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Biomedical subjects

O Lundgren

Publications and source records attributed to O Lundgren.

At least 73 records · Page 4Linked to original sources
PubMed1989

Radical production during in vivo intestinal ischemia and reperfusion in the cat.

Free radical formation was studied with electron spin resonance during 2 h of intestinal ischemia in the cat, at a blood flow less than 5 ml.min-1.100 g-1, followed by 30-min reperfusion. A modification of the spin trapping technique was used to stabilize highly reactive free radicals. The rate of secondary radical formation was 0.32 +/- 0.06 mumol.min-1.100 g intestine-1 before ischemia and increased to a maximum of 0.66 +/- 0.09 mumol.min-1.100 g-1 during the first minutes of reperfusion (mean +/- SE, n = 5). This could be prevented either by maintaining intestinal blood flow at 8-15 ml.min-1.100 g-1, by administering allopurinol before and during ischemia, or by perfusing the intestinal lumen with an O2-saturated buffer solution during ischemia, resulting in maximum rates of radical production during reperfusion of 0.37 +/- 0.04 (n = 6), 0.33 +/- 0.04 (n = 5), and 0.39 +/- 0.13 mumol.min-1.100 g-1 (n = 5), respectively. The results demonstrate that free radicals are produced in the intestine during reperfusion after a period of reduced blood flow below a certain critical level, and that inhibition of xanthine oxidase and prevention of hypoxia will eliminate this radical production.

Animals↗
PubMed1989

Autoregulation of intestinal blood flow: physiology and pathophysiology.

This paper reviews the published work on the autoregulation of intestinal blood flow. Under certain experimental conditions, total intestinal blood flow is autoregulated at arterial pressures varying between 80 and 160 mmHg. Flow autoregulation is more pronounced in the villus circulation than in the vascular bed of the intestinal muscle layers. The autoregulatory vascular adjustments occur in the small precapillary vessels. Some observations have suggested that not only flow but also mean capillary hydrostatic pressure is autoregulated. The importance of this mechanism is that even a small increase in mean capillary pressure could induce considerable filtration of fluid across the huge capillary area of the intestinal mucosa. During flow autoregulation the efficiency of the intestinal countercurrent exchanger increases, which is probably an important factor in explaining the villus ulcerations that develop during arterial hypotension.

Animals↗
PubMed1989

Hemodynamics during increased intraluminal pressure in the ileum of suckling swine.

Studies of intestinal hemodynamics during increased abdominal and intraluminal pressure in adult animals (canine and feline) have shown that blood flow is practically unchanged at pressures up to 35-40 mm Hg. In the young animal, however, decreased total intestinal blood flow has been shown at pressures of 15 mm Hg or greater. To help characterize the effect of intraluminal pressure on intestinal circulation, we have studied pressure-flow relationships in an isolated loop of terminal ileum in piglets 2-14 days of age (mean, 6.1 +/- 3.7 SD, n = 14) with a mean weight of 1,745 +/- 345 SD. Intraluminal pressure was increased from 0-50 cm of water pressure in 10-cm steps of two min' duration. Blood flow was reduced with every increase in intraluminal pressure and significantly reduced at pressures of 20 cm of water or more. The calculated peripheral vascular resistance increased with every increment of intraluminal pressure. Analysis of the relationship of arterial blood pressure to changes in blood flow suggests that blood flow reductions are greater in animals with lower blood pressure at every level of intraluminal pressure studied. Increased intraluminal pressure could be a mechanism of intestinal mucosal ischemia in the newborn, particularly affecting those with low arterial blood pressure.

Animals↗
PubMed1988

Nervous control of intestinal fluid transport: physiology and pathophysiology.

1. The enteric nervous system (10(8) neurones in man) consists of the myentric plexus, the submucosal plexus and other minor plexuses. Eighteen different chemicals are candidates for the role of neurotransmitters in the ENS. 2. The ENS together with the autonomic nervous system and the hormonal system controls gut epithelial transport systems.

Animals↗
PubMed1988

The effect of splanchnic nerve stimulation and neuropeptide Y on cholera secretion and release of vasoactive intestinal polypeptide in the feline small intestine.

The effect of sympathetic nerve stimulation and intra-arterial infusion of neuropeptide Y (NPY) on net fluid secretion and release of vasoactive intestinal polypeptide (VIP) was studied in the cat small intestine during a secretion due to cholera toxin. Activation of the splanchnic nerves (4 Hz, 5 ms, 5 V) decreased net fluid secretion to 57 +/- 10% of control. Concomitantly, the release of VIP was reduced to less than 50%. Furthermore, close i.a. infusion of NPY (estimated increase in plasma concentration 75 nmol l-1) reduced the net fluid secretion and VIP release to 27 +/- 5 and 28 +/- 4% of the pre-stimulatory value. The correlation between the decrease in net fluid secretion and reduction in VIP release showed a strong positive correlation (r = 0.83). These results strongly indicate that the antisecretory effect of sympathetic nerve stimulation during cholera diarrhoea is mediated by inhibition of secretory VIP neurons in the intestinal mucosa. A similar mechanism is also proposed for the intravascularly administered NPY.

Animals↗
PubMed1988

Somatostatin and methionine-enkephalin inhibit cholera toxin-induced jejunal net fluid secretion and release of vasoactive intestinal polypeptide in the cat in vivo.

A major part of the net fluid secretion that is elicited by cholera toxin in the small intestine of the cat has been shown to be mediated by intramural nervous reflex(es). The release of vasoactive intestinal polypeptide (VIP) from the small intestine is increased by cholera toxin. We report that close intra-arterial infusions of methionine-enkephalin (met-enk) and somatostatin cause a parallel reduction in cholera toxin-induced net fluid secretion and in VIP release from the small intestine of the cat. Intestinal blood flow was slightly, but significantly increased by met-enk and not influenced by somatostatin. These results strengthen the hypothesis that VIP is involved as a neurotransmitter in the nervous reflex mediating cholera toxin-induced secretion.

Animals↗
PubMed1988

The importance of the subepithelial resistance for the electrical properties of the rat jejunum in vitro.

The aim of the study was to evaluate full-thickness and partially stripped jejunum as a model for neurogenic control of electrogenic ion transport. The electrical properties of full-thickness and partially stripped segments were studied in Ussing chambers. Using square-pulse analysis, subepithelial and epithelial resistances (Rs and Rp) were determined, and by compensating for the potential fall across Rs, the current generated by the epithelium could be measured. In full-thickness tissue, Rs was approximately 80% of total tissue resistance, and the current measured during short-circuiting of the whole tissue (SCC) was therefore only 20-25% of the current generated by the epithelium (Im). Surgical stripping of the tissue decreased Rs by 10-20%. This means that in full thickness as well as in stripped tissue, 70-80% of the potential difference across the epithelial layer remains after traditional 'short circuiting'. Over a 25-min period, none of the electrical parameters changed significantly in the full-thickness tissues. In the stripped group PD, SCC and Im fell significantly, and in parallel during the same period of time. Neither glucose, noradrenaline, met-enkephalin or carbachol had any significant effect on Rs, Rp or the Rs/Rp ratio. The relative effects of these agents on Im and SCC were therefore similar. Substance P and VIP increased the Rs/Rp ratio significantly and, therefore, the effect of these drugs on Im was significantly more pronounced than the effect on SCC. The results show that the subepithelial resistance must be taken into account when the electrogenic activity in the epithelium is to be determined correctly. Conventionally measured SCC reflects the electrogenic effect of the tested putative neurotransmitters, but the magnitude of the responses is grossly underestimated, particularly for substance P and VIP.

Animals↗
PubMed1988

Assessment of gastric blood flow with laser Doppler flowmetry.

The use of laser Doppler flowmetry (LDF) to measure gastric blood flow was evaluated in the cat and man. The reproducibility of laser Doppler flowmetry recordings was studied in the feline stomach. In five cats flowmeter signals and venous outflow of the stomach were simultaneously recorded. The flowmeter recordings were made during operation and gastroscopy in 140 patients by means of two different (PF1-4-kHz and PF2-12-kHz) laser Doppler systems. The flowmeter recordings were highly reproducible during the cat experiments, with a coefficient of variation varying between 4% and 13%. Angulation of the probe within 60-120 degrees against the tissue under study did not affect the flowmeter signal. Pressure of the probe against the studied tissue attenuated the flowmeter signal 42 +/- 13% (n = 10). A significant correlation coefficient (r = 0.76; p = 0.01; n = 30) was obtained between flowmeter signal and venous outflow of the stomach. In man the PF2-12-kHz system yielded a higher flowmeter signal (14.5 +/- 6.9 V; 32 patients) than the PF1-4-kHz system (7.9 +/- 2.5 V; 108 patients). Flow dimensions were calculated by using results previously obtained in the intestines. The estimated blood flow values amounted to 31 +/- 10 and 57 +/- 27 ml min-1 100 g-1 for the PF1-4-kHz and PF2-12-kHz systems, respectively. In conclusion, laser Doppler flowmeter is a promising technique for studying gastric perfusion during operation and endoscopy. Motion artifacts are the major drawback of the present laser Doppler systems.

Adult↗
PubMed1987

Evidence for the existence of an endogenous inhibitor of Na, K-ATPase in plasma from cats and rats.

Plasma samples from cats and rats were filtered through molecular filters to obtain a concentrate of the plasma molecules with a mass between 500 and 10,000. This concentrate was placed on a gel filtration column and eluted with a Tris buffer. Fractions corresponding to a molecular mass of 1500-2000 exhibited a marked Na,K-ATPase inhibitory 'activity', which was not influenced by heating to 95 degrees C for 10 min or by enzymatic degradation by pronase or trypsin.

Animals↗
PubMed1987

Changes in cyclic 3'5'-adenosine monophosphate tissue concentration and net fluid transport in the cat's small intestine elicited by cholera toxin, arachidonic acid, vasoactive intestinal polypeptide and 5-hydroxytryptamine.

We have analysed tissue cyclic 3'5'-adenosine monophosphate (cAMP) concentration in different fractions of the cat's small intestinal mucosa during secretion elicited in vivo by four different secretagogues: cholera toxin (administered intraluminally), vasoactive intestinal polypeptide (VIP; given i.a.), arachidonic acid (AA; administered intraluminally) and 5-hydroxytryptamine (5-HT; given i.a.). Cholera toxin was found to increase cAMP concentration in the villi but not in the crypts. The VIP, AA and 5-HT did not influence tissue cAMP concentration despite a profuse net fluid secretion. Hexamethonium inhibited secretion elicited by cholera toxin and AA but did not significantly influence tissue cAMP concentration. There is strong evidence for the view that villus and crypt regions of the small intestinal mucosa have different functions, secretion taking place in the crypts and absorption in the villi. However, the lack of cAMP increase in the crypts reported in this study suggests that cholera toxin in this model does not reach the crypts. The results are not in agreement with a role for cAMP in mediating secretion from the crypts, but are compatible with a role of cAMP in inhibiting absorption in the villi. It is suggested that the observed fluid secretion from the crypts elicited by cholera toxin, AA and 5-HT is to a major part mediated by intramural enteric reflexes.

Animals↗
PubMed1987

Mechanisms of neurotensin-induced fluid secretion in the cat ileum in vivo.

Neurotensin (NT) is released from N cells in the small intestinal epithelium. Among other effects NT is known to elicit fluid secretion in the small intestine. This study was carried out in order to elucidate the mechanism by which NT elicits this secretion. Neurotensin infusions at two rates (4.5 and 45 pmol min-1 kg-1 body wt) to isolated segments of cat ileum in vivo, caused a steady rate of net fluid secretion and a release of vasoactive intestinal polypeptide into the mesenteric vein. The secretion was totally inhibited by tetrodotoxin. Hexamethonium, a nicotinic receptor antagonist, inhibited the secretion elicited by the lower but not by the higher dose of NT. Met-enkephalin also inhibited the induced secretion while pyrilamine, a histamine-I receptor antagonist had no effect. No significant change in enteric blood flow was caused by the NT infusion. These results indicate that NT elicits a nervous reflex in the enteric nervous system which, accordingly, turns the transport of the enterocytes into net fluid secretion.

Animals↗
PubMed1987

Autoradiographic location of beta-adrenoceptor subtypes in cat colon smooth muscle.

In order to localize beta-adrenoceptors 125I-(-)pindolol (IPIN) was used in binding to sections from cat colon. The binding characteristics for IPIN to beta-adrenoceptors on colon sections were estimated by demonstrating reversible binding in the presence of isoprenaline and by steroselective binding to the isomers of propranolol. The binding of IPIN to both beta 1- and beta 2-adrenoceptors was shown by biphasic displacement curves in the presence of the selective beta-adrenoceptor compounds betaxolol, ICI 118.551 and procaterol. The colon sections were found to contain proportions of beta 1-adrenoceptors (30-50%) and beta 2-adrenoceptors (50-70%). In the autoradiographic studies, 100% of the developed grains after exposure of IPIN to the photographic emulsion were displaced by 50 microM of isoprenaline. By microscopic counting at autoradiographic grains, 30-40% of the grains were found in the circular smooth muscle, while 60-70% of the grains were found in the longitudinal smooth muscle. A concentration of 2 nM ICI 118.551 completely displaced all grains in the circular smooth muscle and partly displaced those found in the longitudinal smooth muscle. A high concentration of ICI 118.551 (1 microM) displaced all grains above background from the smooth muscle. It is concluded that the circular smooth muscle only contains beta 2-adrenoceptors, while longitudinal smooth muscle may contain a proportion of beta 1-adrenoceptors. Whether such a location of beta adrenoceptors can be related to the beta 1-adrenoceptor-mediated inhibition of colon motility can not be clarified from these studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1987

Influence of sodium deoxycholate on morphology, net fluid transport and motility in the small intestine of the rat.

Intestinal fluid secretion and motility were induced by luminal perfusion of rat small intestine with sodium deoxycholate, a dihydroxy bile salt for 1-3 h. Changes in intestinal morphology were studied simultaneously with the changes in fluid transport and motility. The results suggest that the bile salt causes epithelial lesions which may lead to a reduced fluid absorption in the villi, thereby explaining part of the total change in net fluid transport caused by the bile salt. Pyrilamine and indomethacin did not influence the bile salt-induced secretion. Based on earlier studies, it is proposed that the major part of the bile salt-evoked secretion is mediated via activation of intramural nervous reflex(es), which also stimulate the intestinal smooth muscle cells.

Animals↗