Elevated Pressure Gradient Research Articles

Reduced EGFR causes abnormal valvular differentiation leading to calcific aortic stenosis and left ventricular hypertrophy in C57BL/6J but not 129S1/SvImJ mice

Epidermal growth factor receptor (EGFR) signaling contributes to aortic valve development in mice. Because developmental phenotypes in Egfr-null mice are dependent on genetic background, the hypomorphic Egfr(wa2) allele was made congenic on C57BL/6J (B6) and 129S1/SvImJ (129) backgrounds and used to identify the underlying cellular cause of EGFR-related aortic valve abnormalities. Egfr(wa2/wa2) mice on both genetic backgrounds develop aortic valve hyperplasia. Many B6-Egfr(wa2/wa2) mice die before weaning, and those surviving to 3 mo of age or older develop severe left ventricular hypertrophy and heart failure. The cardiac phenotype was accompanied by significantly thicker aortic cusps and larger transvalvular gradients in B6-Egfr(wa2/wa2) mice compared with heterozygous controls and age-matched Egfr(wa2) homozygous mice on either 129 or B6129F1 backgrounds. Histological analysis revealed cellular changes in B6-Egfr(wa2/wa2) aortic valves underlying elevated pressure gradients and progression to heart failure, including increased cellular proliferation, ectopic cartilage formation, extensive calcification, and inflammatory infiltrate, mimicking changes seen in human calcific aortic stenosis. Despite having congenitally enlarged valves, 129 and B6129F1-Egfr(wa2/wa2) mice have normal lifespans, absence of left ventricular hypertrophy, and normal systolic function. These results show the requirement of EGFR activity for normal valvulogenesis and demonstrate that dominantly acting genetic modifiers curtail pathological changes in congenitally deformed valves. These studies provide a novel model of aortic sclerosis and stenosis and suggest that long-term inhibition of EGFR signaling for cancer therapy may have unexpected consequences on aortic valves in susceptible individuals.

Hemodynamic and functional assessment of mechanical aortic valves using combined echocardiography and multidetector computed tomography

Limitations are found in the ability of transthoracic echocardiography to evaluate mechanical aortic valve replacements (AVR). We evaluated the ability of combined echocardiography and computed tomography (CT) to enhance the hemodynamic and functional evaluation of AVR. We performed a retrospective evaluation of 41 consecutive patients with AVR (27 bileaflet, 14 single disc) and both transthoracic echocardiography and 64-detector electrocardiographic-gated CT. Each study was interpreted by 2 independent, blinded readers. The effective orifice area was compared with the corrected energy-loss coefficient area and the geometric orifice area. Patients with an elevated mean pressure gradient (>15 mm Hg) were assessed for potential abnormal findings, including patient-prosthesis mismatch, elevated cardiac index, valve dysfunction, significant regurgitation, or pressure recovery effect. Significant differences (P<0.05) and moderate-to-high correlations (r=0.55-0.98) were observed between the effective orifice area (2.2+/-0.8 cm(2)), corrected energy-loss coefficient area (3.0+/-1.5 cm(2)), and geometric orifice area (3.6+/-0.9 cm(2)). At least one abnormality was observed in 7 of 25 patients with normal gradients and in 14 of 16 patients with elevated gradients (P<0.001). In 16 patients with elevated mean pressure gradient, a potential cause could be determined in 4 with echocardiography alone and in 14 patients with combined echocardiography and CT (P=0.001). CT aids in the interrogation of prosthetic valve function, enhancing evaluation for patient prosthesis mismatch, and correction for pressure recovery by the corrected energy-loss coefficient. CT is additive to the assessment of mechanical AVR with transthoracic echocardiography, and the combination permits a more complete assessment of both AVR function and hemodynamics.

高度の肺高血圧症を合併した高齢者Basedow病の1例

An 83-year-old woman was admitted to our hospital with dyspnea. A chest X-ray showed cardiomegaly and pulmonary congestion. An echocardiogram revealed severe tricuspid regurgitation and markedly elevated transtricuspid pressure gradient of 103 mmHg. There was no left ventricular systolic or diastolic dysfunction. Laboratory evaluation revealed elevated free T4 and suppressed TSH levels. Serum level of anti-TSH receptor antibody was significantly elevated. A thyroid echogram demonstrated increased internal flow pattern in the thyroid gland. As a result of these findings, she was given a diagnosis of Basedow's disease associated with severe pulmonary hypertension and congestive heart failure. After treatment for hyperthyroidism with thiamazole, propranolol, furosemide, and warfarin, she made good recovery with gradual resolution of pulmonary hypertension. The severity of pulmonary hypertension in this case was significantly higher than that in previous reports, possibly because of concomitant minor pulmonary embolism, thiamine deficiency and anemia. In summary, we report a rare case of Basedow's disease with severe and reversible pulmonary hypertension that appeared in very old age.

Left ventricular mass regression following implantation of MIRA bileaflet valves in patients with severe aortic stenosis

The aim of this study was to evaluate the factors that determine the course of left ventricular mass regression in a homogeneous group of patients following aortic valve replacement by use of the mechanical Edwards MIRA bileaflet prosthesis. Furthermore, we examined if the 19-mm valve leads to an equally good outcome when compared with larger 21- and 23-mm valves. We included 79 patients (49 men) with a mean age of 65+/-9 years operated on for isolated aortic valve replacement with the MIRA valve prosthesis. The analyses included preoperative and postoperative echocardiograms during a follow-up of at least 18 months (995+/-439 days) after valve surgery. Indication for valve replacement was aortic stenosis in 59 and combined disease (aortic stenosis and regurgitation) in 20 patients. Concomitant coronary artery bypass grafting was performed in 28 patients. Left ventricular mass index declined from 155.6+/-47 g/m(2) to 128.8+/-35 g/m(2) (P<0.001) at final visit and normalized in 49% of the patients. Female sex and a preoperatively highly elevated left ventricular mass index were identified as risk factors for residual hypertrophy. However, age and valve size did not have a predictive value for completeness of left ventricular mass regression. This study supports the evidence that an extensive preoperative left ventricular hypertrophy results in an incomplete postoperative mass regression in patients with aortic bileaflet valves. It shows that the slightly elevated pressure gradient in MIRA 19-mm valves does not affect left ventricular mass regression.

Surgical Treatment of Hypertrophic Obstructive Cardiomyopathy in Pediatric Patients With Severe Hypertrophy

We have undertaken a study over a period of 5 years on 35 hypertrophic obstructive cardiomyopathy (HOCM) patients with severe hypertrophy in the age range between 8 and 15 years. The indication for surgery was based on the diagnosis of severe myocardial hypertrophy in association with serious cardiac failure (New York Heart Association class III or IV) or elevated intraventricular pressure gradients refractory to medical therapy. Furthermore, patients were considered for operation if they met a history of sudden death within their families. A new technique of HOCM surgical correction in pediatric patients with severe hypertrophy was proposed. Conceptually, this approach offers a number of advantages: it affords the excision of the asymmetrically hypertrophied area of the ventricular septum without penetration into the left ventricle cavity; it avoids mechanical damage to the heart conduction system and aortic valve; and for the surgeon, it improves visual inspection of the area to be resected. Here, we describe the disease history of 35 patients, their diagnostic evaluations, the surgical procedure, and the postoperational observations as well as the results of follow-up assessments. We state that the surgery was successful in all 35 cases. There were no early or late deaths. Acute postoperative pericarditis developed in three patients early after surgery. The follow-up period was 38 +/- 7 months, and complications were not observed so far.

The bidirectional Glenn operation: A risk factor analysis for morbidity and mortality

Patients with single ventricle heart defects often undergo a palliative bidirectional Glenn operation. For this operation, we analyzed potential risk factors for morbidity and mortality. We also evaluated the effects of a persistent left superior vena cava by comparing the outcomes of unilateral and bilateral operations. We reviewed the clinical records of 270 consecutive patients who underwent a bidirectional Glenn operation between 2001 and 2007. A total of 226 patients underwent unilateral operations and 44 patients underwent bilateral operations. Patient characteristics included weight and age, single ventricle morphology, vena caval anatomy, and previous surgery. Operative details included cardiopulmonary bypass technique and duration, pulmonary artery management, hemi-Fontan construction, concomitant procedures, and hemodynamics. Outcome data included duration of chest tube drainage, lengths of intensive care unit and hospital stay, morbidity, and mortality (<30 days). The median length of chest tube drainage was 2.4 days (range 1-20 days). Risk factors for prolonged drainage were elevated central venous pressure (P = .015) and transpulmonary gradient (P = .011). The median lengths of stay in the intensive care unit and hospital were 50 hours (range 20-1628 hours) and 5 days (range 2-83 days), respectively. Risk factors for both included prolonged cardiopulmonary bypass time, elevated central venous pressure and transpulmonary gradient, and right ventricular morphology. Overall, 72 of 270 patients (27%) had 116 postoperative complications. Risk factors included prolonged cardiopulmonary bypass time (P = .002) and elevated central venous pressure (P = .029). Mortality was 2 of 270 patients (0.7%). No risk factors for death were identified. Weight (median 6.8 kg vs 6.2 kg, P = .038) and age (median 186 days vs 159 days, P = .001) at the time of surgery were significantly greater in the bilateral bidirectional Glenn group compared with the unilateral group. However, there was no difference in any of the outcome variables. Outcomes were adversely affected primarily by prolonged cardiopulmonary bypass time, elevated central venous pressure and transpulmonary gradient, and right ventricular morphology. Specifically, outcomes were unaffected by the presence of a left superior vena cava, cannulation strategy, or antegrade pulmonary blood flow. There were few differences between the unilateral and bilateral groups, none of which were postoperative outcomes.

On the possible formation of a vortex flow in a supersonic inlet with three-dimensional compression

The structure of the flow in an inlet with three-dimensional compression and an adjoining channel of rectangular cross-section is experimentally investigated for the external flow parameters M∞ = 4 and Re ≈ 52 · 106 1/m. The phenomenon of vortex generation in the air-intake and its breakdown at the channel entry, where it encounters an elevated pressure gradient, is studied

Percutaneous balloon mitral valvuloplasty in patients with severe mitral stenosis and low transmitral diastolic pressure gradient.

An elevated left atrial pressure and high diastolic pressure gradient (DPG) across the mitral valve are the major hemodynamic abnormalities in mitral stenosis (MS). However, a subgroup of patients with severe MS is characterized by low initial DPG. The authors reviewed the clinical, echocardiographic and hemodynamic data as well as procedural results in 180 patients who underwent percutaneous balloon mitral valvuloplasty (PBMV). An initial mean DPG > 10 mmHg was found in 144 patients (80%) (group A) and mean DPG < or = 10 mmHg in 36 patients (20%) (group B). Patients in group A had higher left ventricular ejection fraction (LVEF) than in group B (61 +/- 5% versus 42 +/- 6%, respectively) and higher cardiac index (2.8 +/- 0.4 versus 2.0 +/- 0.3 l/min/m(2) ). In group B 12 patients (33%) had normal LVEF, whereas 24/36 (67%) had reduced LVEF. All the latter had wall motion abnormalities on ventriculography. Unlike group A, intraprocedural echocardiography was essential for monitoring and evaluating immediate results of PBMV in group B. On follow-up of three years, 75% of group A patients and 55% in group B were in functional class I (p < 0.05). PBMV did not significantly improve symptoms in patients in group B who had preprocedure LVEF < or = 35%.

Pressure-driven capillary snap-off of gas bubbles at low wetting-liquid content

Abstract Snap-off is an important mechanism for generating discontinuous gas bubbles in porous media. Here, we use a hydrodynamic, corner-flow theory to re-examine the breakup of gas threads in constricted pores. Our primary focus is on the initial liquid volume within the corners of a pore and on the possibility of a minimum liquid content below which snap-off is inhibited. It is found that smoothly constricted pores with relatively small throats connected to large bodies exhibit excellent ability to snap-off regardless of their initial liquid content. Where such pores are present in porous media, it is predicted that strong foam is generated. Additional factors contributing to snap-off include elevated pressure gradients in the liquid phase and lamella or lens movement that establishes gradients in the axial profile of interfacial curvature. Our new results re-support successive snap-off as a viable mechanism of steady foam generation in homogeneous porous media at low overall aqueous-phase liquid content and at high liquid-phase pressure gradient.

Current management of the complications of cirrhosis and portal hypertension: Variceal hemorrhage, ascites, and spontaneous bacterial peritonitis

GASTROENTROLOGY 2001;120:726-748

Transient dysfunction of the freestyle stentless xenograft

After replacement of a bicuspid aortic valve with a Freestyle stentless xenograft, right coronary leaflet dysfunction and an elevated pressure gradient developed. Attempts to match the right and left ostia of the prosthesis, which were located at an angle of less than 120 degrees, to the native right and left ostia, which were located at 180 degrees, may have resulted in the leaflet distension. This is a suggestive finding about its implantation technique.

Catheter obstruction effect on pulsatile flow rate--pressure drop during coronary angioplasty.

The coupling of computational hemodynamics to measured translesional mean pressure gradients with an angioplasty catheter in human coronary stenoses was evaluated. A narrowed flow cross section with the catheter present effectively introduced a tighter stenosis than the enlarged residual stenoses after balloon angioplasty; thus elevating the pressure gradient and reducing blood flow during the measurements. For resting conditions with the catheter present, flow was believed to be about 40 percent of normal basal flow in the absence of the catheter, and for hyperemia, about 20 percent of elevated flow in the patient group. The computations indicated that the velocity field was viscous dominated and quasi-steady with negligible phase lag in the delta p(t)-u(t) relation during the cardiac cycle at the lower hydraulic Reynolds numbers and frequency parameter. Hemodynamic interactions with smaller catheter-based pressure sensors evolving in clinical use require subsequent study since artifactually elevated translesional pressure gradients can occur during measurements with current angioplasty catheters.

Patency and reintervention rates during routine TIPSS surveillance.

To assess the medium-term outcome of transjugular intrahepatic portosystemic stent shunts (TIPSS) by measuring the incidence of shunt obstruction or failure during routine surveillance and the number of interventions performed. This is a retrospective study covering a 4-year period, from 1992 to 1996, during which 102 TIPSS procedures were performed. Indications for treatment were variceal bleeding (76%) and refractory ascites (24%). Follow-up protocol after TIPSS included transfemoral or transjugular portal venography and measurement of portosystemic pressure gradient (PPG) at 3 months, 12 months, and then at yearly intervals. The results of the first 155 venograms on 62 patients (mean follow-up 14 months) have been reviewed and Kaplan-Meier analysis performed. One hundred and thirty-seven of 155 (88%) examinations showed patent shunts. Fifty-six of 137 (41%) of the patent TIPSS had elevated PPG with signs of stenosis. The majority (41/56) of shunt stenoses with elevated pressure gradients were related to neointimal hyperplasia in the hepatic venous aspect of the shunt. Interventions used to reduce the pressure gradient or to restore patency included: angioplasty (62/102 interventions), additional stents (21/102), a second TIPSS procedure (2/102), and thrombolysis or thrombectomy (4/102). The primary patency rate was 66% at 1 year (52% at 2 years). Primary assisted patency was 72% at 1 year (58% at 2 years). Secondary patency was 86% at 1 year (63% at 2 years). The majority of TIPSS shunts will remain patent when regular portal venography, with appropriate intervention, is undertaken. Although there is a high reintervention rate this mainly takes the form of balloon angioplasty.

Increased stiffness and persistent narrowing of the aorta after successful repair of coarctation of the aorta: Relationship to left ventricular mass and blood pressure at rest and with exercise

Fifteen children and adolescents who had repair of coarctation of the aorta before age 15, who were not hypertensive at rest, and who had resting arm-leg blood pressure gradients of <20 mm Hg underwent noninvasive evaluation of left ventricular structure and function, aortic stiffness, and residual coarctation as well as bicycle exercise testing. These results were compared with those in 15 age- and sex-matched control subjects. The mean resting age-related systolic blood pressure percentiles (63% versus 46%), transverse aortic stiffness measured by the elastic modulus (Ep) (42.1 versus 23.2 kPa), stiffness index beta (β) (3.66 versus 2.17), echocardiographic left ventricular fractional shortening (0.42 versus 0.36), left ventricular mass index (99.3 versus 81.0 gm/m 2), maximum exercise right arm systolic blood pressure (173 versus 156 mm Hg), and exercise arm-leg blood pressure gradient (35 versus 6 mm Hg) were significantly increased in the coarctectomy patients compared with controls. Univariate correlations in the coarctectomy group showed significant relationships of residual aortic narrowing with left ventricular mass index ( r = 0.68, p < 0.01) and resting systolic blood pressure percentile for age ( r = 0.55, p < 0.05). Residual aortic narrowing did not significantly correlate with aortic stiffness, resting blood pressure gradient, or exercise blood pressure gradient. Neither left ventricular mass index nor resting systolic blood pressure percentile significantly correlated with age of repair or years after repair. These results demonstrate persistent abnormalities in aortic stiffness and left ventricular mass and function after successful repair of coarctation of the aorta in childhood and adolescence. Mild degrees of residual aortic narrowing may affect resting blood pressure and left ventricular mass. Elevated blood pressure and blood pressure gradients between upper and lower extremities during exercise may be a reflection of increased arterial stiffness in the upper body as well as mild persistent coarctation.

Fire Affects Ecophysiology and Community Dynamics of Central Wisconsin Oak Forest Regeneration

In order to understand better the ecophysiological differences among competing species that might influence competitive interactions after, or in the absence of, fire, we examined the response to fire of four sympatric woody species found in intermediate—sized gaps in a 3—yr—old mixed oak forest in central Wisconsin. Selected blocks in the forest were burned in April 1987 by a low—intensity controlled surface fire. The fire had significant effects during the following growing season on community structure, foliar nutrient concentrations, and photosynthesis. Acer rubrum seedling density declined by 70% following the fire, while percent cover increased several—fold in Rubus allegheniensis. In general, leaf concentrations of N, P, and K were increased by the fire in all species, although the relative enhancement decreased as the growing season progressed. Daily maximum photosynthetic rates were 30—50% higher in burned than unburned sites for Prunus serotina, Quercus ellipsoidalis, and R. allegheniensis, but did not differ between treatments for A. rubrum. Mean sunlit photosynthetic rates and leaf conductances were stimulated by the burn for all species, with the greatest enhancement in photosynthesis measured in Q. ellipsoidalis. Leaf gas exchange in R. allegheniensis was most sensitive to declining leaf water potential and elevated vapor pressure gradient, with Q. ellipsoidalis the least sensitive. Fire had no discernable effect on water status of these plants during a year of relatively high rainfall. In comparison with other species, A. rubrum seedlings responded negatively after fire–both in terms of survival/reproduction (decline in the number of individuals) and relative leaf physiological performance. Fire enhanced the abundance of R. allegheniensis and the potential photosynthetic performance of R. allegheniensis, P. serotina, and particularly Q. ellipsoidalis. We conclude that post—fire stimulation of net photosynthesis and conductance was largely the result of enhanced leaf N concentrations in these species.

Effect of obesity on esophageal transit

Esophageal transit time as measured by radionuclide scintigraphy using a swallowed technetium sulfur colloid bolus was measured in obese patients with gastroesophageal reflux, lean patients with reflux, and lean volunteers without reflux. The esophageal transit time was significantly prolonged in the obese group compared with both lean groups (p less than 0.001). Esophageal manometric measurement also confirmed that obese patients have an elevated gastroesophageal pressure gradient, presumably caused by increased intraabdominal pressure resulting from the mechanical burden of excess fat. The esophageal transit time is significantly related to the gastroesophageal pressure gradient. This finding, coupled with those in previous manometric investigations showing that esophageal muscle has a decreased maximum velocity with increasing afterload, explains in part why obese patients have delayed esophageal transit time. Therapy for reflux in obese patients should be aimed at improving esophageal transit.

Capillary pressure gradients in cremaster muscle of normotensive and spontaneously hypertensive rats

The purpose of this investigation is to test the hypothesis that capillary pressure gradients are elevated in spontaneously hypertensive rats (SHR) and to determine the mechanism for the elevation. The cremaster muscle was prepared for microscopic examination under chloralose-urethane anesthesia in seven SHR and eight Wistar-Kyoto (WKY) rats 4–6 weeks of age. Capillary hematocrit, diameter, and red cell velocity were measured. Capillary flow induced by a time-varying pressure gradient was treated mathematically. A finite Hankel transformation was applied to the Navier-Stokes equation for capillary vessels. The solution was expressed as a Fourier-Bessel series, and the fluctuation of capillary flow induced by a time-varying pressure gradient was studied. It was shown that if the velocity fluctuation depended only on the pressure gradient, then the velocity fluctuation would be diminished almost instantly after the capillary started to flow. Capillary pressure gradient and shear stress were evaluated according to two different flow models, Newtonian and Casson. The capillary viscosity was obtained from the capillary hematocrit based on the empirical correlation of viscosity vs hematocrit. Calculations based on both flow models indicate that the capillary pressure gradient and shear stress of SHR is higher than in WKY, especially in vessels near 6 μm in diameter. The elevated pressure gradient is due to a combination of reduced capillary density, causing a higher red cell velocity and a tendency toward smaller capillary diameters in the SHR. Capillary hematocrit and viscosity were not elevated in the SHR.

HEPATOBILIARY IMAGING WITH Tc-99m-HIDA

Availability of the Tc-99m-hepatobiliary agents has permitted an evaluation of the liver-biliary tree-gallbladder-small bowel complex even in the face of elevated bilirubin levels. Although the sequence of events is usually well defined, variations can be found which tend to contribute to diagnostic uncertainties. We wish to point out 2 major variants, which are likely related to increased pressure in the biliary system. 1) Stasis pattern. As long as hepatic ability to extract the radiotracer is still present, the blood level of Tc-99m-HIDA will progressively fall and that within the liver will increase. Once within the liver however, the radiolabel may not progress into the biliary system. This stasis pattern has been recognized in patients with intrahepatic cholestasis. An identical pattern has been noted in 2 males with acute high obstruction of the biliary tree. Hepatic accumulation of tracer occurred, but there was total lack of collection in the larger biliary radicals and no excretion. The diagnosis of high obstruction was confirmed surgically. The presence of acute high obstruction should be considered when a stasis pattern is accompanied by signs and symptoms of cholecystitis (severe pain was present in both cases). 2) Intrahepatic reflux. As the gallbladder contracts, the pressure generated is usually greater than that in the cystic and common bile ducts; hence, the pathway of excretion is from gallbladder toward the small bowel. If this pathway is obstructed, then bile may pass in another direction. A woman was seen with intermittent right upper quadrant pain. The Tc-99m-HIDA study proceeded normally with filling of the gallbladder. Upon administration of a fatty meal, there was prompt emptying of the gallbladder with reflux of activity into the major intrahepatic ducts. At ERCP, there was delayed runoff, and an inferred elevated pressure gradient preventing downward drainage. Hence, increased pressure within the bile excretory pathway can result in unusual distribution of the Tc-99m-HIDA. (Supported by USPHS CA 17802).

Stimulation of insulin release by elevated pressure gradient.

In an attempt to stimulate the contractile events which presumably lead to intracellular translocation and exocytosis of the beta granule, the effect of elevated pressure on the rate of insulin release was studied. In vitro preparations of pancreas were incubated in media of low glucose content (1.65 mM) for several consecutive 15 min periods. The effect of pressure gradients, ranging from 0 to 45 mm Hg above atmospheric pressure, on insulin release was tested during the second period by introducing a mixture of 95% O2-5% CO2 into the incubation flasks. The results have shown that: 1) a rise in the pressure gradient over the gas phase was accompanied by an increase in the concentration of insulin released into the medium; 2) there was a direct relationship between the pressure gradient and the rate of insulin release; 3) the enhanced rate of insulin release caused by elevated pressure was not reversed immediately after release of pressure, but the effect was completely abolished within a period of 15 min; and 4) the stimulating effect of high glucose concentration on the rate of insulin release was completely blocked in the presence of 1 mM DNP, but the pressure-induced stimulation of insulin release was insensitive to this agent. In view of recent evidence implicating the microtubular-microfilamentous system in the secretory process of insulin, it is suggested that the application of pressure to the islet cells provides the necessary motive force to facilitate the intracellular translocation and extrusion of the beta granules normally performed by the beta cell contractile structures.

Cerebral vasoparalysis, arterial hypertension and brain edema (author's transl)

The present studies were performed in order to determine whether "filtration edema" will develop as a consequence of cerebral vasoparalysis, vasoparalysis in combination with arterial hypertension or arterial hypertension alone. A series of dogs, anaesthetised with i.v. Chloralose-Urethane were exposed 1) to cerebral vasoparalysis, produced by hypercapnia (PaCO2 about 150 mm Hg) and hypoxaemia (PaO2 40-60 mm Hg); 2) to arterial hypertension and 3) to a combination of cerebral vasoparalysis and arterial hypertension. Following cerebral vasoparalysis and arterial hypertension, a significant decrease of total cerebrovascular resistance and moderate increase of venous resistance was observed. Regional cerebral blood flow (133Xe), intracranial pressure, as well as the pressure in postcapillary venous outflow (sinus sagittalis wedge pressure and confluence sinuum pressure) were increased. Neither normotonic vasoparalysis nor vasoparalysis in combination with slight arterial hypertension (MABP more than 90 min above 180 mm Hg) resulted in cerebral edema. In contrast, cerebral vasoparalysis in combination with severe arterial hypertension (MABP more than 90 min above 220 mm Hg) resulted in a statistically significant increase in the water content in the white matter without evidence of protein extravasation. Multiple small foci of Evans blue extravasates, however, were found in the cortex following arterial hypertension in combination with vasodilation, indicating a damage of the blood brain barrier. In these blue stained cortical areas the water content was significantly in creased. The following conclusions were drawn from the results. Vasoparalysis during normotension does not produce brain edema despite the slightly elevated hydrostatic pressure gradient between intravasal and extracellular space. Only considerable increase of this hydrostatic pressure gradient caused by a combination of vasoparalysis with severe arterial hypertension is able to produce brain edema in the white matter. In addition, acute hypertension may cause minor multifocal damage of the blood brain barrier in the cerebral cortex. It is concluded that so-called brain swelling, which has been described by several authors in states of cerebral vasoparalysis, is not predominantly caused by brain edema but by vascular congestion. The clinical aspects of the result are discussed.