SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Hepatic arterial blood flow (HABF) and portal blood flow (PBF) were measured in 18 dogs while awake and during isoflurane and halothane anesthesia. Surgical preparation 1 week before the measurements consisted of a left thoracotomy, placement of a left atrial catheter, and insertion of another catheter into the distal aorta via the left femoral artery. Cardiac output and liver blood flow were determined using microspheres at three stages: stage 1-awake state; stage 2-after 45 min of 1 MAC of isoflurane (eight dogs) or halothane (10 dogs) anesthesia; and stage 3-after 45 min of 2 MAC of inhalation anesthesia. Half-life and fractional clearance for indocyanine green (ICG) were determined 1 day before the experiment (awake state), and at the end of stages 2 and 3. Mean arterial pressure (MAP) and cardiac index (CI), as well as PBF, decreased during isoflurane and halothane anesthesia. HABF increased significantly during isoflurane anesthesia, remained unchanged during 1 MAC of halothane anesthesia, and significantly decreased during 2 MAC of halothane anesthesia. Apparently, hepatic oxygen supply was maintained much better during isoflurane than during halothane anesthesia. PBF correlated with CI during halothane (r = 0.97) and, to a certain extent, with MAP during isoflurane (r = 0.66). HABF correlated with CI and MAP during halothane (r = 0.74 and 0.71, respectively) but did not correlate with systemic hemodynamic variables during isoflurane. ICG half-life significantly increased during 1 and 2 MAC of halothane anesthesia. The degree of increase did not correlate with the level of anesthesia or the decrease in total hepatic blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The ultrasonic-Doppler technique is a very simple method for flow measurement. With this method the generally accepted mechanism of hepatic arterial flow increase after reduction or interruption of the portal vein flow could be confirmed. The increase was not related to cardiac output. Previous doubts about the portal vein flow behaviour after suppression of hepatic artery flow were decided, joining the little group of authors, who did not observe a variation of the portal vein flow in this condition. The concept of the autoregulation of the liver blood supply seems to be connected to the hepatic arterial system only. Although an increase of the hepatic artery flow after infusion of isoproterenol supports the existance of beta-receptors in the hepatic arterial system, it could be proved, that there was no reduction after propranolol infusion. This suggests, that autoregulation of the liver blood supply is not connected to the beta-receptors only.
In acute tests set up on 13 dogs the pressure and blood flow in the portal vein and hepatic artery, the pressure in the inferior vena cava along with lymph- and bile currents were registered following intraportal introduction of CCI4. Subject to determination were also the resistance of venous and arterial hepatic vessels and of the splachnic zone, as well as the summary blood flow. The rising pressure and diminished blood flow in the portal vein were found to be the result of the growing resistance of venous vessels in the liver. Falling pressure and reduced blood flow in the hepatic artery bore witness to the general toxic effect of CCl4 on the animal organism. Increased portal pressure and disturbed permeability of biological membranes was attended by a greater lymph outflow. The inhibition of bile secretion came as a result of hypoxic and toxic damage of the liver.
Intravenous dopamine (4 and 8 microgram/kg/min) causes an increase of hepatic flow and cardiac index, while the ratio hepatic flow:cardiac index remains unchanged. The increase of renal flow after dopamine therefore does not occur at the expense of hepatic flow.
As measured by electromagnetic blood flow transducers, direct infusion of epinephrine, norepinephrine, and dopamine into the portal vein (PV) produced a 40-50% decrease in hepatic arterial (HA) blood flow; isoproterenol increased HA flow by about 69%. No changes in PV flow or pressure were observed. Direct HA infusion of the vasoconstrictors decreased HA flow by amounts comparable to those occurring after PV infusion. However, HA infusion of isoproterenol increased HA flow only 15% suggesting a difference in beta-receptor population in the two vessels. When infused directly into the superior mesenteric artery (SMA), epinephrine and norepinephrine reduced SMA flow by about 45% and PV flow by 20-25%; HA flow increased 6-8%. Infusion of isoproterenol and dopamine into SMA increased SMA flow by 115% and 206% and PV flow by 60% and 70%, respectively, whereas HA flow decreased by 25% and 50%. Portal vein pressure increased less than 3 mmHg. Alpha- and beta-receptor blockade of the liver did not change significantly the alterations in hepatic arterial blood flow that were secondary to changes in portal venous blood flow. It is likely that regulation of hepatic arterial flow resides in mechanisms located within the liver sinusoids.
Under study were 66 children with diffuse purulent peritonitis of the appendicular genesis and 18 adults with bile peritonitis resulting from gangrenous cholecystitis. The analysis of their rheohepatograms showed sharply increased tone of hepatic arterioles, slower outflow of the venous blood, especially in the group of patients with bile peritonitis. Such changes were found to stay long and not to return to normality by the time of discharge of the patient from the hospital. Such patients should be purposefully treated in the polyclinics.
The hepatic hemodynamic effect of 20 mg sublingual nifedipine was evaluated in 15 patients (13 men, 2 women) during heart catheterization. The liver blood flow was measured 10 min after administration of nifedipine by continuous thermodilution (Baim coronary sinus flow analyzer). Nifedipine was associated with a decrease in systolic blood pressure (from 156 +/- 14 to 138 +/-13 mmHg), an increase in heart rate (from 73 +/- 13 to 81 +/- 8.6 beats/min), and increase in cardiac output (from 6.0 +/- 1.6 to 6.5 +/- 1.3 l/min). In 2/15 patients no significant change was derived. The liver blood flow increased in 13/15 patients from 218 +/- 171.7 to 336.7 +/- 247.7 ml/min (22%-194%, P less than 0.01). The study demonstrates that the vasodilation of nifedipine involves the hepatic circulation. If the hepatic clearance of drugs is high and flow dependent, nifedipine-induced increase of hepatic blood flow may impair drug clearance.
Regional hepatic blood flow has been determined by 4 methods with the aid of the 133Xe washout technique: scintisplenoportography (direct application of 133Xe into the spleen by means of a thin needle); arterial method (133Xe is injected into the A. hepatica by means of a catheter); retrograde-venous method (133Xe administered by an occluding hepatic vein catheter); percutaneous intrahepatic method (133Xe administered directly into the parenchyma by means of a Chiba needle). Ad 1.: Scintisplenoportography (SSP) was executed with 97 patients: 8 patients with a healthy liver presented a hepatic blood flow of 103.37 +/- 11.5 ml/100 g/min. 4 patients with a chronic hepatitis showed a hepatic blood flow of 105.67 +/- 10.2 ml/100 g/min. In 38 patients with compensated cirrhosis, hepatic blood flow was determined with 58.15 +/- 11.5 ml/100 g/min and 19 patients with decompensated cirrhosis showed a blood flow of 34.54 +/- 7.2 ml/100 g/min. Of the 19 patients, who did not present any liver image, 2 patients suffered from a prehepatic block, 1 patient (female) from a posthepatic block, the rest were decompensated cirrhoses. In 5 patients suffering from steatosis only collateral circulation was determined and in 4 patients the spleen could not be punctured. In the patients with compensated and decompensated cirrhosis of the liver, hepatic blood flow differentiated significantly (p less than 0.001) from patients with healthy livers and chronic hepatitis. In the patients with bioptically assured steatosis only the washout constant was determined. Reproducibility of this method was tested in 4 patients and no statistical difference of hepatic blood flow values could be found and the correlation coefficient amounted to 0.9856. The advantage of SSP lies in the possibility of recording the portal vein circulation: cranial collaterals were found in 33 patients, 2 patients had caudal collaterals exclusively and 29 patients cranial and caudal collaterals. 33 cirrhosis patients presented evidence of hepatic shunts. In nearly all patients hepatic blood flow was higher in the right lobe than in the left. Ad 2.: Arterial method was executed in 26 patients: 2 patients with healthy livers had a hepatic blood flow of 89.85 +/- 2.9 ml/100 g/min, 19 compensated cirrhoses with 49.28 +/- 11 ml/100 g/min and 3 decompensated cirrhoses with 36.43 +/- 3.4 ml/100 g/min.(ABSTRACT TRUNCATED AT 400 WORDS)
Regional hepatic blood flow has been determined by 4 methods with the aid of the 133Xe washout technique: scintisplenoportography (direct application of 133Xe into the spleen by means of a thin needle); arterial method (133Xe is injected into the A. hepatica by means of a catheter); retrograde-venous method (133Xe administered by an occluding hepatic vein catheter); percutaneous intrahepatic method (133Xe administered directly into the parenchyma by means of a Chiba needle). Ad 1.: Scintisplenoportography (SSP) was executed with 97 patients: 8 patients with a healthy liver presented a hepatic blood flow of 103.37 +/- 11.5 ml/100 g/min. 4 patients with a chronic hepatitis showed a hepatic blood flow of 105.67 +/- 10.2 ml/100 g/min. In 38 patients with compensated cirrhosis, hepatic blood flow was determined with 58.15 +/- 11.5 ml/100 g/min and 19 patients with decompensated cirrhosis showed a blood flow of 34.54 +/- 7.2 ml/100 g/min. Of the 19 patients, who did not present any liver image, 2 patients suffered from a prehepatic block, 1 patient (female) from a posthepatic block, the rest were decompensated cirrhoses. In 5 patients suffering from steatosis only collateral circulation was determined and in 4 patients the spleen could not be punctured. In the patients with compensated and decompensated cirrhosis of the liver, hepatic blood flow differentiated significantly (p less than 0.001) from patients with healthy livers and chronic hepatitis. In the patients with bioptically assured steatosis only the washout constant was determined. Reproducibility of this method was tested in 4 patients and no statistical difference of hepatic blood flow values could be found and the correlation coefficient amounted to 0.9856. The advantage of SSP lies in the possibility of recording the portal vein circulation: cranial collaterals were found in 33 patients, 2 patients had caudal collaterals exclusively and 29 patients cranial and caudal collaterals. 33 cirrhosis patients presented evidence of hepatic shunts. In nearly all patients hepatic blood flow was higher in the right lobe than in the left. Ad 2.: Arterial method was executed in 26 patients: 2 patients with healthy livers had a hepatic blood flow of 89.85 +/- 2.9 ml/100 g/min, 19 compensated cirrhoses with 49.28 +/- 11 ml/100 g/min and 3 decompensated cirrhoses with 36.43 +/- 3.4 ml/100 g/min. Patients suffering from cirrhosis demonstrated significantly lower hepatic blood flow than patients with healthy livers (p less than 0.001). In arterial application also, with the exception of a single patient, the values for hepatic blood flow were higher for the right than the left lobe of the liver.(ABSTRACT TRUNCATED AT 400 WORDS)
Membrane-bound liver alkaline phosphatase (Mem-LiALP, EC 3.1.3.1) is a high-molecular-mass liver alkaline phosphatase (ALP) present in metastatic, infiltrative and cholestatic liver disease. Shedding of hepatocyte plasma membrane fragments (LiPMF) is thought to be responsible for the appearance of Mem-LiALP in the circulation. Several other membrane-bound enzymes, such as gamma-glutamyltransferase (gamma-GT), leucine aminopeptidase (LAP), and 5'-nucleotidase (5'-Nu) are present in the membrane of the shedded LiPMF. By means of immunohistochemical and immunoassay procedures, we presently show that AD-1, a specific monoclonal antibody originally produced against Mem-LiALP, reacts with LAP, a constituent of the human liver plasma membrane. Using AD-1 as an immunosorbant, we isolated circulating LiPMF from cholestatic sera to a high level of purity and separated it from other high-molecular-mass material, such as liver ALP or similar lipoprotein-X complexes. These purified membrane fragments retained their biochemical characteristics. Glycosyl-phosphatidylinositol anchor bearing liver ALP (Anch-LiALP) could be released from the LiPMF by Triton X-100. Whereas ALP was released upon treatment of AD-1 purified LiPMF with phospholipase C, phospholipase D only cleaved the glycosyl-phosphatidylinositol anchor following detergent solubilization of the enzyme. Serum LiPMF from patients with different kinds of cholestatic liver disease were bound onto AD-1 coated nitrocellulose disks and the activity of four membrane-bound enzymes (LAP, ALP, 5'Nu, gamma-GT) was analyzed. A considerable interindividual variation of enzyme activities was observed, suggesting some heterogeneity in the membrane composition of these fragments.
Explore the source record for details and available documents.