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Biomedical subjects

H Thiel

Publications and source records attributed to H Thiel.

At least 55 records · Page 3Linked to original sources
PubMed1980

Liver hemodynamics and portacaval shunt.

The hepatic circulation, which is essentially important in supplying liver cells with oxygen and substrates needed for securing metabolic homeostasis, is well regulated by extrahepatic and intrahepatic mechanisms. Autoregulation of hepatic artery flow, as well as pressure mediated vascular interactions between hepatic-arterial, portal venous and hepatovenous blood flow, secure a constant low pressure sinusoidal liver perfusion. Apart from these hemodynamic mechanisms, there are also specific morphologic features in the hepatic vascular bed responsible for regulating liver blood flow. Functional aspects concerning the arterial and portal venous contributions in liver circulation give strong evidence that portal blood may be of greater importance than arterial, especially for hepatic nutrition and trophics, as well as for metabolic homeostasis of the whole organism. In portacaval shunt operations, portal venous flow to the liver should be preserved to the greatest extent possible.

Esophageal and Gastric Varices↗
PubMed1979

[Bone marrow insufficiency and hemangioendothelioma of the liver after thorotrast application: Late effects of thorotrast (thorium dioxide) in man (author's transl)].

The report details with the late effects following administration of thorotrast in two patients: multicentre metastating hemangioendothelioma of the liver respective bone marrow insufficiency developed after application of thorotrast 34 respective 36 years ago. The clinical and autoptical findings are described and attention is drawn to the relevance of this disease at present time.

Alkaline Phosphatase↗
PubMed1979

[New aspects of liver circulation: effects and consequences for the portocaval shunt therapy in liver cirrhosis].

Hepatic circulation, which is of essential importance in supplying the liver cells with oxygen and substrates needed for securing metabolic homeostasis of the organism, is characterized by well-regulated mechanisms of intrahepatic arterial, portal and hepatovenous interaction. Furthermore, the hepatic circulation is integrated in the systemic and splanchnic hemodynamic as interposed in a high, or respectively low, pressure system. Beside these hemodynamic mechanisms there are also specific morphologic features in the hepatic vascular bed responsible for regulating liver blood flow. For hepatic nutritions and trophics, and for the metabolic homeostasis of the organism, portal blood is of greater importance than arterial. In porto-caval shunt surgery it is recommended that any remaining portal flow to the liver be preserved to the greatest extent possible.

Homeostasis↗
PubMed1978

["Hepatogenic ulcer": theories and facts (author's transl)].

A review of literature is given concerning the incidence, pathogenesis and clinical relevance of peptic ulcer in chronic liver disease. 1. Today there is no doubt about a highly significant incidence of peptic ulcer in chronic liver diseases, especially in cirrhosis of the liver. Therefore it seems reasonable to use the term "hepatogenic ulcer". 2. Assuming a relation between chronic liver disease and peptic ulceration several theories are discussed with regard to the causality and etiology. Most investigators suppose the diseased liver as "primum movens" in peptic ulceration by means of conditioning different ulcerogenic factors. 3. The clinical finding of increased frequency of peptic ulcer in cirrhotics despite of reduced gastric acid output is no contradiction. It can be explained by relative disturbance of the balance between aggressive and protective mechanism, the latter being diminished. Although a dysfunction of gastric mucus is recently assumed, the specific pathogenetic factor is not clear up to now. 4 Nevertheless, there is no doubt about the clinical relevance of this type of ulcer, given by diagnostic and therapeutic problems and pitfalls.

Chronic Disease↗
PubMed1977

[Hemodynamic studies on liver circulation with special reference to the hepatic artery].

Hepatic and systemic hemodynamics were studied in the rat under different experimental conditions. It could be demonstrated that the hepatic arterial blood flow in normal as well as in sick liver of animals is well regulated: for example by means of the venovasomotorical reaction (portoarterial interaction) and systemically by autoregulation. There exists an inverse correlation between arterial and portalvenous liver blood flow: As portal liver blood flow decreases hepatic arterial flow increases. Especially a marked increase of hepatic artery flow was found after portocaval end-to-side anastomosis. Yet, the hepatic artery flow improvement after portocaval shunt could not compensate the diverted portalvenous blood supply at all. In states of portal hypertension with a relevant portocaval collateral circulation, also after surgical portocaval shunt, the systemic circulation becomes more hyperdynamic. There also exists a remarkable relation between the extent of portocaval shunt flow to circulating blood volume, cardiac output and circulation time. Some correlates of the experimental findings with the altered hemodynamics in human liver cirrhosis were found and discussed from the viewpoint of portocaval shunt surgery in man.

Animals↗
PubMed1977

"To select better--to shunt better" prerequisites for better shunt therapy in liver cirrhosis. Review.

Essentially 3 facts are responsible for the poor clinical outcome after porta-caval shunt in liver cirrhosis today: 1. Further reduction of hepatic blood flow, 2. total or nearly complete deprivation of the liver of portal venous blood supply with essential substances and functions and 3. insufficient criteria for selection. Since there exists no alternative procedure in decompressing bleeding varices in the end, porta-caval anastomoses will have to be performed also in the future. Therefore all efforts must be undertaken to improve the operative and longterm results, including a better preoperative selection and a better shunting. Determination of "functional" liver volume, knowledge of hepatic arterial reaction and preoperative determination of the intrahepatic shunt-flow might be very promising aspects in the selection today. In porta-caval surgery a differentiated choice of the available shunting methods to be applied, especially techniques for selective decompression and liver arterialization, may improve the results. Finally, the aim in each case should be a porta-caval shunt adapted to the individual situation of the cirrhotic patient.

Blood Pressure↗
PubMed1976

Hepatic blood flow and cardiac output after porta-caval anastomosis in the rat.

Investigations were performed in rats with portacaval anastomosis (PCA) in order to measure hepatic hemodynamics and cardiac output (CO) 3, 6, 14 and 28 days after operation under pentobarbitone anesthesia using the flow fraction distribution method (131I-MAA) of CO. The latter was calculated using Vierordt's principle from blood volume (BV) (125RIHSA-dilution method) and ICG-appearance time (ICG-AT) (ear-densitometry). Even 3 days after PCA CO was increased to 38.7 +/- 5.0 (SD) ml/min/100 g b.w. (normal 23.8), due to an increase of BV from 6.3 +/- 1.4 to 7.5 +/- 0.6 ml/100 g b.w. and a decrease of ICG-AT from 3.6 +/- 0.4 to 2.8 +/- 0.5 s. Arterial hepatic flow fraction of CO increased to 8.7 +/- 2.8% (control: 5.5 +/- 2.4%). Changes could be observed up to day 28. Hepatic blood flow per g liver tended to stabilize but was still decreased at day 28: 1.5 +/- 0.6 ml/min/g liver (control: 2.0 +/- 0.3). The typical hemodynamic changes in human liver cirrhosis can be reproduced by PCA alone. They are considered to be compensatory mechanisms for a reduced portal liver blood flow, which are not found to compensate completely.

Animals↗
PubMed1976

[Effects of endotoxinemia on renal and intrarenal hemodynamics of rats with or without portacaval anastomosis].

Renal dysfunction in patients with cirrhosis of the liver is frequent especially in connection with endotoxaemia. Renal and intrarenal haemodynamics were investigated, therefore, in normal rats with or without portacaval anastomosis (PCA) by means of the cardiac output (CO) fractionation technique using microspheres. The intrarenal blood distribution was estimated after anatomical separation of renal cortex and medulla. In normal rats the total renal fraction of CO was 22.5 +/- 7.2%, and the renal medulla fraction 0.8 +/- 0.4% of CO. After a single injection of E. coli-endotoxin (1.5 mg/kg b.w.) the animals developed a high-cardiac-output state, the mean arterial pressure decreased from 110 +/- 15 mm Hg to 81 +/- 6 mm Hg. Renal fraction of CO was unaltered but the blood flow through the kidney was increased due to the high CO. The blood flow of the medulla increased five to tenfold of control values whereas renal cortical blood flow decreased. During the first eight hours after endotoxin administration the animals developed polyuria with a decrease of urine osmolality. Comparable systemic and renal haemodynamics were present in untreated PCA-rats, in which endotoxaemia was present spontaneously (Limulus Gelation Test). Additional endotoxin administration in these animals caused severe shock syndrome with a decrease in total renal perfusion and a further decrease in renal cortical blood flow. Endotoxin administration in normal rats caused minimal morphological alterations in the kidneys which were comparable with those found in PCA-rats. Endotoxin administration in PCA-rats however leads to severe damage of the kidney with fibrin deposits in the glomerula and acute tubular necroses. The haemodynamic, functional and morphological changes caused by endotoxin in the experiments are observed in principle in patients with cirrhosis of the liver too. This indicates that endotoxin should be taken into considerations concerning the pathogenesis of renal failure in patients with cirrhosis of the liver.

Animals↗
PubMed1975

Endotoxin-induced liver necrosis and intravascular coagulation in rats enhanced by portacaval collateral circulation.

The effects of intravenously administered endotoxin on the hepatic and systemic circulation as well as on the coagulation system were evaluated in normal rats (n = 26), in rats with experimental portal hypertension (n = 15), and in rats with portacaval anastomosis (n = 22). Endotoxin (1-5 mg/kg) in the normal rat leads to a prompt increase of transaminase activity and to a hyperdynamic circulation with a consequent increase in the total hepatic blood flow. In a later phase (6 h postoperatively) the hepatic artery dilated with a consequent hepatic arterial hyperperfusion. The coagulation system was affected with signs of consumption coagulopathy. In the rats with portal hypertension and portacaval collaterals as well as in those with portacaval anastomosis, the endotoxin injection resulted in acute liver necrosis within 12 to 15 hours. The hepatic artery became overdilated with a cardiac output fraction of 25% (normal 5-5%). Blood extravasates and thrombi, rich in fibrin, were detected in the liver. It is suggested that this exaggeration of the endotoxin effect was due to an impaired clearance function of the reticuloendothelial system, probably as consequence of portacaval collateral circulation. It is concluded that endotoxins (1) damage the liver even in a normal organism; (2) are potent to induce acute liver necrosis, if the reticuloendothelial system is altered; (3) have to be taken into consideration as contribution to the pathogenesis of acute as well as chronic liver diseases.

Alanine Transaminase↗