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F M Fouad

Publications and source records attributed to F M Fouad.

At least 19 recordsLinked to original sources
PubMed1997

Automated cardiac output measurement by spatiotemporal integration of color Doppler data. In vitro and clinical validation.

BACKGROUND: A new Doppler echocardiographic technique has been developed for automated cardiac output measurement (ACOM) that assumes neither a flat flow profile nor collinearity with the scan line, but clinical validation of this method is lacking. METHODS AND RESULTS: In 165 subjects (50 intensive care patients, 10 dobutamine echocardiography patients, and 105 normal volunteers; age, 49.4 +/- 19.3 years; 92 men), ACOM was performed in the left ventricular outflow tract (LVOT), with the color baseline shifted to avoid aliasing. ACOM was also tested in a pulsatile in vitro model. Stroke volume was calculated by double integration of Doppler signals in space (across the LVOT) and in time (through the systolic period), assuming hemiaxial symmetry: integral of integral of pi r v(r,t) dr dt, where v(r,t) is the velocity at a distance r from the center of the LVOT at time t during systole. Stroke volume from ACOM was compared with thermodilution (TD), aortic valve pulsed-wave Doppler (PWAO), and left ventricular echocardiographic (two-dimensional [2D]) methods. There was good correlation between ACOM and PWAO (r = .93). TD (r = .86), and 2D (r = .74), with close agreement seen. ACOM had higher correlation and agreement with TD than did either PWAO (P < .02) or 2D (P < .01). ACOM was also able to track accurately the changes in cardiac output with dobutamine infusion in comparison with PWAO (r = .94). In vitro assessment demonstrated excellent correlation (r = .98, y = 1.0x + 1.94) with little impact of pulse repetition frequency or misalignment up to 30 degrees. Gain dependency was noted but could be optimized by visual inspection of the color image. CONCLUSIONS: Automatic integration of numerical data within color Doppler flow fields is a feasible new method for quantifying flow. It is simpler and faster, requires fewer assumptions, and uses only one apical view. ACOM is a promising new approach to echocardiographic quantification that deserves further study and refinement.

Adolescent↗
PubMed1996

Acute-phase response in rat to carbon tetrachloride-azathioprine induced cirrhosis and partial hepatectomy of cirrhotic liver.

Irreversible liver cirrhosis was induced in rats by supplementing their diet with 0.02% azathioprine and intubating them twice a week with carbon tetrachloride in corn oil. Over period of 3 mo, intoxicated rats showed an atypical acute-phase reaction (APR). The relative concentrations of haptoglobin, beta-lipoprotein, alpha-1-antitrypsin, an unknown peak "X, " and transferrin increased exponentially following a mild initial drop, while albumin, C3c + C3, alpha-1-acid glycoprotein, alpha-1-lipoprotein, and macroglobulin declined continually during the experiment. The accumulated peritoneal fluid was found to contain a similar spectrum of APR proteins. On the other hand, histological examination revealed gradual liver damage manifested as a gradual increase in the areas of collagen separating liver cells, and at the end of the experiment, severe liver damage was evident with isolated hepatocytes in a matrix of collagen. The available data point to the disparity that exists between the physical status of hepatocytes and their biochemical function, which suggests that the remaining metabolically fatigued hepatocytes of the cirrhotic liver continue to biosynthesize and release elevated concentrations of some secretable APR proteins and less of others. Changes in the spectrum of APR plasma components during the progression of inflammatory or physical lesion remain a valid biochemical measure of the pathological function of the acutely intoxicated liver. Partial hepatectomy (PH) of cirrhotic liver displayed a mute APR and no regenerative activity of the remnant hepatic tissue, most likely due to the substantial depletion of hepatic DNA and possible chemical damage to DNA of the remaining viable hepatocytes. A possible cause for the depressed APR to the surgical insult of PH is that the initial azathioprine-CCl4 intoxication had maximally affected APR gene expression and a second injury would then elicit minimal further changes in mRNA levels. Thus, in a compounded pathological condition, the initial inflammatory stimulus on various pre-rRNAs, rRNAs, and mRNAs is rate-limiting to the hepatic biosynthesis and secretion of APR proteins and may not respond linearly, if at all, to a second stimulus.

Acute-Phase Reaction↗
PubMed1996

Measurement of cardiac output with first-pass determination during rubidium-82 PET myocardial perfusion imaging.

In addition to providing useful clinical information, cardiac output determined during rubidium-82 positron emission tomographic (PET) myocardial perfusion studies can be used in the measurement of absolute regional myocardial blood flow using Sapirstein's method. This investigation was conducted to compare cardiac output values obtained by post-processing data acquired in a list mode PET myocardial perfusion study with those obtained using a technetium-99m-labeled red blood cell method on the same patients. Results from 14 patients showed that cardiac output can be accurately measured simultaneously in a 82Rb PET myocardial study, allowing determination of multiple perfusion and functional parameters of the heart, thus improving the cost-effectiveness of the 82Rb PET study.

Cardiac Output↗
PubMed1996

Artificial liver support: the pipe dream of today should be the reality of the near future.

The title of this article is taken from an interesting Letter to the Editor entitled 'Artificial liver support-Pipe dream or reality' by Cattral and Levy of the Toronto Hospital, Canada, published in the New England Journal of Medicine 1994, in which the authors persuasively propose possibilities of artificial liver support and suggest its advantages. We find that their suggestions agree with the core of our thoughts on this subject. The present article deals with the concept of implanting livers taken from humans, primates or non-primates (e.g. hog) into patients in parallel with their own metabolically fatigued or cirrhotic livers, with minimal surgical manipulation, as a prelude to total artificial liver support via a liver dialysis device. While the possibility exists that the host liver may recover function, a donor liver, whether implanted into the patient's abdomen or connected in vitro to the patient's circulatory system extracorporeally, may provide the host liver respite and a period for recovery and proliferation, if possible. Once recovery is under way, the donor liver may be removed and the patient will not experience the usual risks of rejection and the necessary side-effects of immunosuppression associated with conventional full hepatectomy and donor transplantation. The viability of a liver implantation model in rats is correlated in this article with hepatic acute phase response.

Animals↗
PubMed1996

Biogenesis of hepatic acute-phase response to trauma.

The bioorganic pathway(s) of hepatic acute-phase response in rat to single and compounded traumata triggered either by chemical or physical injury has been re-evaluated for the purpose of advancing a better understanding of mechanisms of hepatic regeneration. These insights would be useful in cases of liver cirrhosis and end-stage liver diseases and may allow avenues of surgical management other than liver transplantation. Mechanisms of acute-phase response in rat to a single inflammatory stimulus, e.g. intoxication with phalloidin, alpha-amanitin, subcutaneous administration of carageenan, subcutaneous implantation of Yoshida sarcoma or i.p. administration of Zajdela ascites are discussed and compared with (a) acute-phase response to intoxication by various factors leading to the development of liver cirrhosis, and (b) acute-phase response of nascent hepatocytes where hepatic regenerative activities were induced by chemical intoxication or surgical partial hepatectomy. Interestingly, hepatic acute-phase response was not limited only to these injuries outlined above but also to psychological conditions.

Acute-Phase Proteins↗
PubMed1995

Comparison of thermally oxidized lipids and acetaminophen with concurrent consumption of ethanol as inducers of liver cirrhosis.

The mechanism(s) of liver damage initiated by ingestion of toxic components of thermally oxidized lipids was compared in a rat model with the documented mechanisms of hepatic failure and necrosis initiated by acetaminophen. Acetaminophen (50 mg/kg body weight) or oxidized lipids (0.15 ml oxidized trilinolein or 1.05 ml oxidized butter oil per rat) were intubated at 12-h intervals to rats. Treated rats were allowed free access to food and water containing 3% ethanol. Changes in relative concentration of acute-phase plasma proteins, determined by two-dimensional (2D) immunoelectrophoresis, were taken as a marker of liver damage. In contrast to simple inflammation, acute-phase plasma proteins in this study disproportionately increased or decreased as histological damage of the liver due to intubation oxidized lipids or acetaminophen. Histological examination of liver of rats intoxicated with oxidized lipids revealed severe liver cirrhosis at the end of the trial, where the remaining viable hepatocytes were separated in a matrix of collagen. [3H1]Thymidine incorporation in hepatic DNA of acetaminophen or oxidized lipid intoxication increased in the early stages of intoxication, indicative of regenerative activity of the liver. Further progression of the cirrhosis inhibited continued liver regeneration and [3H1]thymidine incorporation into hepatic DNA. The cirrhotic liver at this stage failed to regenerate to the original mass upon 75% partial hepatectomy. Therefore, it may be concluded that hepatic necrosis produced by oxidized lipids or by acetaminophen may have similar mechanisms.

Acetaminophen↗
PubMed1993

Acute-phase plasma protein response to cholera intoxication in healthy and diabetic rats.

The aim of the present study is twofold: to establish the response of hepatic machinery of plasma protein biosynthesis to cholera intoxication, and to examine the same response of alloxan-diabetic hepatocytes with minimal capacity of synthesis of plasma proteins. Direct lesion of hepatic plasma membranes via ip administration of cholera toxin to male rats resulted in a typical acute-phase response (APR) of plasma proteins, which had regressed to levels similar to those of healthy controls approximately at 240 h postintoxication. The d 2 response to a single 0.16 mg/kg body weight dose was typified by a 23% reduction in the level of albumin, but a 6- and 24-fold increase in the levels of fibrinogen and alpha-1-acid glycoproteins, respectively. This response was similar (in direction but not in magnitude) to the acute-phase reaction to a simple subcutaneous administration of carrageenan. The intoxication was accompanied by a massive leakage, into the peritoneal cavity, of plasma fluid, which embraced the complete profile of acute-phase reactants. A three-step mechanism is proposed to account for the observations as follows: (1) There is a rapid formation of a stable complex between subunit B of the toxin and ganglioside GM1 of hepatic plasma membrane. An APR is induced in response to the alteration(s) of hepatic plasma membranes. (2) The release, from the choleragen-membrane complex, of polypeptide A1 and its subsequent penetration of the hepatic membrane result in both activation of adenylate cyclase and increased vascular permeability of hepatic membranes. This leads, in turn, to exudation of components of plasma fluid in the peritoneal cavity of intoxicated rats. An alternate rationale for this exudation is the slow leakage of plasma proteins out of the blood vascular system (possibly through microvesicles) into the peritoneal cavity of cholera intoxicated rats. The spectrum of acute-phase hepatic secretory components was mirrored in the corresponding peritoneal exudate. (3) The increased hepatic membrane flow provides the continued renewal of plasma membrane proteins required for its eventual repair by either endocytosis or sloughing off the toxin-bound membrane segments into the circulatory system, thus producing regression of APR. Livers of diabetic rats, an already established model in terms of APR, responded to ip administration of cholera toxin by increased biosynthesis of the identified plasma proteins and a marked reduction in total free-glucose in serum.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute-Phase Proteins↗
PubMed1993

Immunoelectrophoretic pattern of native mucosal intracellular glycoproteins of hog healthy and drug-intoxicated stomachs and of hog body fluids.

Naturally occurring glycoproteins have been extracted from fundic and antral mucosal tissue of the hog stomach by means of nondegrading techniques. Major and retarded glycoprotein fractions separated by gel filtration were further dissociated from appreciable amounts of noncovalently bound proteins by CsCl density gradient centrifugation. Antisera to glycoprotein fractions of fundic and antral regions of the stomach were prepared in rabbits. The major fractions from both gastric regions have similar molecular mass (approximately 2 x 10(6)), sedimentation coefficient (approximately 31.5 s), and specific viscosity (approximately 1.6). Purified fractions from each region were further separated into two subfractions by affinity chromatography on wheat germ lectin. Glycoprotein subfractions from antrum and fundus differ appreciably in their carbohydrate and amino acids content, share antigenic determinants, but do not cross-react with anti-hog serum protein antisera. Further diversity in native mucin glycoproteins was observed by the use of one-(D) and two-dimensional (2D) immunoelectrophoresis; subfractions that cross-react with specific anti-hog gastric glycoproteins were found to contain three or more components. D-Immunoelectrophoretic analyses demonstrated (1) in vivo degradation of glycoprotein components of the major fundic fraction isolated from mucosal tissue of alcohol/acetyl salicylate-intoxicated hog stomachs and (2) in vitro catabolism of major fundic glycoproteins by corresponding mitochondrial lysosomal (ML) acid hydrolases. Furthermore, 2D-immunoelectrophoretic analyses showed that (1) hog synovial fluid and plasma proteins have similar prosthetic moieties as either reacted with anti-hog serum proteins antisera. Nonetheless, locations, shapes, and staining intensities of the immunoprecipitate lines differed, which is indicative of different structures of the carbohydrate moieties of components of synovial fluid and plasma proteins, and (2) only a minor fraction of hog cerebrospinal fluid cross-reacted with anti-hog serum protein antisera. This is contrary to the generally accepted deduction based on high-resolution 2D-electrophoresis, indicative of different compositional patterns of plasma and cerebrospinal fluids.

Animals↗
PubMed1993

Sensitivity and specificity of the tilt table test in young patients with unexplained syncope.

UNLABELLED: The usefulness of the head-up tilt testing (HUT) has been previously addressed in diagnosing vasovagal neuroregulatory syncope in the teenage population. However, data concerning sensitivity and specificity is deficient due to the lack of control groups. We compared the response to HUT in young patients referred because of syncope or near syncope (n = 44, mean age 16 +/- 3 years SD) to healthy young volunteers with a normal physical examination and no previous history of syncope (n = 18, mean age 16 +/- 2 years) and to determine the sensitivity and specificity of HUT. The graded tilt protocol was performed at 15 degrees, 30 degrees, and 45 degrees (each for 2 min), and then 60 degrees for 20 minutes. Cuff blood pressure was measured every minute and lead II ECG was continuously monitored. RESULTS: 25 of the 44 patients (57%) developed a vasovagal response or became symptomatic after 13.8 +/- 5.7 minutes of HUT. Three of the 18 volunteers (17%) had a vasovagal response and became symptomatic after 9 +/- 3 minutes of HUT. There was no statistical difference among the four groups (with and without tilt induced vasovagal response) in terms of age and baseline hemodynamic data. The sensitivity of 20 minutes HUT was 57% and its specificity was 83%. The presyncopal hemodynamic response in patients with history of syncope that was characterized by a significant decrease in systolic blood pressure and lack of increase of diastolic blood pressure as compared with baseline and with other groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Partially hepatectomized rats: a model for the study of the effect of toxins on the plasma protein profiles of nascent hepatocytes.

A useful framework is proposed for unifying the synthesis of plasma proteins and their degradation by, or release from, liver cells of intact and partially hepatectomized rats, in which synthesis and release of acute-phase plasma proteins occur in synchrony with the internalization and catabolism of plasma and extracellular proteins. The catabolism of proteins and other hepato-intracellular glycoproteins during sepsis or trauma is essential to provide constituent amino acids and carbohydrates for the synthesis of acute-phase plasma proteins. Increases in the plasma levels of acute-phase response proteins in sham-operated rats reached a maximum between 1 and 2 d after mock surgery, and had returned virtually to control levels within 6 d. By contrast, acute-phase proteins in the plasma of partially hepatectomized rats were decreased by 10-20% of their initial values after 24 h. A maximum acute-phase response on d 7 after the operation was characterized by an increase of 181, 445, and 19% for alpha-1-acid glycoprotein, hepatoglobin, and hemopexin, whereas other acute-phase proteins remained below control levels, for example, by 11, 25, and 38% for albumin, transferrin, and prealbumin, respectively. This delayed response suggests that the nascent liver cells had inherited the capacity of the parent cells to respond to inflammatory signal and had synthesized acute-phase plasma proteins. Accordingly, a time frame for the application of toxin to nascent hepatocytes is suggested. An increased activity (300 +/- 50%) for both bound and free neuraminidase in remnant liver tissue 19 h post partial hepatectomy suggested that hepatic regenerating factor(s) were produced in liver tissue via the hepatic bound and/or free neuraminidase-mediated desialylation of humoral substrates. By contrast, circulating levels of lysosomal enzymes alpha-fucosidase and beta-N-acetyl-D-glucosaminidase were increased marginally after 24 h but had returned nearly to control levels after 7 d, suggesting that lysosomal acid hydrolases do not play a major role in regenerative DNA synthesis, mitosis, or in the synthesis of acute-phase plasma proteins.

Acute-Phase Proteins↗
PubMed1989

On the genesis of gastric haemorrhage.

An hypothesis involving a three step mechanism to account for the initiation of gastric lesions is described. The mechanism necessitates: (a) A drop in the internal energy (ATP) of the mucosal cells of the stomach upon being subjected to stress; either pathological or psychological. (b) Membranes of mucosal "suicidal sacs" containing potent lysosomal acid-hydrolases are rendered fragile and burst, thus releasing hydrolytic acid-hydrolases into the cytoplasm of the mucosal cells as the latter develop an energy deficit under stress. (c) Gastric mucosal cell necrosis, via the degradation of cytoplasmic and mucinous gastric glycoproteins by these lysosomal acid- hydrolases and subjection of the submucosal tissue to the corrosive effects of the luminal fluid containing hydrochloric acid and pepsin, i.e., initiation of gastric haemorrhage. The above mechanism is a general one that describes events associated with the development of gastric lesions regardless of the factor(s) or the agent(s) initiating gastric mucosal haemorrhage.

Animals↗
PubMed1989

Study of hepatotoxicity in isolated perfused liver versus cultures of rat hepatocytes.

Isolated perfused liver and cultures of rat hepatocytes were assessed for the quantitative evaluation of hepatotoxicity. Release of de novo biosynthesized plasma proteins and acid hydrolases into perfusion or culture media was taken as an indication of the integrity of hepatocytes in both systems. The activities of six acid hydrolases, alpha-L-fucosidase, alpha-D-galactosidase, beta-D-galactosidase, beta-D-N-acetylgalactosaminidase, beta-D-N-acetylglucosaminidase, and cathepsin D, were assayed in collagenase-segregated hepatocytes and in monolayer cultures of rat liver cells obtained via collagenase perfusion of rat liver. In situ, liver perfusion with collagenase led to a loss of 45 +/- 5% of the total acid hydrolase activity in the mitochondrial-lysosomal pellet of the liver cells with concomitant increase of these enzymes in the cytosol. In monolayer cultures over a period of 30 h, increased activity of cathepsin D, beta-D-galactosidase, and beta-D-N-acetylglucosaminidase in the mitochondrial-lysosomal pellet and the cytosol fraction was evident with concurrent biosynthesis of plasma proteins. The use of radioactive tracing techniques with the isolated perfused liver revealed that the rate of catabolism of intracellular protein was approximately 5 times that of plasma protein synthesis. Both methods described here are suitable for the study of the effects of toxins on the function of hepatocytes.

Animals↗
PubMed1987

Inhibition by the mushroom toxins alpha-amanitin and phalloidin of hepatopoietin-induced 3H-thymidine incorporation into rat liver DNA and of plasma protein production in hepatocyte cultures.

In primary cultures of rat hepatocytes the induction of 3H-thymidine uptake into DNA of liver cells by the liver cell proliferation factor hepatopoietin demonstrates that this factor is active not only in vivo but also in vitro. Addition of the mushroom toxins alpha-amanitin or phalloidin to liver cell culture decreased the uptake of 3H-thymidine into hepatocytes (in the absence or presence of hepatopoietin) as well as the attachment of the hepatocyte cultures. Mushroom toxins also inhibited the production of plasma proteins in hepatocyte cultures. The inhibition, observed at toxin concentrations from 10(-5) to 10(-7) M, was dose-dependent. At low concentrations of phalloidin the inhibition appears to be selective for certain proteins.

Amanitins↗
PubMed1987

Localization of autonomic nervous system dysfunction in dialysis patients.

Autonomic nervous system dysfunction has been described frequently in uremic patients. The purpose of this study is to determine the localization of this abnormality and to study the possible relationship between autonomic dysfunction and the occurrence of dialysis hypotension. Sixteen consecutive patients participated in the study, 5 of whom had a history of dialysis-induced hypotension. These 5 patients were compared to the other 11 as regards the cardiovascular response to isoproterenol infusion, tilt test and arteriovenous (AV) fistula occlusion. None of the responses to the above mentioned stimuli was significantly different between the 2 groups. In the whole study population, an index of parasympathetic control of heart rate (variation of heart period, VHP) was reduced (31 +/- 5 vs. 59 +/- 9 ms in age-matched controls; p less than 0.025). Heart rate and diastolic blood pressure response to isoproterenol infusion was normal (+23 +/- 2 beats/min and -9 +/- 3 mm Hg; p less than 0.005 for both), indicating normal response of effector organs to beta-adrenergic agonist stimulation. Similarly, plasma norepinephrine increased significantly (+294 +/- 51 pg/ml; p = NS from normal laboratory values) in response to head-up tilt, and heart rate increased simultaneously in all but 5 patients. Blood pressure response was within normal after 10 min of head-up tilt at 60 degrees in all but 3 patients; only 1 of these 3 patients was in the group of dialysis hypotension. However, during AV fistula occlusion, heart rate did not change markedly, despite the significant increase in systolic blood pressure, suggesting an altered sensitivity of baroreceptor reflex arc.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Converting-enzyme inhibition and coronary blood flow.

The effects of converting-enzyme inhibition (25 mg oral captopril) on coronary hemodynamics in the presence and absence of activation of the renin-angiotension system were studied in 10 patients with mild essential hypertension with no evidence of ischemic heart disease. Coronary blood flow was determined by thermodilution before and after 1 week of diuretic therapy in six patients and before and after placebo in four patients. The diuretic (50 mg/day furosemide) reduced coronary blood flow and increased coronary vascular resistance; in these same patients, captopril reduced mean arterial pressure and the rate-pressure product but increased coronary flow significantly. There was no change in any of these variables after captopril in the placebo group. Similar results were obtained in normotensive rats treated with hydrochlorothiazide; the increase in coronary flow after captopril correlated significantly with the control plasma renin activity. These results in hypertensive humans and normotensive experimental animals indicate that diuretic therapy reduces coronary blood flow significantly, and angiotensin can play a significant role in modulating coronary vascular resistance under conditions associated with activation of the renin-angiotensin system.

Adult↗
PubMed1987

Left ventricular diastolic function in hypertensive patients.

Left ventricular filling rate has been shown to be depressed in hypertensive patients before any alteration in indexes of systolic function. The mechanism(s) underlying this abnormality is not known. However, several factors were found to influence left ventricular filling rate. The relative importance of these factors is emerging from studies performed at various centers. Of these, the adrenergic drive, coronary blood flow, heart rate, afterload, and calcium reuptake mechanisms seem to be important. Physiologically, the index of left ventricular filling should therefore be normalized to allow comparison between different individuals. Using a normalized index (filling rate/emptying rate), we found in a small group (n = 13) of hypertensive patients that the increase in total peripheral resistance during head-up tilt was blunted in those with reduced left ventricular filling, suggesting that this abnormality in diastolic function accompanying hypertension plays a role in cardiovascular regulation by altering sensitivity of cardiopulmonary reflexes.

Animals↗
PubMed1986

Nitrendipine, a calcium-entry blocker. Renal and humoral effects in human arterial hypertension.

Thirteen patients with hypertension and normal renal function received nitrendipine, a calcium entry blocker. Nitrendipine did not modify renal blood flow (RBF) or glomerular filtration rate (GFR), decreased mean arterial pressure (MAP) and total peripheral resistance, and did not significantly change cardiac output. Individual RBF changes did not correlate with MAP or cardiac output modifications. Mean arterial pressure changes were inversely correlated with basal renin levels and directly associated with age. Plasma catecholamines and plasma renin activity increased, but plasma aldosterone and plasma volume did not change significantly. However, the greater decrements of MAP tended to be associated with the greater increases in plasma volume. Data show that long-term calcium entry blockade by nitrendipine does not modify RBF or GFR despite the decreased renal perfusion pressure. Further, nitrendipine may be more effective in older patients and the presence of low renin.

Adult↗