotid blood flow (CCBF). Control values were obtained under light general anesthesia, and ventricular fibrillation was induced. External CPR (ECPR) was performed with a mechanical compressor before opening the chest and pericardium through the left fifth interspace. The following sequence of three hand positions was used for OCPR: technique A, one-handed technique with thumb on left ventricle, fingers over the right ventricle, and apex in palm; technique B, two-handed technique with right ventricle cupped in left hand and fingers of right hand over left ventricle; and technique C, one-handed technique with fingers of right hand over left ventricle and heart against sternum. Each was done at a rate of 60 compressions per minute with the operator blind to results during performance. All three techniques produced significantly (P less than .05) greater DBPs and CCBFs when compared with ECPR. All three also produced significantly lower (P less than .05) ICPs when compared with ECPR. DBPs, SBPs, CCBFs, and cerebral perfusion pressures were similar for techniques B and C, and all were significantly greater (P less than .05) than those achieved with technique A.(ABSTRACT TRUNCATED AT 250 WORDS)     

Control of cardiac output by systemic vessels: Circulatory adjustments to acute and chronic respiratory failure and the effect of therapeutic interventions

The circulation requires the heart to pump blood from the venous to the arterial bed. The factors that determine venous flow into the heart are mean pressure in the systemic vasculature, right atrial pressure and the resistance to venous return. The mean pressure in the systemic vasculature is a function of the stressed vascular volume and the systemic vascular compliance. Right atrial pressure depends on many factors. These include the contractile state of the right and left ventricles, the load on the right and left ventricles, the presence or absence of pericardial effusion, and alterations in pleural pressure that might occur with positive pressure ventilation. The resistance to venous return tends to stay remarkably constant, but can be reduced by significant arteriovenous shunting.The right ventricle has a relatively high diastolic compliance. Because of this, changes in volume of the right ventricle are associated with only modest increases in right atrial pressure. Therefore, as load on the right ventricle increases, mean systemic vascular pressure needs to increase only a small amount to maintain cardiac output. If right atrial pressure increases sufficiently as a result of a greatly increased load on the right ventricle, as in pulmonary embolism, hypoxic pulmonary vasoconstriction or chronic respiratory failure, the increase in mean systemic vascular pressure necessary to maintain normal venous return, and therefore cardiac output, may lead to signs of right heart failure, with no change in the slope of the right heart function curves. The implications of this phenomenon are important in managing patients with acute and chronic respiratory failure. Positive pressure ventilation, diuretic agents, cardiac glycosides and other inotropic or vasoactive drugs will influence the relation between the mean systemic pressure and right atrial pressure. Therefore, these treatment modalities may unexpectedly alter cardiac output if the systemic vascular effects are not kept in mind.     

Dimensional changes of the left ventricle during acute pulmonary arterial hypertension in dogs

Left ventricular dimensions and volumes were measured by an endocardial marker technique in eight closed chest dogs during progressive increases of 10 mm Hg in mean pulmonary arterial pressure. Right ventricular volumes were measured by biplane cineanglography.

Increasing mean pulmonary arterial pressure caused a progressive increase in right ventricular volume; at a mean pulmonary arterial pressure of 60 mm Hg, right ventricular end-diastolic volume increased by 48 percent and end-systolic volume by 50 percent. Left ventricular volumes began to decrease significantly at a mean pulmonary arterial pressure of 30 mm Hg, and when a mean pulmonary arterial pressure of 60 mm Hg was reached, left ventricular end-diastolic volume had decreased by 30 percent and left ventricular end-systolic volume by 19 percent. Changes in ventricular filling pressure dlrectionally followed the volume changes of the respective ventricle. Left ventricular stroke volume decreased 45 percent at a mean pulmonary arterial pressure of 60 mm Hg but increasing heart rate prevented a decrease in cardiac output.

The decrease in left ventricular volume as pulmonary arterial pressure was Increased was associated with a disproportionate reduction in the left ventricular septal-lateral axis. At end-diastole, this dimension decreased by 22 percent at a mean pulmonary arterial pressure of 60 mm Hg, the anterior-posterior axis decreased by 8 percent and the base-apex axis by 4 percent. A similar disproportionate decrease of the septal-lateral axis occurred at end-systole. Even at the modest increase in mean pulmonary arterial pressure to 20 mm Hg, only the septal-lateral dimension was significantly shortened, and the right ventricular end-diastolic volume had increased by 17 percent but left ventricular end-diastolic volume was not significantly changed. Thus, during acute pulmonary hypertension, the right ventricle progressively dilates resulting in a distinctive change in the shape of the left ventricle that suggests septal buiging and that may impair left ventricular function.     

Beneficial effects of atrioventricular synchrony in dogs with right coronary artery embolization, and complete heart block

Complete heart block complicating right ventricular infarction frequently is accompanied by shock. Hemodynamic responses to different pacing modes were studied in six anesthetized, closed chest dogs following right coronary artery embolization with mercury and heart block induced by repetitive trans-septal DC shock. Hemodynamics were recorded at control, following right coronary artery embolization, during atrioventricular sequential pacing (DVI) and ventricular pacing (VVI). With respect to the hemodynamics recorded during VVI and DVI pacing; (1) The mean arterial pressure increased by 29.4% during DVI pacing (92.1 +/- 31.3 mm Hg vs 73.4 +/- 28.9 mm Hg p less than 0.005). This increase was primarily due to an augmentation in systolic arterial pressure. (2) The left ventricular end diastolic pressure increased by 35.8% during DVI pacing (16.3 +/- 5.3 mm Hg vs 12.0 +/- 4.3 mm Hg p less than 0.01). (3) Cardiac output improved by 33.8% during DVI pacing (2.34 +/- 0.75 L/min vs 1.76 +/- 0.59 L/min, p less than 0.0005). This was a consistent improvement in cardiac output with a narrow range of 27.1% to 39.0%. (4) There were no significant changes in right atrial, pulmonary, pulmonary capillary wedge pressures or in systemic vascular resistance. In dogs with right coronary artery occlusion and complete heart block DVI pacing is clearly superior to VVI pacing. This is probably because the atrial contribution to ventricular filling, in this model, is critically important to maintain an adequate cardiac output.     

Intravenous isosorbide dinitrate during open-heart surgery and its role in the treatment of right-sided congestive heart failure

Recent awareness of the importance of the functional integrity of the right ventricle and the effect of raised pulmonary vascular resistance on cardiac output after cardiopulmonary bypass has focused attention on means of protecting right ventricular myocardium and reducing right ventricular afterload during open-heart surgery. A study of the acute effects of bolus intravenous isosorbide dinitrate (ISDN) has shown that after cardiopulmonary bypass, bolus intravenous ISDN produced highly significant (p less than 0.001) decreases in mean pulmonary arterial pressure (13%), pulmonary vascular resistance (23%) and the ratio of pulmonary to systemic vascular resistance (20%), indicating that active pulmonary vasodilation had occurred in the absence of other hemodynamic changes. The results suggest that possibly the acute effect of low-dose ISDN after cardiopulmonary bypass is predominantly exerted on the right ventricular afterload if systemic arterial pressure is not elevated. Two different clinical situations are described in which intravenous ISDN proved beneficial, one being acute pulmonary hypertension after protamine sulphate and the second being acute right-sided congestive heart failure with systemic hypotension unresponsive to conventional therapeutic measures. Thus, ISDN may prove a useful agent for alleviating right ventricular dysfunction at a time of not infrequent cardiovascular instability, the period after bypass.     

Therapie des akuten Herzversagens, medikament?se Strategie

The leading pathophysiology of acute heart failure and cardiogenic shock is acute or subacute myocardial infarction. Reperfusion of the occluded coronary vessel accompanied by adequate support of cardiac function via assist systems, preferentially the intraaortic balloon counterpulsation, is the therapy of choice. Adjustment of preload (high pulmonary capillary pressure in-acute myocardial infarction with small heart, low pulmonary capillary wedge pressure in patients with large ventricles and chronic heart failure, high central venous pressure in patients with right heart failure, and right ventricle myocardial infarction) and afterload (peripheral arterial vasodilatation, recommended systolic arterial pressure 80-90 mm Hg) but not maximization of cardiac output play an important role. Positive inotropic drugs should be considered when these strategies fail. In acute right heart failure in pulmonary hypertension, a preferential pulmonary vasodilatation with intravenous or inhalative prostaglandins or inhalative NO are of utmost importance. Systemic hypotension is not a contraindication in this pathophysiology.     

Measurement of right ventricular volumes using 131I-MAA

A method has been presented for determining the right ventricular residual ratio, that is, the ratio of the end-systolic volume to the end-diastolic volume during each cardiac cycle. ¹³¹I-MAA was injected as a bolus into the right ventricle, and the ratio of isotope remaining in the chamber during the succeeding cardiac cycles was determined with a collimated scintillation counter placed over the right ventricle. Since the counter detected the radioactivity from the entire right ventricular cavity, potential errors from incomplete mixing were minimized. The washout curve from the ventricle was distorted somewhat by the accumulation of isotope in intervening lung tissue. This distortion was eliminated by subtracting the build-up curve of radioactivity in the lung recorded simultaneously with a second scintillation counter positioned over the lateral chest wall.In 14 dogs anesthetized with chloralose, the right ventricular residual ratio was relatively constant at 40.4 ± 3.1 per cent. Duplicate measurements differed by less than 3 per cent indicating the good reproducibility of the method.Right ventricular stroke volume was determined from cardiac output (dye dilution) and heart rate. With this and the simultaneously determined residual ratio (¹³¹I-MAA), end-diastolic volume could be calculated. Stroke volume and stroke work were highly correlated with end-diastolic volume, in keeping with the Frank-Starling mechanism.     

Effects of isometric exercise on the right ventricular function and on the pulmonary circulation, in normal subjects (author's transl)]

The pulmonary circulatory response and right ventricular haemodynamics were assessed in normal subjects who sustained hand-grip exercise (HG) at 50% of the maximum voluntary contraction (M.V.C.) for 3 minutes. Ten normal subjects, aged 25 to 66 years, who underwent full right catheterization were studied. The following parameters were taken into consideration: heart rate (HR), end diastolic right ventricular pressure (EDRVP) end diastolic right ventricular volume (EDRVV), mean pulmonary arterial pressure (PAP), pulmonary wedge pressure (PWP), total pulmonary resistance (TPR), cardiac output (CO) and right ventricular sistolic work minute index (RVSWMI). These data were obtained by means of a tip-micromanometer connected with an polygraphic recorder and by means of thermodilution cardiac output computer. The statistical significance of the difference between the resting control values and those after isometric exercise was calculated with the Student's paired t test. A comparison of the control data with those obtained after isometric exercise, demonstrate a statistical significant (p less than 0,001) increase of the HR, PAP, PWP, TRP, CO, RVSWMI, a less significant (p less than 0.01) increase RVEDP. Our findings show that the HG causes changes in the pulmonary circulation and the right ventricular function. Our data seem to sustain that the pulmonary circulation respondes differently under isometric stress than it does under isotonic stress. The use of HG can thus be postulated as a useful means of evaluation of the response of the pulmonary circulation and right ventricular function.     

Pulmonary vasodilatory action of endogenous atrial natriuretic factor in rats with hypoxic pulmonary hypertension. Effects of monoclonal atrial natriuretic factor antibody.

We administered ascitic fluid containing atrial natriuretic factor (ANF) monoclonal antibody to rats after 3 weeks of exposure to hypoxia while the rats were still hypoxic. In additional chronically hypoxic rats, we infused synthetic rat ANF. In conscious chronically instrumented rats, after a bolus dose of 5 micrograms i.v. ANF, pulmonary arterial pressure fell significantly from 26.5 +/- 2 to 21 +/- 2 mm Hg (p less than 0.01), reaching its nadir at 5 minutes without change of systemic arterial pressure, cardiac output, or heart rate. Pulmonary arterial pressure increased gradually from 26 +/- 4 to 34 +/- 4 mm Hg within 30 minutes (p less than 0.05) after acute administration of ANF monoclonal antibody and decreased transiently to return to baseline within 15 minutes after infusion of control ascitic fluid containing monoclonal antibody against an apolipoprotein. Cardiac output and heart rate remained unchanged after both ANF monoclonal antibody and control ascitic fluid. In normoxic rats, acute administration of ANF monoclonal antibody did not cause significant changes in pulmonary arterial pressure, cardiac output, or heart rate. Rats receiving weekly intravenous injections of ANF monoclonal antibody that were started before initiation of exposure to hypoxia experienced significantly aggravated pulmonary hypertension and right ventricular hypertrophy compared with rats receiving repeated infusions of control ascitic fluid. However, there was no significant difference in small pulmonary arterial wall thickness or percentage of muscularized arteries at the alveolar duct level. These results suggest that endogenous ANF attenuates hypoxic pulmonary hypertension by decreasing pulmonary vascular tone.     

Enhanced responsiveness to carotid baroreceptor unloading in conscious dogs during development of perinephritic hypertension

The effects of unloading the carotid sinus baroreceptors before and during the development of perinephritic hypertension were studied in conscious dogs instrumented with aortic catheters to measure arterial pressure and heart rate, and electromagnetic flow probes to measure cardiac output and calculate total peripheral resistance. Prior to hypertension, bilateral carotid occlusion (BCO) increased mean arterial pressure by 38 +/- 2 from 101 +/- 2 mm Hg and total peripheral resistance by 19 +/- 2 from 46 +/- 3 mm Hg/l/min, while cardiac output and heart rate did not change from 2,299 +/- 128 ml/min and 84 +/- 4 beats/min, respectively. At 2 weeks after renal wrapping, there were significant increases in baseline mean arterial pressure, cardiac output, and total peripheral resistance and decreases in heart rate; BCO increased mean arterial pressure by 59 +/- 5 from 130 +/- 4 mm Hg, heart rate by 36 +/- 5 beats/min from 69 +/- 3 beats/min, and cardiac output by 458 +/- 103 from 2,711 +/- 239 ml/min. By 4 weeks after renal wrapping, heart rate and mean arterial pressure responses to BCO were approaching baseline levels. After beta-adrenergic receptor blockade, responses to BCO of mean arterial pressure, cardiac output, and heart rate were no longer significantly enhanced during the development of hypertension. Thus, in conscious dogs, reflex pressor responses to baroreceptor unloading via BCO were enhanced during the development of hypertension but no longer present 3 weeks later. The augmented mean arterial pressor responses to BCO were mediated by increases in cardiac output and heart rate, which in turn, appeared to be controlled by beta-adrenergic receptor mechanisms.     

Plasma brain natriuretic peptide and atrial natriuretic peptide concentrations correlate with left ventricular end-diastolic pressure

The present study was designed to investigate whether brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) plasma concentrations correlate with left ventricular end-diastolic pressure (LVEDP), pulmonary capillary wedge pressure (PCWP), diastolic pulmonary arterial pressure (DPAP), right atrial pressure (RAP), or ejection fraction (EF). Plasma BNP and ANP levels were determined by commercial radioimmunoassays (Peninsula) after Sep Pak C₁₈ extraction in blood samples withdrawn from the pulmonary artery and the left ventricle or from the left ventricle and the femoral vein in 85 patients undergoing diagnostic cardiac catheterization. Linear and nonlinear regression analysis and the paired sample f-test were applied to the data. Pulmonary arterial plasma BNP and ANP levels showed a close nonlinear correlation with LVEDP (BNP: r=0.94, p < 0.001; ANP: r=0.81, p < 0.001), a significant linear correlation with PCWP, DPAP, and RAP, and a significant negative correlation with EE ANP concentrations decreased significantly from the pulmonary artery to the left ventricle and from the left ventricle to the femoral vein (p < 0.001). BNP levels also decreased significantly between the left ventricle and the femoral vein (p < 0.001), but there was no significant difference between pulmonary arterial and left ventricular BNP concentrations. BNP and ANP concentrations correlated significantly between pulmonary arterial and left ventricular blood samples (BNP: r = 0.99, ANP: r = 0.93, p < 0.001) and between left ventricular and peripheral blood samples (BNP: r=0.99, ANP: r=0.94, p<0.001). The present data suggest that peripheral plasma BNP and ANP levels are useful noninvasive indices of cardiac performance.     

Left ventricular myocardial edema. Lymph flow, interstitial fibrosis, and cardiac function

We hypothesized that both acute and chronic accumulation of myocardial interstitial edema (extravascular fluid [EVF]) would compromise cardiac function. We also postulated that excess fluid within the myocardial interstitial space would potentiate interstitial fibrosis, thus further compromising function. Dogs were divided into three groups: 1) control, 2) chronic pulmonary hypertensive with right heart failure, and 3) chronic arterial hypertensive. The quantity of EVF, expressed as the unitless blood-free (wet weight-dry weight)/dry weight ratio, and interstitial fibrosis (collagen content) were determined and correlated with cardiac function at baseline and after acute elevation of coronary venous pressure and reduction of cardiac lymph flow. Control EVF was 2.90 +/- 0.20 (mean +/- SD), which increased to 3.45 +/- 0.16 after acute (3-hour) elevation of coronary sinus pressure. This EVF significantly compromised cardiac function. The EVF in chronically hypertensive dogs and in dogs with chronic right heart pressure elevations was 3.50 +/- 0.30 and 3.50 +/- 0.08, respectively. End-diastolic left ventricular interstitial fluid pressure increased from a control value of 14.9 +/- 3.1 (at EVF = 2.9) to 24.8 +/- 3.7 (at EVF = 3.5). An EVF of 3.5 produced approximately 30% reduction of the heart's ability to maintain cardiac output at a left atrial pressure of 15 mm Hg. The compromised function in these chronic models is exacerbated after acute elevation of coronary venous pressure and reduction of cardiac lymph flow. Collagen levels were elevated by at least 20% in the chronic hypertensive dogs and in the nonhypertrophied left ventricles of dogs with chronic right heart pressure elevation.(ABSTRACT TRUNCATED AT 250 WORDS)