Biomedical subjects
Publications and source records attributed to J B Bülow.
Based on a review of the literature, the effect of physical training on bone mineral density (BMD) has been evaluated. There seems to be evidence for increased BMD in children and adults performing weight-bearing physical training, whereas the loss of BMD in the elderly is reduced. No study has documented the necessary level of physical training needed for a positive effect on BMD.
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Ischaemia has been implicated in the pathogenesis of gastric mucosal disorders. The aim of this investigation was to study the gastric mucosal electrical potential difference (PD), pH, blood flow and morphology during hypoxia, gastric ischaemia, and gastric ischaemia following inhibition of free radical formation with allopurinol. PD and pH were measured simultaneously with an intragastric microelectrode, and the PD values were corrected for the liquid junction potentials created by the intragastric pH variation. Blood flow was measured by the radiolabelled microsphere technique in 18 anaesthetized dogs. Short general hypoxia and short ischaemia caused reversible declines in PD, increases in pH, and no morphological damage. Ischaemia for 1 h caused a significant decline in PD persistent after reperfusion, an increase in pH, and morphological PD, but after reperfusion PD was normalized. Gross morphology was normal, and histology showed only minor damage. The results therefore support the hypothesis that oxygen-derived free radicals are involved in gastric mucosal injury occurring during ischaemia and reperfusion.
A man aged 33 years developed an arterio-venous fistula following a gunshot wound from behind in the right calf. The quality of the fistula could be demonstrated employing digital subtraction angiographic technique while the quantity was demonstrated employing 99Tc macroaggregated albumin. The localization of the fistula is important in view of the surgical procedure and the haemodynamic amount is important to determine cardiac involvement.
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Indomethacin inhibits prostaglandin synthesis and causes gastric mucosal damage. The correlation between the gastric mucosal function and gastric blood flow was investigated. The intragastric liquid junction corrected potential difference (PD) across the stomach wall was used to characterize the gastric mucosal function. Mucosal blood flow was determined by the radiolabelled microsphere technique. Seven dogs were anaesthetized, intragastric PD was measured continuously and blood flow determined at basal condition during sympathetic activation, and after IV indomethacin (7.5 mg/kg). PD was unchanged during the basal period and during mild sympathetic activation. After indomethacin PD was reduced significantly (-40 +/- 6 mV to -20 +/- 5 mV, measured with gastric lumen negative, mean and SD, P less than 0.05). Mucosal blood flow decreased during sympathetic activation and a further significant reduction was seen after indomethacin. PD and flow reductions correlated (R = 0.92). As indomethacin given IV caused a parallel impairment of gastric mucosal function and blood flow, part of the indomethacin-related mucosal damaging effects might be due to the flow reduction.
The gastric blood flow and the gastric mucosal potential difference (p.d.) was studied in anaesthetized Göttingen mini-pigs under normal conditions and during increased FFA/albumin ratios. The antrum mucosal p.d. was measured continuously with a newly developed intragastric microelectrode principle. The gastric blood flow was measured with the radioactive microsphere technique: at basal conditions, during high FFA/albumin ratios, and after normalization of the plasma lipids. The antrum p.d., expressed with gastric lumen negative, decreased during the increased FFA/albumin ratios; from -25 +/- 3 mV to -17 +/- 4 mV, (P less than 0.05). A further reduction to -12 +/- 3 mV (P less than 0.05) was observed during the normalization of the FFA/albumin ratios. The antrum and corpus mucosal blood flow values were reduced by 37 and 26% during the increased FFA/albumin ratios, and the gastric mucosal blood flow returned to initial values after normalization of the plasma lipids. The p.d. reduction during and after the increased FFA/albumin ratios could reflect a reduced active ion transport across the mucosa caused by a changed gastric mucosal metabolism.
Plasma concentrations of insulin, C-peptide, and proinsulin were measured in different vascular beds in order to determine renal, hepatic, and systemic kinetics of the endogenous peptides in the fasting condition. Nineteen nondiabetic subjects were studied, two were normal, nine had minor vascular disorders, four had cirrhosis without organic kidney disease, and four had organic kidney disease with moderately decreased glomerular filtration rate. In subjects without organic kidney disease the arteriorenal venous extraction ratios of insulin, C-peptide, and proinsulin were mean 0.27, 0.20, and 0.21, respectively (n = 14). These values were significantly reduced in kidneys with organic disease. Renal plasma clearance values of insulin, C-peptide, and proinsulin were mean 113, 87, and 90 mL/min, respectively (n = 6). Urinary clearances were substantially lower (0.8, 13, 3.5 mL/min, respectively), indicating that a significant degradation of these peptides also takes place in the normal kidney. In subjects without liver disease the estimated hepatic extraction ratio of insulin was mean 0.48, under the assumption that no C-peptide is removed by the liver. Endogenously released insulin was removed from plasma in kidney, liver, and elsewhere in the approximate proportion 10%:65%:25%, whereas, C-peptide was removed by one half in kidney and the other half elsewhere. The overall metabolic clearance rates of insulin and C-peptide were estimated to be 15 and 4.5 mL/min/kg, respectively. The results indicate that the kidney contributes substantially to removal of insulin, C-peptide, an proinsulin, mainly by degradation, less by urinary excretion.
The plasma concentration of pancreatic polypeptide (PP-like immunoreactivity) was measured in different vascular beds in order to determine regional kinetics of endogenous PP in fasting, supine subjects with normal or moderately decreased kidney function. Patients with kidney disease (n = 10) had a significantly higher level of circulating PP than controls (n = 10): median PP = 52 (range 21 to 352) v 20 (6 to 143) pmol/L, respectively (P less than 0.02). Circulating PP was inversely correlated to 51Cr-EDTA plasma clearance (r = -0.57, P less than 0.02, n = 14) and directly correlated to serum creatinine concentration (r = 0.70, P less than 0.01). Hepatic venous PP was significantly higher than systemic PP in both controls and patients with kidney disease (P less than 0.001, n = 15). The values were positively correlated (r = 0.98, P less than 0.001; slope = 1.37 +/- 0.05, P less than 0.001), indicating a progressively increasing rate of PP secretion in subjects with raised circulating PP. No statistically significant difference could be detected between systemic and renal venous PP or across the lung, left adrenal gland, or lower limb. Assuming steady state between secretion and biodegradation, the metabolic clearance rate of the peptide was estimated to be approximately 600 to 800 mL/min in controls and slightly below this value in patients with nephropathy. These results suggest that the raised circulating PP found in patients with decreased kidney function is due to both increased secretion and decreased degradation.(ABSTRACT TRUNCATED AT 250 WORDS)
The concentrations of substance P (SP) and vasoactive intestinal polypeptide (VIP) were determined in plasma in normal volunteers during acute occlusive ischaemia (n=5) and in patients with chronic ischaemia (n=5) due to obliterative arterial disease in the lower limbs. Venous SP, but not VIP, increased significantly in the early post-occlusive period in normal volunteers (P less than 0.02). In the patients no significant veno-arterial difference in plasma concentration of SP or VIP could be detected across normal or chronic ischaemic areas. The results may suggest a role for SP in the acute post-occlusive vasodilation and/or in the post-occlusive heat-pain sensation. A role for SP in chronic ischaemia could not be defined. Plasma VIP was unchanged in both acute and chronic ischaemia.
Elevated concentrations of circulating substance P in patients with liver insufficiency have been ascribed to decreased hepatic degradation. To establish a possible biodegradation of the peptide in liver-intestine and kidneys, the concentration of endogenous immunoreactive substance P was determined in various vascular beds during a right-sided catheterization in 13 subjects without liver insufficiency. All subjects had normal values of circulating substance P, and no significant difference was found between systemic plasma and hepatic venous or renal venous concentrations of substance P. The results indicate that degradation of circulating endogenous substance P in man is not confined to liver-intestine or kidney but may take place in many tissues.