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N Korsgaard

Publications and source records attributed to N Korsgaard.

31 records · Page 2Linked to original sources
PubMed1991

Microcirculatory and trophic effects of short chain fatty acids in the human rectum after Hartmann's procedure.

Short chain fatty acids (acetic, propionic and butyric) were instilled into the rectum of patients who had undergone Hartmann's procedure. The following parameters were examined before and after a 2-week treatment period with short chain fatty acids (100 ml twice daily at a total concentration of 150 mM): (1) microcirculatory effects in vivo using a laser Doppler flow technique, and (2) morphometrical changes in mucosal biopsies. The following parameters were significantly increased in all patients after treatment: (1) mucosal blood flow, (2) the fractional crypt cell epithelium plus surface epithelium volume in relation to total tissue volume down to the muscularis mucosa, (3) nuclear volume in the crypt and the surface epithelium, and (4) the fractional nuclear volume to total cell volume in the crypt and the surface epithelium. These data suggest that short chain fatty acids in the human colon have trophic and vasodilatory effects.

Acetates↗
PubMed1991

Angiotensin II causes vascular hypertrophy in part by a non-pressor mechanism.

Angiotensin II, when given in low doses, raises blood pressure slowly. When tested in vitro on vascular smooth muscle cells, it has mitogenic and trophic effects; it is not known if it has these effects in vivo. Our purpose was to determine whether vascular hypertrophy develops during slow pressor infusion of angiotensin II and, if so, whether it is pressure induced. Three experiments were done in rats infused subcutaneously with angiotensin II (200 ng/kg/min) by minipump for 10-12 days. Experiment 1: Angiotensin II gradually raised systolic blood pressure (measured in the tail) from 143 +/- 2 to 208 +/- 8 mm Hg (mean +/- SEM), significantly suppressing plasma renin and increasing threefold (NS) plasma angiotensin II. There was no loss of peptide in the pump infusate when tested at the end of the experiment. Experiment 2: In the perfused mesenteric circulation, vasoconstrictor responses to norepinephrine, vasopressin, and KCl were enhanced in rats given a slow pressor infusion of angiotensin II, but sensitivity of responses was not altered. This combination of changes suggests that vascular hypertrophy develops during slow pressor infusion of angiotensin II. Experiment 3: Vessel myography was done after angiotensin II infusion with and without a pressor response. Angiotensin II raised systolic blood pressure, increased heart weight, and produced myographic changes of vascular hypertrophy in the mesenteric circulation, increasing media width, media cross-sectional area, and media/lumen ratio. Hydralazine given with angiotensin II prevented the rise of pressure and the cardiac effect but not the vascular changes. Two-way analysis of variance showed that angiotensin II significantly increased media width, media cross-sectional area, and media/lumen ratio, all independent of hydralazine. Thus, although hydralazine inhibits the pressor and cardiac effects of angiotensin II, suggesting a pressor mechanism for the cardiac change, it does not inhibit structural vascular change, which suggests that at least part of the effect has a non-pressor mechanism.

Angiotensin II↗
PubMed1991

Cellular morphology in mesenteric resistance vessels from antihypertensive treated spontaneously hypertensive rats.

The effects on media smooth muscle cell size of long-term antihypertensive treatment with four different drugs were studied in isolated segments of mesenteric resistance arteries from spontaneously hypertensive rats (SHRs) using an unbiased stereological principle (the "disector"). Young SHRs were treated from age 4 weeks to 24 weeks with metoprolol (130 mg/kg/day), isradipine (42 mg/kg/day), captopril (60 mg/kg/day) or perindopril (1.5 mg/kg/day). At 24 weeks, when all drugs had lowered the blood pressure in SHRs compared to untreated controls (order of efficacy perindopril greater than captopril greater than isradipine greater than metoprolol), random arterial samples were taken from the mesenteric vascular bed close to the intestine and mounted on an isometric myograph, allowing standardized measurements of vascular dimensions. Although, taken together, the four treatments reduced blood pressure as well as the media:lumen ratio of the vessels and the number of cell layers, there was no significant effect of the treatments, taken together, on cell volume, cell number or on the ratio between interstitium and cells. However, cell volume correlated with blood pressure (P less than 0.05), suggesting that the most effective treatments (perindopril and captopril) had inhibited cell growth. It is, however, not clear whether the effect on cell volume was a specific effect of the drugs used, or whether it was only due to the blood pressure reduction.

Animals↗
PubMed1990

Active wall tension--length curve and morphology of isolated bovine retinal small arteries: important feature for pharmacodynamic studies.

The active and passive wall tension--internal circumference (diameter) relations of isolated ring segments of bovine retinal small arteries (i.d. ca. 200 microns) were studied in vitro using an isometric myograph. The active tension of the vessels (when fully activated with 10(-5) M 5-HT and 10(-5) M PGF2 alpha in high K(+)-saline) reached a maximum (1.2 N m-1) at an internal circumference, L0, where the passive tension (measured in Ca2(+)-free solution) were 0.89 N m-1. Below and above L0 the active tension fell linearly, the zero tension intercepts being 0.48 L0 and 1.61 L0. The passive wall tension rose exponentially as a function of the internal circumference (diameter) and was 43 times higher at 1.4 L0 than at L0. A small transient spontaneous contraction was observed after rapid stretch of the arteries. Papaverine and Ca2(+)-free solution did not change the wall tension of vessels stretched to L0, indicating absence of stable spontaneous myogenic tone in the vessels. Histological examination showed that the retinal artery media on average had three smooth muscle cell layers which in total were 12 microns thick. The media/lumen ratio was 7%. Smooth muscle cell volume was 1228 micron3, constituting about 72% of the media volume. The active wall tension--internal circumference relation and morphology of bovine retinal small arteries is generally equal to that of arteries of similar size from other species, but active force generation of the retinal vascular smooth muscle cells is considerably lower.

Animals↗
PubMed1988

Atrial content and plasma levels of atrial natriuretic peptides in rats with chronic renal failure.

The possible role of atrial natriuretic peptides (ANP) for the adaptive changes in renal Na excretion during chronic renal failure was studied in 5/6 nephrectomized (NX) rats maintained on a normal (100 mmol/kg) and a high (800 mmol/kg) Na diet. Atrial content of natriuretic substances was determined by bioassay and plasma ANP by radioimmunoassay. Nephrectomized rats showed a twofold increase in plasma ANP irrespective of their Na intake. Atrial ANP content was increased by high Na diet but unchanged by NX. Nephrectomized rats maintained on high Na diet showed partial depletion of atrial ANP stores. There were no significant changes in the volume fraction of atrial granules determined. The results suggest that ANP is involved in the regulation of renal Na excretion during chronic renal failure and acute Na loading; other mechanisms are probably involved in the adaption to chronic Na loading.

Animals↗
PubMed1988

Cellular hypertrophy in mesenteric resistance vessels from renal hypertensive rats.

To determine whether the increased thickness seen in media of mesenteric resistance vessels of Wistar-Kyoto rats made hypertensive by a Goldblatt procedure (one-kidney, one clip model) was due to hypertrophy or hyperplasia of smooth muscle cells, the cellular dimensions of these vessels were estimated using a new, unbiased stereological method (the disector). Furthermore, to investigate whether the changes seen could be secondary to the increased blood pressure, morphometric measurements were also made in renal arcuate arteries, which, due to the constricting silver clip, probably had not been exposed to the increased pressure load. Vessels were mounted on a myograph, and their media thickness, lumen diameter, and maximum active wall tension response were measured. In the mesenteric vessels media thickness had increased by 58%, whereas no changes were seen in the renal vessels. Vessels were then fixed, and serial sections were made in the mesenteric vessels. The disector was used to calculate the numerical cell density in each vessel. By combining the myograph measurements and the estimated numerical cell density, the number of cells per segment unit length was calculated (renal hypertensive rats, 6.8 micron-1; sham-operated Wistar-Kyoto rats, 6.3 micron-1; p greater than 0.40) and mean cell volume was determined (renal hypertensive rats, 1541 micron 3; sham-operated Wistar-Kyoto rats, 1256 micron 3; p less than 0.02). No morphometrical changes were found in single sections of the renal arteries. We conclude that the increased media thickness observed in mesenteric resistance vessels of one-kidney, one clip Goldblatt hypertensive rats mainly was caused by smooth muscle cell hypertrophy.

Animals↗
PubMed1988

A case of thromboangiitis obliterans affecting coronary, pulmonary, and splenic vessels. Is thromboangiitis obliterans a generalized vascular disease?

We describe a 53 year old man who died following his 3rd myocardial infarction. Before death there were scintigraphic signs of infarctions in the lung and spleen. Postmortem examination revealed an occlussive vascular disease in coronary, pulmonary, and splenic vessels. The histological findings were consistent with thromboangiitis obliterans. We suggest that thromboangiitis obliterans probably is a generalized vascular disease.

Coronary Vessels↗
PubMed1986

Neonatal sympathectomy of normotensive Wistar-Kyoto and spontaneously hypertensive rats with 6-hydroxydopamine: effects on resistance vessel structure and sensitivity to calcium.

6-Hydroxydopamine (6-OHDA) was injected on alternate days from birth to 3 weeks of age into spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) control rats. The effects of this neonatal treatment on cardiovascular structure and mesenteric resistance vessel calcium sensitivity was studied in young (6 week) and adult (5 month) rats. Mean arterial pressure of treated SHRs and WKYs was reduced by 10% compared with control rats, but the heart:body weight ratio was unaffected by treatment. Both pharmacological and histological studies suggested that at 6 weeks of age, mesenteric resistance vessels from treated WKYs were completely denervated, but that vessels from treated SHRs still had sparse innervation. At 5 months all vessels from the treated rats had some adrenergic innervation, but less than the control rats. In the WKYs, treatment was associated with reduced media:lumen ratio and reduced calcium sensitivity of the mesenteric resistance vessels, while no such changes were observed in the SHR vessels. The results indicate that the sympathetic nervous system in SHRs is more resistant to chemical denervation than the sympathetic nervous system of the WKYs. The results also suggest that sympathetic innervation of mesenteric resistance vessels may affect vessel structure and sensitivity.

Animals↗
PubMed1983

Correlations and otherwise between blood pressure, cardiac mass and resistance vessel characteristics in hypertensive, normotensive and hypertensive/normotensive hybrid rats.

We have measured heart weight and properties of 150-200 microns mesenteric resistance vessels from spontaneously hypertensive (SHR), Wistar-Kyoto (WKY), two-kidney, one clip Goldblatt renal hypertensive (RHR) and outbred Wistar rats, as well as in SHR/WKY F2-hybrid rats. All rats were 14-weeks-old. In the SHRs, WKYs, RHRs and Wistars the mean blood pressures (measured intra-arterially) were, respectively: 136, 111, 164 and 100 mmHg. In the SHR/WKYs the systolic blood pressures (measured regularly over a two-week period by the tail cuff method) were normally distributed between the values obtained from control SHRs and WKYs. Relative heart weight and resistance vessel media thickness/lumen diameter ratio correlated (P less than 0.001) with blood pressure between SHRs, WKYs, RHRs and Wistars; however, no significant correlation was seen in SHR/WKYs. By contrast, the calcium sensitivity of the resistance vessel noradrenaline response did correlate (P less than 0.01) with blood pressure in the SHR/WKYs, but did not correlate between the pure strains (calcium sensitivity of the SHR and Wistar vessels was similar, but higher than that of the WKY vessels; induction of renal hypertension did not affect calcium sensitivity). The results suggest that although the cardiac enlargement and increased resistance vessel media/lumen ratio of 14-week SHRs may be advantageous for these animals, these structural abnormalities may not be primary causes of the hypertension. Furthermore, the results indicate that it is the WKYs which are abnormal in having a low calcium sensitivity of their resistance vessels, but suggest also that this reduced sensitivity may be associated with mechanisms which help to keep the WKYs normotensive.

Animals↗
PubMed1982

Potentiating and depressive effects of ouabain and potassium-free solutions on rat mesenteric resistance vessels.

We have investigated the in vitro effects of ouabain and K-free solutions on some pharmacological and electrophysiological properties of rat mesenteric resistance vessels (internal diameter approximately 190 micrometers). Vessels were mounted as ring preparations on a myograph capable of measuring their isometric wall tension. In normal saline solutions, vessels did not exhibit any tone and had a membrane potential of -54 mV. Both 1 mM ouabain and K-free solutions caused a transient depolarization of 5-8 mV; thereafter the membrane slowly depolarized to about -45 mV after 30 minutes. There was no mechanical response to ouabain, but K-free solutions caused a transient development of tension which could be inhibited by phentolamine (1 microM). In norepinephrine-activated vessels, exposure to ouabain or K-free solutions caused a small depolarization and an increase in tension. Long-term (30-minute) exposure to 1 mM ouabain or K-free solutions reduced the amplitude of norepinephrine responses and, for the lower (but not the higher) norepinephrine concentrations, the membranes were about 14 mV more depolarized than control. The mechanical responses to a cocktail of norepinephrine in a high potassium solution were, however, unaffected. Re-exposure to normal saline solution produced a transient hyperpolarization and transiently eliminated the norepinephrine response, but thereafter the membrane potential and response returned to normal. The results indicate that ouabain and K-free solutions can have both short-term potentiating and long-term depressive effects on the mechanical response of rat mesenteric resistance vessels to norepinephrine.

Animals↗
PubMed1981

Evidence that the increased calcium sensitivity of resistance vessels in spontaneously hypertensive rats is an intrinsic defect of their vascular smooth muscle.

We have investigated media thickness and noradrenaline- and calcium-sensitivity of isolated mesenteric resistance vessels from spontaneously hypertensive (SHR) and control Wistar-Kyoto (WKY) rats, which had been treated in various ways. Vessels from untreated SHRs had an increased media thickness and increased noradrenaline- and calcium-sensitivity. Anti-hypertensive treatment of SHRs and WKYs with Felodipine reduced blood pressure, eliminated the difference in vessel media thickness, but did not reduce vessel noradrenaline- or calcium-sensitivity. Chemical sympathectomy of SHRs and WKYs at birth likewise resulted in reduced blood pressure, but did not eliminate the difference in vessel media thickness although again vessel noradrenaline- and calcium-sensitivity remained unchanged. Induction of renal hypertension in WKYs caused an increase in blood pressure and increase in vessel media thickness, but did not affect vessel noradrenaline-sensitivity. The results suggest that while vessel media thickness is influenced by blood pressure, the sensitivity differences of SHR resistance vessels are an intrinsic defect of their vascular smooth muscle, independent both of blood pressure and neurogenic influences.

Animals↗