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Biomedical subjects

A Falk

Publications and source records attributed to A Falk.

At least 91 records · Page 5Linked to original sources
PubMed1983

The role of 5-hydroxytryptamine in the feline response to intravenous infusion of live E. coli.

A standardized septic shock was induced in cats by intravenous infusion of a live E. coli bacteria strain. The bacterial infusion induced a rapid haemodynamic response characterized mainly by a pulmonary arterial hypertension and a late phase characterized by systemic hypotension and hypodynamic circulation. Systemic arterial, pulmonary arterial, portal venous, left atrial pressures, max inspiratory-expiratory pressure difference in the trachea, aortic and intestinal blood flows were monitored. Arterial blood samples were taken for recording the number of circulating platelets and white blood cells and for determining the acid-base balance. The effect of pretreatment with ketanserin, a specific 5-hydroxytryptamine2 (5-HT2)-receptor blocker on these haemodynamic reactions was studied. In short term experiments on non-bacteriaemic control cats, ketanserin prevented the pulmonary hypertension induced by intravenous 5-HT infusions but not the increase in intestinal blood flow. Ketanserin induced a reduction of total peripheral (including intestinal) vascular resistance to blood flow but had no effect on aortic blood flow. After infusion of bacteria, ketanserin pretreated cats were more hypotensive due to a relative peripheral dilatation of the resistance vessels. Ketanserin pretreatment had no effect on the pulmonary vascular reactions, the tracheal pressure difference or the number of circulating platelets or white blood cells. Thus, except for a more pronounced hypotension early after bacterial infusion, ketanserin pretreatment did not influence the haemodynamic response. It is concluded that 5-HT is not of significant importance in the pathogenesis of the haemodynamic reactions following experimental bacteraemia.

Animals↗
PubMed1983

Sympathetico-adrenergic influences on the small intestinal vascular reactions in experimental septic shock.

The objective of this study was to explore the vascular reactions in the small intestine and the possible role of sympathetico-adrenergic influences. The experiments were performed on 23 cats. The small intestinal blood flow was estimated using a drop counting technique. In one series of cats (n = 7) the small intestine and the adrenal glands had intact vascular and nervous supply (I), in another series (n = 7) the small intestine was sympathetically denervated and the adrenal vessels ligated (II), and in a third series (n = 9) the small intestine was innervated but the adrenal vessels ligated (III). The septic state was induced by i.v. infusion of live E. coli bacteria for two hours. The small intestinal blood flow decreased and intestinal blood flow resistance increased in all series within 3 min upon bacterial infusion. The intestinal vasoconstriction was maintained in cats with intestinal denervation as well as in cats with the adrenal vessels ligated, favouring that other humoral factors than catecholamines are involved. During the later phase of bacteremic shock the intestinal blood flow remained in the preseptic range in the series with a denervated small intestine and ligated adrenals as well as in intact cats, but declined gradually and significantly in cats with adrenal ligation only (III). This pattern of reactions favours a local rather than a remote sympathetico-adrenal influence.

Adrenalectomy↗
PubMed1983

The effects of 5-HT blockade in graded intestinal vascular obstruction in the rat.

Intestinal vascular obstruction with an obstruction pressure of 120 cm of water for one hour induces a 75% mortality in rats. The mortality is associated with intestinal mucosal lesions, release of cardiotoxic material to the intestinal venous blood and trapping of platelets in the lungs. The present series of experiments was performed to study the role of released serotonin in the pathogenesis of the circulatory collapse that follows in this shock model. This was done by pretreating rats subjected to standardized intestinal vascular obstruction with Ketanserin, a selective 5-HT2 receptor blocking agent. It was found that Ketanserin reduced the increase in hematocrit otherwise induced but had no significant effect on mortality, trapping of platelets or the intestinal mucosal lesions. It is concluded that serotonin is probably not of significant importance in the pathogenesis of the circulatory collapse following intestinal vascular obstruction.

Animals↗
PubMed1983

Surgical management of pancreatic injuries. Report of three cases with major pancreatic trauma.

Pancreatic trauma is associated with high mortality and high incidence of complications. A pancreatic injury is easily overlooked at laparotomy, unless complete exploration of the gland is performed. There are often associated visceral and vascular injuries. Three cases of severe pancreatic trauma treated during the past three years are discussed as regards surgical management and the treatment of subsequent complications.

Adult↗
PubMed1982

Paragonimiasis in the United States. A report of nine cases in Hmong immigrants.

Nine cases of paragonimiasis have been encountered in Laotian Hmong immigrants from Camp Ban Vinai in Thailand. Symptoms included cough, hemoptysis, and fever. Chest x-ray films showed segmental infiltrates and pleural effusions, often bilateral. The clinical presentation mimics tuberculosis. All Hmong patients with chronic infiltrates and pleural disease in whom tuberculosis has not been proven should have parasitologic and serologic evaluation to exclude paragonimiasis.

Adolescent↗
PubMed1982

[Not Available].

Explore the source record for details and available documents.

Austria↗
PubMed1982

Cardiopulmonary function as related to intestinal mucosal lesions in experimental septic shock.

The purpose of the present investigation was to explore a possible relationship between cardiopulmonary function and small intestinal mucosal lesions in experimental septic shock. The filling pressure of the left ventricle of the heart (LVEDP) and the maximal pressure change during systole (max dP/dt) were monitored continuously by a tip-transducer catheter. The pulmonary and femoral arterial pressures and pressure changes in the trachea were recorded. The aortic blood flow was measured electromagnetically. Stroke volume, external cardiac work, and the pulmonary vascular resistance could be calculated. Twenty-two cats were made septic by i.v. infusion of live E. coli bacteria. Controls received saline i.v. After 2 hours of bacteremia, preload was increased by a rapid infusion of dextran to unmask cardiac dysfunction. Small intestinal specimens were taken for microscopical examination. The occurrence and the degree of mucosal damage was established. Thirteen cats had virtually normal mucosal appearances, whereas nine disclosed severe lesions. The loading procedure revealed a more pronounced cardiac dysfunction in cats with severe mucosal damage, compared to those without. Pulmonary vasoconstriction, bronchoconstriction, and impaired ventilation-perfusion ratio were also demonstrated, but these signs of pulmonary dysfunction did not differ when comparing animals with and without mucosal damage. A correlation between impaired cardiac function on one hand and hypotension--intestinal mucosal lesions on the other, suggests cardiotoxic material released from the damaged intestine as one contributing mechanism.

Animals↗
PubMed1982

Mucosal lesions in the feline small intestine in septic shock.

The incidence and possible pathogenic mechanisms in the development of small intestinal mucosal lesions in experimental septic shock were investigated in cats. Mucosal lesions were found in 50% of the animals following a standardized bacteremia, and 15% had pronounced mucosal damage. The development of these lesions was not correlated with intestinal vasoconstriction or to portal hypertension but with decreased systemic arterial blood pressure during the last hour of the experiments. The correlation between mucosal damage and arterial hypotension in septic shock supports the view that these lesions are caused by hypoxia secondary to an increased efficiency in the countercurrent exchange mechanisms of oxygen in the villi.

Animals↗
PubMed1982

An evaluation of the functional implications of the intestinal mucosal lesions in shock.

Small intestinal mucosal lesions are reported in clinical shock and are commonly found in experimental shock. Experimental series in which shock is induced by regional intestinal ischemia or IV infusion of live Escherichia coli in cats or by graded intestinal vascular occlusion in rats are described. In all series mucosal damage was related to pronounced hypotension or mortality. In the cat models myocardial dysfunction was demonstrated in vivo by IV volume load and recording of changes in left ventricular filling pressure as related to cardiac performance. Following intestinal ischemia in cats and intestinal vascular obstruction in rats the intestinal venous plasma was found to contain cardiotoxic factors when tested in vitro. It is proposed that the development of small intestinal mucosa lesions in shock tends to further aggravate hypotension by causing intestinal release of cardioinhibitory material.

Animals↗
PubMed1981

Central hemodynamic responses to venous, aortal or portal infusion of live E. coli bacteria in the cat.

The central hemodynamic responses were studied in experimental sepsis in cats, following various routes of infusion of live E. coli bacteria. The aortic blood flow (ABF) was electromagnetically recorded. The pulmonary artery was cannulate for pressure recording. Platelet and white blood cell concentrations, PO2, PCO2, pH and oxygen saturation were measured at intervals. I.v. infusion of bacteria induced initially decreased ABF, systemic hypotension, pulmonary hypertension. Portal infusion evoked, on the other hand, increased ABF, but induced no significant change in systemic or pulmonary arterial blood pressures. Aortal infusion induced responses in between. The initial hemodynamic changes were followed by relative normalization after 5-10 min. Then, in all series, a progressive fall in ABF and systemic blood pressure were noticed. Within 5 min following bacterial infusion the platelet and white blood cell concentrations fell to 65 and 50%, respectively. In all series a moderate metabolic acidosis developed. Thus, the initial hemodynamic response following infusion of live E. coli was dependent on the route of infusion; intraportal infusion induced initially a more hyperdynamic state. The different initial central hemodynamic responses did not influence the subsequent development of a hypotensive shock state.

Animals↗
PubMed1981

Intestinal hemodynamic effects of varying the route of infusion of live E. coli bacteria in the cat.

The responses of the series-coupled vascular sections in the feline small intestine were studied in experimental sepsis induced following various routes of infusion of live E. coli bacteria. The intestinal hemodynamics were followed by means of plethysmography combined with direct recording of the intestinal venous outflow. After 2 hours of bacterial infusion the experiments were terminated. Infusion of E. coli in the inferior caval vein induced initially hypotension, decreased intestinal blood flow (Q) and increased intestinal vascular resistance (R). Portal venous infusion induced, on the other hand, an initial arterial blood pressure increase, an increase of Q and a decrease of R. Aortal infusion evoked only minor initial changes. The early response was in all series followed by a progressive hypotension during which Q decreased and R increased gradually. There were no changes in intestinal tissue volume, indicating that there was no pooling of blood or extravasation of fluid, during the experiments. Intestinal mucosal lesions were equally distributed in the three series. Thus, depending on the route of infusion live E. coli induced intestinal vasoconstriction or vasodilatation. Regardless the route, there was no intestinal pooling of blood or fluid. Hypotension developed in most cats after 120 min, regardless the site of infusion and the initial vascular response.

Animals↗
PubMed1980

Clonal regulation of the induction of macrophage-and granulocyte-inducing proteins for normal and leukemic myeloid cells.

A cloned line of myeloid leukemic cells can be induced by the alkylating agent nitrosoguanidine for two macrophage- and granulocyte-inducing (MGI) activities. One activity, MGI-I, induced the formation of macrophage and granulocyte colonies from normal myeloblasts. Another activity, MGI-2, induced differentiation of MGI+D+ myeloid leukemic cells to macrophages and granulocytes. Experiments on the time course of induction of the two activities have shown that MGI-I was induced before MGI-2, MGI-1 was first detected in cell extracts and this was followed by detection of both activities in culture supernatants (conditioned medium). After induction with bacterial lipopolysaccharide, another inducer of both MGI activities in this clone, MGI-I was also detected before MGI-2 in cell extracts. The steroid dexamethasone, which is an effective inducer of some differentiation-associated properties in this clone, did not induce either MGI-1 or MGI-2. Studies with different clones of myeloid leukemic cells have shown a clonal variation in the induction of MGI-1 and MGI-2. Different clones were induced by nitrosoguanidine either for MGI-1 and MGI-2, for MGI-1 without MGI-2, or for neither MGI-1 nor MGI-2. None of the clones were induced for MGI-2 without MGI-1. The results indicate that the induction of MGI-1 and MGI-2 is differently regulated in the same clone, and that there is a clonal and thus presumably genetic variation in inducibility for these two activities of MGI.

Animals↗
PubMed1980

Intestinal vascular and central hemodynamic responses in the cat following i.v. infusion of live E coli bacteria.

Septic shock was induced in cats by i.v. infusion of live E. coli bacteria. The reactions of the series-coupled sections of the small intestinal vascular bed were followed continuously by a plethysmographic technique. Intestinal venous outflow was recorded using a drop counting technique. Intestinal venous outflow was recorded using a drop counting technique. The chest was opened and blood flow in the ascending aorta was followed electromagnetically. Pulmonary arterial blood pressure was recorded after direct cannulation. Following infusion of washed E. coli bacteria suspended in saline, a rapid early response was evident. This was characterized by arterial hypotension, unchanged aortic blood flow, pulmonary hypertension, and intestinal vasoconstriction. After 5-10 min a period of relative normalization followed. After 30-60 min a second phase, characterized by general circulatory deterioration, developed. The induced septic shock was initially characterized by a slight intestinal vasoconstriction. There was no accumulation of blood or fluid in the intestinal vascular bed; an isovolumetric state was thereby maintained in intestinal tissue throughout the experiments.

Animals↗
PubMed1980

Pulmonary vascular reactions in experimental septicemia, A preliminary report.

Septicemia was induced in cats by infusion of live E. coli bacteria into the inferior vena cava, the portal vein or the aortic arch. Systemic arterial blood pressure, aortic blood flow, pulmonary arterial blood pressure, intestinal blood flow and portal venous pressure were recorded continuously and arterial platelet and white blood cell counts and acid-base balance measured at intervals. Infusion of E.coli into the inferior vena cava induced an initial response characterized by systemic pressure reduction, unchanged or increased aortic blood flow and pulmonary hypertension. Intestinal blood flow decreased moderately, while portal pressure remained unchanged. The arterial infusion evoked a similar response. After portal infusion there was a more pronounced increase of aortic blood flow, a significantly less elevation of the pulmonary artery pressure, and the intestinal blood flow was maintained. The changes induced in arterial acid-base balance or in platelet and white cell counts were not influenced by the route of administration. It is concluded that the route of administration of bacteria is of importance when considering the relevance of experimental data to clinical septic states.

Animals↗
PubMed1980

Hemodynamic effects of systemic or portal IV infusion of live E coli bacteria in the cat. A preliminary report.

The reactions in the series-coupled vascular sections of the small intestine and the changes in aortic blood flow, systemic arterial, and pulmonary arterial blood pressure were followed continuously in cats made septic by IV infusion of live E coli bacteria for 2 hours. Peripheral venous infusion initially induced systemic hypotension, pulmonary hypertension, and increased aortic blood flow, but decreased intestinal blood flow. These changes were normalized within 5-10 minutes. During the next 110 minutes systemic arterial blood pressure, aortic blood flow, and intestinal blood flow decreased continuously while intestinal blood flow resistance remained in the control range. Portal venous infusion induced a significantly less pronounced initial pulmonary arterial blood pressure increase. No initial intestinal vasoconstriction was noticed and intestinal blood flow resistance decreased during the bacterial infusion. In both series only small and insignificant changes of intestinal tissue volume were seen. The data suggest that the route of infusion is important to the response in experimentally-induced sepsis. The constant intestinal tissue volume argues against intestinal pooling as being of importance to the development of low blood pressure in septic shock.

Animals↗
PubMed1978

Preferential charging of tRNA-Met-f in Escherichia coli K12.

The charging of tRNA-Met-f and tRNA-Met-m in vivo and in vitro and initiation of polysomes during methionine limitation were studied in two strains of Escherichia coli K12. In the wild-type strain the distribution of polysomes as well as the kinetic parameters of methionyl-tRNA synthetase indicate preferential acylation of tRNA-Met-f. This preferential charging of tRNAM-et-f does not take place in a mutant strain which is also defective in initiation of polysomes during methionine limitation.

Adenosine Triphosphate↗