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Biomedical subjects

M Papp

Publications and source records attributed to M Papp.

At least 127 records · Page 7Linked to original sources
PubMed1977

Humoral influences on local blood flow and external secretion of the resting dog pancreas.

Graded doses of glucagon (2--8 microgram/kg b. w.), prostaglandin E1 (PGE1) (125--1000 ng/kg b. w.), caerulein (1--32 ng/kg b. w.) and a synthetic C-terminal octapeptide of cholecystokinin-pancreozymin (CCK--PZ) 50--400 ng/kg b. w.) were infused into the superior pancreatioduodenal artery in chloralose-anaesthetized dogs to study the effect on blood flow and external secretion of the resting pancreas. Local blood flow was measured by a heated thermocouple inserted into pancreatic tissue supplied by the superior pancreaticoduodenal artery. Blood flow through this artery was measured by electromagnetic flowmeter. Juice was collected from the cannulated main pancreatic duct. Each of the four agents significantly increased pancreatic blood flow. There was a linear correlation between the doses and the blood flow responses. Caerulein and the synthetic C-terminal octapeptide of CCK--PZ increased the amount of secreted juice from the resting pancreas. The C-terminal octapeptide of CCK--PZ elevated the protein concentration of the secreted juice in proportion to the dose. Glucagon and PGE1 did not influence the amount of secreted juice from the resting gland.

Animals↗
PubMed1976

Fine structrual relation between pancreatic excretory ductules and intercellular spaces.

Horse-radish peroxidase injected into the femoral vein of intact rats, or infused at 30 cm H2o pressure into the main pancreatic duct of intact dogs, entered easily the interstitial spaces surrounding acini and acinar cells. The latter are interconnected at their luminal segments by zonulae occuldentes. These junctions form a barrier to tracer penetrating from the interstituim towards the lumen of terminal ductules. However, the intraductally infused peroxidase entered the interstitial spaces, probably through the pressure injured acinar cells, as did colloidal carbon particles when infused intraductally.

Animals↗
PubMed1976

The distribution of 3H-gastrin and 14C-pentagastrin in the blood and lymph of rats.

3H-gastrin (0.83 mug/rat) or 14C-glycine-pentapeptide amide (100 mug/rat) were injected into the femoral vein in various groups of rats and radioactivity was measured in the arterial blood plasma and thoracic duct lymph in consecutive 5--10 min. periods for 60 minutes. Radioactivity excreted in the bile for 30 minutes was injected into the blood and lymph was followed for 120 minutes. It has been observed that labelled gastrin or pentagastrin activity reaches its peak in the plasma in the 5th minute after intravenous injection. Next, activity in the plasma decreased after the injection of labelled gastrin, but remained unchanged after the injection of labelled pentagastrin. In the lymph, radioactivity reached its peak value between 5--15 min. after the injection of the labelled hormones. This peak value was two- to threefold of plasma radioactivity measured at the same periods. After the intravenous injection of labelled pentagastrin radioactivity was excreted in the bile; injecting this radioactive bile into the jejunal lumen, radioactivity was reabsorbed mainly into the blood circulation.

Animals↗
PubMed1976

Pathogenesis of acute pancreatitis: pancreatic ductal-interstitial-vascular and lymphatic pathways.

The generally accepted theory explaining the pathogenesis of pancreatic autodigestion (acute pancreatitis) is analysed. The pathways are discussed through which the content of the pancreatic duct system, the digestive enzymes, may escape to enter the acinar cells and the pancreatic interstices, together with the effect of the enzymes on the pancreatic vessels and thus on pancreatic blood flow. The potential consequences of vascular damage are described as well as the importance of pancreatic lymphatics in the transport of the escaped enzymes from the interstices. Although no definite answer can be given to the basic problem whether acute autodigestion of the pancreas is a result of some intra- or extra-acinar process, it is suggested that the intra- and extra-acinar processes are linked and are decisive in launching the pathological process.

Acute Disease↗
PubMed1975

Impeded interstitial fluid movement: a factor in pancreatic oedema.

Pancreatic oedema was induced by physiological saline infused into the superior pancreatico-duodenal artery of 34, chloralose anaesthetized dogs. Both lymph flow from cannulated pancreatico-duodenal lymphatics and intralymphatic pressure in the non-transected ones increased significantly. The increase in pressure may be due to the regional lymph nodes obstructing increased lymph flow. The development of gross pancreatic oedema preceded the peak values of pancreatico-duodenal lymph flow and pressure. This suggested impeded fluid movement along tissue interstices and from tissue interstices into the pancreatic lymphatics. The progression of the oedema ran roughly parallel with the increase in fluid pressure measured by a perforated capsule implanted two weeks earlier into pancreatic tissues supplied by the artery. The results suggest that both the rise in lymph flow and pressure during the development of oedema in lobular organs like the pancreas are rather the consequences and not the causes of oedema.

Animals↗
PubMed1975

Glucagon treatment of experimental acute pancreatitis.

CFY male rats anaesthetized with pentobarbital were used in different groups for inducing acute pancreatitis by the retrograde injection either of 1 mg elastase, 5 mg trypsin, 4 mg lysolecithin, 10 mg Na-taurocholate in 0.2 ml volume or of 0.3 m. sunflower oil. In each group laparatomized animals served for control. The animals with pancreatitis were treated either with 15 mug/b.w.kg/hour glucagon or with physiological saline for 72 hours. Twenty-four and 72 hours after inducing pancreatitis glucagon did not influence the significant fall in blood pressure elicited by the intraductal injection of trypsin or elastase or in the plasma calcium level in pancreatitis induced by trypsin or sunflower oil. Neither did glucagon affect the significant increase of plasma lipase activity in pancreatitis induced by trypsin or taurocholate. It also failed to reduce the 24-hour mortality rate and the extension of fat tissue necrosis in the abdominal cavity of pancreatitic animals. In contrast, glucagon treatment significantly reduced the amount of abdominal exudate associated with bile salt induced pancreatitis and, probably due to its pancreatic blood flow increasing effect, seemed to moderate the degree of tissue damage elicited in the pancreas by detergents such as taurocholate or lysolecithin.

Acute Disease↗
PubMed1975

Effect of hypocalcaemia and lipid peroxidation on experimental acute pancreatitis.

It has been studied whether hypocalcaemia increased the mortality rate of experimental acute pancreatitis in the rat, and whether lipids injected into the pancreas underwent peroxidation, damaging thereby the gland. Prolonged hypocalcaemia was induced by bilateral parathyrodectomy and intensified by a calcium-deficient diet. Parathyroidectomy significantly decreased also arterial blood pressure. Three hours after their intraductal injection, both 0.2 ml sunflower oil and 5 mg trypsin significantly decreased arterial blood pressure in the non-parathyroidectomized animals and so did 5 mg trypsin in the parathyroidectomized ones; sunflower oil decreased the blood calcium level below 5 mg/100 ml in parathyroidectomized rats fed a calcium-deficient diet. No differences were found in the mortality rates of nonparathyroidectomized normocalcaemic rats and parathyroidectomized hypocalcaemic ones, or in the extent and gravity of pancreatic injury and in the extent of fat tissue necrosis at 3 and 24 hours after the intraductal injection of 0.2 ml sunflower oil or 5 mg trypsin. Sunflower oil, oleic acid and linoleic acid injected by retrograde way into the pancreas in 0.2 ml volume each induced extensive danage to the acinar parenchyma, while liquid paraffin failed to do so. Among these agents, only linoleic acid increased, as a sign of lipid peroxidation, malonaldehyde concentration in the pancreatic tissue. Linoleic acid injected into the submaxillary salivary gland in 0.1 ml volume induced extensive tissue damage, while sunflower oil, oleic acid failed to do so.

Acute Disease↗
PubMed1975

Structure of cutaneous lymphatics propelling lymph.

In serial sections from the oedematous skin of hind limb of rats the lymph vessel walls were studied for structures active in propelling the lymph. To dilate the lymphatics lymph formation and transport were increased by dextran-oedema. A special type of sack-like structure lined almost exclusively by endothelial cells was observed at the postcapillary segment between the lymph capillaries and lymph vessels proper. The lymph flow from the capillaries into these postcapillary sack-like sinuses is regulated by valves. The postcapillary sacks joined the lymph vessels proper the media of which was built up of a muscle cell sheath. In these artery-type lymph vessels proper the lumen was found to be varying in diameter; some vessels seemed to have practically no lumen while other segments were open. Under the electron microscope thin, actin-type and thick, myosin-type myofilaments were seen in the muscle cells of lymphatic post-capillaries and lymph vessels proper. The lymph is accumulated in the postcapillary sack-like sinuses and from there is transported towards the centre by the contractions of artery-type lymph vessels. Thus, these structures may function as "lymph hearts" in the oedematous skin.

Animals↗