Search PubMed⌕ Search

Biomedical subjects

O Lundgren

Publications and source records attributed to O Lundgren.

At least 163 records · Page 9Linked to original sources
PubMed1979

On the protective role of the liver in the hypotensive state following intestinal ischemia.

Regional intestinal hypotension (arterial inflow pressure about 30 mmHg) was induced in cats by partially occluding the superior mesenteric artery with an adjustable clamp. The superior mesenteric vein was cannulated and the intestinal venous outflow recorded by a drop counter. The intestinal venous blood bypassed in one series the liver and was returned to the animal via the jugular vein. In two other series it was returned via the portal vein and in one of these also the hepatic arterial pressure was kept at 30 mmHg. Following two hours of regional intestinal shock a general cardiovascular derangement was evident in all series. This was not influenced by directing the intestinal venous blood flow through a normotensive or hypotensive liver. Characteristic intestinal mucosal lesions were found in all series. It is concluded that bypassing or directing the intestinal venous blood through a normotensive or hypotensive liver did not affect the local and general cardiovascular effects of regional intestinal hypotension.

Animals↗
PubMed1978

Cardiac and pulmonary function in regional intestinal shock.

After a two-hour period of regional intestinal shock (arterial inflow pressure 30 to 35 mm Hg; electrical stimulation of regional vasoconstrictor fibers at 6 Hz) a pronounced cardiovascular derangement is observed as reflected in a rapid fall in arterial blood pressure. In this study, central hemodynamics and lung function were investigated to elucidate if functional changes in the thoracic organs might explain the cardiovascular collapse. No alteration of pulmonary function was observed. A negative inotropic influence on the heart was, however, noted as judged by a decreased left ventricular stroke volume and left ventricular maximal pressure change in the face of an increased left ventricular end diastolic pressure. Based on earlier observations with the same shock model, it is proposed that the cardiac effects were caused by cardiotoxic material released from the hypoxic gut.

Animals↗
PubMed1978

Tissue osmolality in intestinal villi during luminal perfusion with isotonic electrolyte solutions.

A cryoscoptic technique has been developed that makes it possible to determine tissue osmolality in the core of the intestinal villi. During absorption from an isotonic electrolyte solution containing glucose an osmolality gradient was demonstrated from tip to base of the villi in both the jejunum and the ileum. The tissue osmolality at the villous tips was measured to 1 000-1 200 mOsm/kg H2O while the osmolality at the villous base was approximately isotonic with plasma. Increasing intestinal blood flow by i.a. administration of a vasodilator drug, or making the intestine ischemic by clamping the intestinal vascular supply while supplying the mucosa with oxygen, markedly decreased tissue osmolality. Substituting all sodium ions with choline in the luminal perfusate abolished almost completely the tissue hyperosmolality and the intestine became a secretory organ. These observations are consistent with the view that the observed villous tissue hyperosmolality was created by a countercurrent multiplication of sodium chloride. The physiological implications of this mechanism is discussed and it is, among other things, proposed that the hyperosmolar region represents the hyperosmotic compartment necessary for explaining intestinal water absorption.

Animals↗
PubMed1978

The effects of cholera toxin on intramural blood flow distribution and capillary hydraulic conductivity in the cat small intestine.

Blood flow distribution to the mucosa-submucosa and to the muscularis in the cat small intestine was investigated with a 85Kr elimination technique before and after exposing the intestinal mucosa for 30 min to cholera enterotoxin. In all experiments the toxin induced an intestinal secretion. Concomitantly, total intestinal blood flow was increased to a level 50 per cent above control 3 h after exposure. This vasodilatation reflected a doubling of mean blood flow in the mucosa--submucosa while muscularis blood flow remained unchanged. In another series of experiments the effect of cholera toxin on intestinal capillary hydraulic conductivity was investigated by determining the capillary filtration coefficient (CFC). A slight increase in CFC was noted during the 3 h observation period but this was not more pronounced than would have been expected from the concomitant vasodilatation. It is concluded that hemodynamic changes in the intestinal mucosa may be one of the several factors that probably are involved in the pathogenesis of cholera.

Animals↗
PubMed1978

On the chemical nature of the blood borne cardiotoxic material released from the feline small bowel in regional shock.

The cardiotoxic material released into blood from the feline small intestine during a 2 or 3 h regional shock period (inflow pressure to the small intestine 30--35 mmHg during a continuous activation of the regional sympathetic vasoconstrictor fibres at 6 Hz) has been analyzed with regard to three properties: 1. molecular mass determined by molecular filtrations; 2. solubility in a nonpolar solvent (ether); 3. heat stability by heating plasma to 80 degrees C for 30 min. The results obtained suggest that the cardiotoxic material consists of at least two heat stable fractions. One is water soluble with a molecular mass between 500 and 1 000 d and the other is lipid soluble with an unknown molecular mass.

Adrenergic Fibers↗
PubMed1978

Nervous release of vasoactive intestinal polypeptide in the gastrointestinal tract of cats: possible physiological implications.

1. The release of vasoactive intestinal polypeptide (VIP) into blood from the gastrointestinal tract was studied when eliciting autonomic nervous effects known to be mediated via non-adrenergic, non-cholinergic nerve fibres. All studies were performed on animals given atropine. 2. Electrical stimulation of the low threshold vagal fibres to the stomach did not significantly change gastric volume or VIP concentration in the venous effluent from the stomach. Stimulating the high threshold fibres, on the other hand, produced a gastric relaxation concomitant with a significant increase of venous plasma VIP concentrations. When eliciting a similar vagal relaxation of the stomach by distending a balloon the oesophagus a significant increase of venous plasma VIP concentration was also recorded. 3. Mechanical stimulation of the mucosa of the small bowel increased intestinal blood flow and a significant increase of venous plasma VIP concentration was observed. 4. Stimulation of the pelvic nerves to the colon produced a transient vasodilation and a significant increase of VIP in the venous effluent from the large bowel. A maintained vasodilation in the colon was induced by mechanically stimulating the rectal mucosa. This vascular response was accompanied by a significant raise of venous plasma VIP concentration. 5. The results demonstrate that all the studied nervous effects known to be mediated via non-adrenergic, non-cholinergic nerve fibres were accompanied by significant increases of the VIP concentration in the venous effluent. The possible physiological implications of these findings are discussed and it is proposed that VIP may be a neurotransmitter in the gastrointestinal tract.

Adrenergic Fibers↗
PubMed1978

Evidence for the existence of a countercurrent exchanger in the small intestine in man.

The vasculature in the human villus forms vascular loops by the supplying arterial vessel and the draining capillaries and/or veins. This study reports two experimental observations that strongly suggest that these vascular loops function as countercurrent exchangers. (1) The elimination of intraarterially injected 85Kr from the human small bowel exhibits an initial very rapid component of the type earlier reported in the feline gut. This component in all probability reflects the extravascular "shunting" in the exchanger of the injected radioactive tracer. (2) When exposing the intestinal mucosa to an isotonic electrolyte solution containing glucose, an osmolality gradient from the tip to the base of the human villi was demonstrated, the tips having an osmolality of around 700 milliosmoles per kg H2O. This hyperosmolality is created by the exchanger acting as a countercurrent multiplier.

Colon↗
PubMed1978

Intestinal ischemia and shock factors.

Perfusion pressure reduction to the small intestinal vascular bed for 2 hours to followed by characteristic villous damage and a general cardiovascular derangement. In an extensive series of experiments on cats it was demonstrated that the cardiovascular derangement could not be ascribed to any pooling of blood and/or fluid in the small intestine. Cardiotoxic material has been demonstrated in the cat intestinal venous blood in in vivo and in vitro experiments using working rat hearts and isolated rabbit papillary muscles. A relationship between the extent of the villous damage and the appearance of cardiotoxic material in the intestinal venous blood has been found. The cardiotoxic material seems to consist of at least two heat stable fractions. One is water soluble with a molecular mass between 500 and 1,000 daltons and the other is lipid soluble with an unknown molecular mass.

Animals↗
PubMed1977

The importance of the intestinal countercurrent exchanger for 85Kr absorption from the feline gut.

The rate of 85Kr absorption from the feline gut was studied at varying intestinal blood flows induced by i.a. infusions of a vasodilator drug or by lowering arterial inflow pressure. The effects on rate of absorption of distending the intestine by increasing intraluminal pressure from 0-1 to 5-7 cm H2O as well as of augmenting the rate of luminal perfusion of the 85Kr solution were also investigated. Distending the small bowel increased rate of 85Kr absorption at all levels of intestinal blood flow except at the very low and the very high blood flow rates. Decreasing blood flow by lowering of arterial perfusion pressure decreased the rate of absorption from the distended gut while it had no effect in the collapsed small intestine. Increasing the rate of luminal perfusion enhanced the rate of 85Kr absorption at all blood flow levels except at the lowest ones. The results are discussed with regard to villous hemodynamics, intestinal countercurrent exchange and intraluminal concentration gradients in the lumen. It is concluded that the countercurrent exchanger represents, under physiological conditions, the major limiting factor for the absorption of lipophilic solutes such as 85Kr.

Animals↗
PubMed1977

Vascular responses to mechanical stimulation of the mucosa of the cat colon.

Mechanical stimulation of the mucosa of the proximal colon evoked a hyperemia which also could be elicited when severing the autonomic fibres to the colon. Mechanical stimulation of the distal colon produced a hyperemia which, on the other hand, was abolished by cutting the pelvic nerves. Afferent pelvic nerve stimulation evoked a response similar to that seen when stimulating the distal colon. Adrenergic and cholinergic receptor blockers did not affect the studied colonic vasodilations. Dihydroergotamine, given in doses abolishing the vascular effects of i.a. injected 5-hydroxytrptamine, abolished the hyperemia to mechanical stimulation of the proximal colon but not that of the pelvic stimulation. It is concluded that a local nervous vasodilator reflex exists in the proximal colon similar to that earlier demonstrated in the small bowel (Biber et al. 1971) and that the reflex vasodilatation evoked by mechanical stimulation in the distal colon is mediated via the pelvic nerves. Hence, the vascular control differs in the proximal and in the distal parts of the colon.

Animals↗
PubMed1977

Sympathetic nervous control of intramural blood flow in the feline and human intestines.

Intramural blood flow and flow distribution in the feline and human intestines were investigated by means of a recently developed inert gas elimination technique during electrical stimulation of the regional sympathetic nerve fibers. The results obtained in man and cat showed qualitative and quantitative similarities. Thus, observations made on man strongly suggested that the intestine exhibited an autoregulatory escape from the vasoconstrictor fiber influence in the same manner as was seen in the cat. During the steady state phase of vasoconstriction induced by nervous stimulation at 8 Hz, blood flow in the mucosa-submucosa and in the muscularis was decreased to the same extent as was total blood flow in the cat, implying that flow distribution to these two major portions of the bowel remained unaltered. In man, the vasoconstriction was somewhat more pronounced in the muscularis than in the mucosa-submucosa. Hence, in man a comparatively larger fraction of total blood flow was diverted to the mucosa-submucosa during nervous vasoconstriction.

Animals↗
PubMed1977

Regional intestinal blood flow in ulcerative colitis and Crohn's disease.

By means of a recently developed isotope washout technique, regional intestinal blood flow and its intramural distribution were determined during surgery and correlated to the morphological inflammatory and vascular features of ulcerative colitis (UC) and Crohn's disease (CD) at different stages and location. In severe colitis total blood flow was significantly increased (64 +/- 9 ml per min X 100 g; mean +/- SE; n = 13) both in UC and CD, the mucosal-submucosal blood flow amounting to 121 +/- 25 ml per min X 100 g (n = 7). The muscularis blood flow was within normal range (18 +/- 10; n = 7), however. In chronic long-standing quiescent or inactive UC, in "healed colitis," and in chronic segmental colitis (CD), colonic blood flow was normal or even reduced (13 +/- 2; n = 8), the decrease in flow comprising both the mucosa-submucosa (21 +/- 3; n = 3) and the muscularis (7 +/- 3; n = 3). In early exudative stage of CD in the ileum total blood flow was normal (26 +/- 5; n = 7) with a normal mucosal-submucosal blood flow (35 +/- 5; n = 3). In late fibrosing stage total blood flow was reduced (11 +/- 1; n = 6) as was the mucosal-submucosal flow (10 +/- 4; n = 3). The muscularis blood flow was reduced in both these stages of ileal CD (7 +/- 1; n = 6). There was a satisfactory agreement between the obtained blood flow figures and the morphologically observed vascular pattern.

Chronic Disease↗
PubMed1977

The significance of sympathetic nervous activity for the development of the intestinal mucosal lesions in shock.

A 2-hour period of regional hypotension at 30-35 mmHg in the feline small bowel was produced by partial occlusion of the superior mesenteric artery. In one series of animals the sympathetic fibres in the splanchnic nerves were stimulated bilaterally at 6 Hz throughout the hypotension. In another group of animals no such stimulation was performed on the denervated intestinal segments. A mucosal damage was observed in both series and it was graded histologically according to Chiu et al. (1970). The two groups were also compared as regards the magnitude of the blood pressure fall occurring during the first hour after the period of intestinal hypotension. No statistically significant difference could be demonstrated between the two series of experiments with regard to mucosal damage or blood pressure fall. It is hence concluded that sympathetic nervous activity does not contribute to any measurable extent to the development of mucosal damage and cardiovascular deterioration observed in connection with regional intestinal hypotension. The explanation for this is discussed.

Animals↗
PubMed1977

Intestinal lysosomal enzyme activity in regional simulated shock: influence of methylprednisolone and albumin.

A 2 hr-period of regional intestinal simulated shock in cats results in small intestinal mucosal lesions and a general cardiovascular derangement, probably secondary to the release of cardiotoxic material into the intestinal venous blood. These phenomenona are accompanied by release of lysosomal and cytoplasmatic enzymes from the intestinal tissue. The effects of methylprednisolone treatment and deposition of albumin in the intestinal lumen during the regional shock period were studied. Administration of methylprednisolone early and late in the regional shock period prevented mucosal lesions and cardiovascular deterioration as well as lysosomal and cytoplasmatic enzyme release. Albumin deposition in the intestinal lumen during the regional shock period prevented lysosomal enzyme release and cardiovascular derangement and to a minor extent mucosal lesions. It is suggested that release of intestinal lysosomal enzymes is of importance for development of mucosal lesions and for production of cardiotoxic material.

Acid Phosphatase↗
PubMed1976

The intestinal mucosal lesions in shock. I. Studies on the pathogenesis.

Mucosal lesions were produced in feline small intestine by evoking a simulated intestinal shock (local hypotension at 30 mm Hg and stimulation of regional sympathetic vasoconstrictor nerves at 6 Hz for 2 h). The degree of mucosal damage was correlated to the level of intestinal blood flow. Microscopically characteristic lesions developed regularly in the small intestinal mucosa when intestinal blood flow was reduced below 12 ml/min X 100 g during the regional shock. The mucosal damage was graded histologically. No difference was found between untreated controls and cats in which the intestinal lumen was perfused with nitrogenated saline. Perfusion with oxygenated saline and i.v. injections of methylprednisolone on the other hand, prevented almost completely the development of the lesions. Albumin, activated charcoal and aprotinin instilled into the intestinal lumen reduced to some extent the mucosal damage. The obtained data support the view that hypoxia is the key factor in the pathogenesis of the mucosal lesions. However, epithelial and intraluminal enzymes are probably important contributing factors.

Albumins↗