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T Kiviluoto

Publications and source records attributed to T Kiviluoto.

71 records · Page 4Linked to original sources

Acute gastric mucosal lesions, haemodynamic and microcirculatory changes in the thermally injured rat.

Early postburn changes in central haemodynamics, organ blood flow distribution and morphology of the gastric mucosa were studied using a standarized thermal skin injury model. Organ blood flow and cardiac output were determined using radioactive microspheres. In the control animals no marked changes in cardiac output or organ blood flow were observed, and the gastric mucosa remained essentially undamaged. After burn injury and no fluid resuscitation, cardiac output decreased by 78 per cent, and blood flow to the stomach, pancreas, spleen, muscle, skin and kidneys also decreased markedly and to about the same degree as the cardiac output, however the adrenal flow remained roughly unchanged at the baseline level. Gross and microscopic lesions developed in the stomach, especially in the corpus. In animals given fluid resuscitation after burn injury cardiac output decreased by 38 per cent during the experiment, but blood flow in the stomach, brain, kidneys and spleen remained fairly constant, while pancreatic and muscle blood flow decreased and adrenal blood flow increased markedly. The gastric mucosa showed only minor microscopic, but no macroscopic lesions at the end of the experiment. The results indicate that acute thermal skin injury induces profound changes in central haemodynamics and organ blood flow which can, however, largely be overcome by adequate fluid resuscitation. The data also suggest that, as in other examples of 'stress ulceration', impaired mucosal blood flow may underlie the stress ulceration which complicates severe burns.

Acute Disease↗

Pancreatic trauma: acute and late manifestations.

A retrospective analysis of 47 patients with pancreatic trauma is presented. A total of 43 patients presented with acute pancreatic injury, 32 after blunt abdominal trauma. Isolated blunt pancreatic injuries were a considerable diagnostic problem with a mean delay from trauma to operation of 9.4 days. At operation peripancreatic drainage in mild injuries and distal resection in cases of ductal injury were the commonest procedures. The overall mortality was 19 per cent, but only three of the eight deaths were attributable to the pancreatic injury. The overall complication rate was 63 per cent and the pancreatic complication rate was 33 per cent. Four patients presented with chronic pancreatitis resulting from previously untreated blunt abdominal trauma 0.5-21 years earlier. Clinically, they did not differ from the manifestations of chronic pancreatitis of other aetiological origins.

Abdominal Injuries↗

Subepithelial tissue pH of rat gastric mucosa exposed to luminal acid, barrier breaking agents, and hemorrhagic shock.

Tissue pH in the immediate subepithelial layer of rat gastric mucosa was measured using H+-selective microelectrodes. Exposure of the mucosa to luminal acid (50-150 mM) caused a significant acidification of the subepithelial tissue. Contrary to expectation, disruption of the mucosal barrier with taurocholate (10 mM), acetylsalicylic acid (10 mM), or ethanol (20% vol/vol) during acid (100 mM HCl) perfusion promoted no further acidification of the subepithelial tissue but rather caused an alkalinization of the primarily acidified subepithelial tissue. When hemorrhagic shock was induced during acid perfusion, a profound acidification of the subepithelial tissue occurred even though a much lower luminal acidity (10 mM HCl) was used. Also, taurocholate had no alkalinizing influence on subepithelial pH during hemorrhagic shock, but caused a rapidly progressing and irreversible drop of the subepithelial tissue pH. The findings suggest that in normal stomach with intact "mucosal barrier," H+ back-diffusion occurs during exposure to acid. However, disruption of the mucosal barrier seems to lead to alkali (HCO3-) efflux from the mucosa, which neutralizes the influxing H+, thus "masking" H+ back-diffusion and protecting the mucosa. Yet, when adequate supply of HCO3- to the mucosa is blocked during exposure to a barrier-breaking agent and acid, increased H+ back-diffusion becomes again "unmasked," leading to extensive acidification and ulceration of the mucosa.

Animals↗

Intracellular pH in isolated Necturus antral mucosa in simulated ulcerogenic conditions.

Intracellular pH (pHi) was measured with proton-sensitive liquid sensor microelectrodes in isolated Necturus antral mucosa, paying special attention to arranging experimental conditions to simulate conditions frequently associated with in vivo "stress ulceration." Intracellular pH in mucosas perfused under standard conditions (Ringer's solution containing HCO3-/CO2) was 7.22 + 0.02 (n = 27). Removal of Na+ and HCO3- or addition of amiloride or 4-acetamido-4-isothiocyanostillbene-2,2-disulfonic acid (blockers of Na+/H+ and Cl-/HCO3-exchangers) had no influence on steady-state pHi, suggesting that these ion exchangers do not significantly contribute to the maintenance of pHi in the presence of normal external pH. Acidification of mucosal (luminal) perfusate to pH 3 (mimicking the presence of gastric acid) had no influence on pHi, but mucosal pH 2 (10 mM HCl) acidified pHi to 6.93 +/- 0.07. Acidification of serosal (nutrient) perfusate to pH 6 (mimicking intramucosal acidosis caused by back-diffusion of luminal H+) acidified pHi to 6.72 +/- 0.10. Removal of Na+ from and addition of amiloride to the serosal perfusate during exposure to serosal pH 6.0 induced further acidification of pHi, suggesting that in this acidotic situation (with very low ambient HCO3- concentration) a Na+/H+ exchanger does contribute to the maintenance of steady-state pHi. Increased PCO2 (10% vol/vol in the gas) in a slightly acidic milieu (mimicking mucosal ischemia) likewise acidified pHi to 6.73 +/- 0.05. A combination of mucosal acid (pH 3), high PCO2 (10% CO2), and low serosal pH (pH 6) (mimicking conditions that prevail, for example, during hemorrhagic shock) acidified pHi and ultimately resulted in cell death. These derangements of intracellular acid-base balance may have pathogenetic importance also in in vivo stress ulceration.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗

Adenosine and the regional differences in adipose tissue metabolism in women.

Adenosine content in abdominal and femoral adipose tissue in menstruating women was 0.38 +/- 0.10 and 0.59 +/- 0.14 nmol/g of wet weight, respectively (mean +/- SEM; N = 17). No difference in adenosine sensitivity was found between abdominal and femoral adipocytes. In lactating women, the adenosine content was lower in femoral than in abdominal adipose tissue (0.40 +/- 0.08 and 0.57 +/- 0.08 nmol/g of wet weight, respectively; N = 10). Adenosine sensitivity in femoral adipocytes was not increased during lactation. As adenosine is a locally acting insulin-like effector, these results suggest that the higher adenosine content in femoral adipose tissue in menstruating women could explain its higher lipoprotein lipase activity and tendency to accumulate fat. During lactation, the lower extracellular adenosine concentration would allow lipid mobilization preferentially from the femoral site.

Abdomen↗

Insulin resistance is a prominent feature of patients with pancreatogenic diabetes.

To compare in vivo insulin action in patients with diabetes secondary to pancreatic diseases (n = 9) to that in type I diabetic patients (n = 13) and in normal subjects (n = 8), we measured insulin-mediated glucose disposal by the euglycemic insulin clamp technique. Five of the nine patients with pancreatogenic diabetes had undergone total pancreatectomy. Similar plasma glucose (approximately 4.8 mmol/l) and insulin (approximately 70 mU/l) levels were maintained in all groups. The rate of glucose metabolism in the pancreatogenic diabetic patients (3.77 +/- 0.55 mg/kg/min) was 47% lower (P less than 0.001) than in normal subjects (7.05 +/- 0.57 mg/kg/min) and 21% lower (P less than 0.05) than in type I diabetic patients (5.54 +/- 0.39 mg/kg/min). The rates of glucose uptake were similarly reduced in totally pancreatectomized patients and in those with pancreatogenic diabetes due to other causes. During hyperinsulinemia induced by the clamp, glucose production (measured using 3-3H-glucose infusion) was completely suppressed in both the pancreatogenic diabetic patients and the normal subjects indicating that the impairment of in vivo insulin action was localized to the peripheral tissues. However, basal glucose production was elevated in the pancreatogenic diabetic patients (2.75 mg/kg/min, P less than 0.001) compared to the normal subjects (1.79 +/- 0.07 mg/kg/min). Glucose production rates were comparable in the totally pancreatectomized patients and in the other patients with pancreatogenic diabetes. The fasting plasma insulin level was, however, lower in the totally pancreatectomized (3.2 +/- 1.6 mU/L, P less than 0.05) than the other pancreatogenic (11.5 +/- 3.7 mU/L) diabetic patients. To examine the mechanisms of peripheral insulin resistance in the pancreatogenic diabetic patients, insulin binding and action were measured in isolated adipocytes. The pancreatogenic diabetic patients displayed normal insulin binding as well as normal rates of glucose transport and oxidation in adipocytes. In conclusion, patients with pancreatogenic diabetes demonstrated marked insulin resistance. Thus, impaired regulation of glucose production is a more likely explanation for the special clinical features of pancreatogenic diabetes than enhanced glucose utilization.

Adipose Tissue↗

Insulin binding and action in adipocytes in vitro in relation to insulin action in vivo in young and middle-aged subjects.

The effect of age on glucose metabolism in vivo was compared to that found in adipocytes in vitro in young (n = 8, age 23 to 31 years) and middle-aged (n = 7, age 37 to 55 years) non-diabetic subjects. During the OGTT, the incremental glucose or insulin areas did not differ significantly between the groups. Fasting and 2 h plasma glucose (P less than 0.01) and the 2 h plasma insulin (P less than 0.05) levels were, however, slightly higher in the middle-aged than in the young group. During iv induced hyperinsulinaemia (approximately 85 mU/l), rates of glucose uptake were comparable between the middle-aged (6.32 +/- 0.94 mg/kg/min) and the young subjects (7.56 +/- 0.78 mg/kg/min, P greater than 0.5). In fat cells, both basal and insulin stimulated rates of glucose transport were 35% lower (P less than 0.05) in the middle-aged than in the young subjects. Basal and insulin stimulated rates of glucose oxidation and lipogenesis were both markedly lower (P less than 0.01) in the middle-aged than in the young group. The rates of glucose transport, oxidation and lipogenesis were inversely related to age, whereas none of these parameters was related to fat cell size. In conclusion, adipocyte glucose metabolism in middle-aged healthy subjects was markedly impaired. In contrast, rates of glucose uptake during iv hyperinsulinaemia and glucose responses during hyperinsulinaemia in the OGTT were comparable in young and middle-aged subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

Pancreatic secretory trypsin inhibitor-like immunoreactivity in pancreatectomized patients.

Pancreatic secretory trypsin inhibitor (PSTI) is a 6000-dalton peptide, that occurs in high concentrations in the pancreas and in pancreatic juice. It is thought to be synthesized by pancreatic acinar cells. We have recently reported the findings of an identical trypsin inhibitor at high concentrations in the urine of patients with gynecological malignancy. Therefore, we have named the inhibitor tumor-associated trypsin inhibitor (TATI). We have now studied patients who have undergone total pancreatoduodenectomy for pancreatic cancer or chronic pancreatitis. By radioimmunoassay (RIA), we found normal levels of this inhibitor in the serum and urine of pancreatectomized patients. The absence of pancreas was confirmed by measuring serum trypsin. By gel filtration and HPLC it was found that PSTI/TATI occurring in pancreatectomized patients was indistinguishable from that found in connection with pancreatitis and ovarian cancer.

Adult↗

Transplantation of pancreatic microfragments in totally pancreatectomized pigs.

Total pancreatectomy was performed on 22 piglets. An intraportal transplantation of pancreatic microfragments was performed on 17 piglets, and 5 piglets were left as controls. After the transplantation, the mean intravenous glucose tolerance curve, K values, and the fasting plasma C-peptide values were normalized during the 1st month. Our results suggest that the method of transplantation of pancreatic microfragments is worth of further development to achieve a status independent of insulin in diabetics.

Animals↗

Assay of adenosine in human adipose tissue.

A method is described to assay the adenosine content of human adipose tissue. Tissue pieces of 10-20 mg were frozen within 1 sec of excision by a conchotome. The pieces were pooled and ground in liquid nitrogen, divided into samples weighing 50-100 mg each and placed in perchloric acid. Neutralized defatted extracts were treated by Dowex AG-1 to remove nucleotides and lyophilized. The adenosine content was measured by RIA using antiserum raised against laevulinic acid (0(2'),3'-adenosine-acetal)-albumin conjugate. The adenosine content in human abdominal sc adipose tissue was 0.56 +/- 0.08 nmol/g of tissue (mean +/- SEM). This shows that adenosine is present in human adipose tissue at concentrations that have been shown to have regulatory effects on cAMP accumulation and lipolysis.

Adenosine↗

Total pancreatectomy for chronic pancreatitis.

Ten instances of total pancreatectomy performed for chronic alcohol induced pancreatitis are reported. There was no hospital mortality, and all of the patients were free of pain. The most difficult problem was labile insulin sensitive diabetes in these patients who were chronic alcoholics. In addition, steatorrhea with weight loss, bleeding marginal ulcers and general weakness diminished working ability. The present data suggest that this procedure should be considered as the last resort in the treatment of severe instances of chronic pancreatitis.

Adult↗

Glycemic control and serum lipoproteins after total pancreatectomy.

Carbohydrate and lipid metabolism were studied in 10 patients who had undergone total pancreatectomy. The results were compared with Type I diabetic patients and normal subjects, all of whom were matched for age, sex and weight. At the same level of glycemic control, the daily need for insulin was significantly lower in the patients with pancreatogenic diabetes than in those with Type I diabetes. Concentrations of serum total VLDL and HDL triglyceride were higher in the pancreatectomized patients than in the diabetic or normal controls, whereas concentrations of serum total and LDL cholesterol were significantly lower. The composition of the VLDL, LDL and HDL particles was abnormal in the totally pancreatectomized patients as all three lipoprotein fractions were enriched in triglyceride. HDL2 cholesterol was similar in the totally pancreatectomized patients to that in the other two groups but HDL3 cholesterol was lower. Postheparin plasma lipoprotein lipase and hepatic lipase activities were normal. It is concluded that in totally pancreatectomized patients the changes in the lipoprotein profile on reflect more the action of various confounding factors, i.e. malabsorption, continuance of alcohol abuse and dietary changes than the impact of the diabetes itself.

Adult↗

Distribution of Ia-positive cells in the pig and human pancreas.

With monoclonal antibody reacting with both human and porcine Ia antigens, we demonstrate with immunoperoxidase staining that Ia expressing endothelial cells are found in Langerhans' islets as well as in exocrine tissue of the pig and human pancreas. However, neither endocrine cells in Langerhans' islets nor acinar or ductal cells do express the Ia antigen.

Animals↗

Site of insulin resistance in type 1 diabetes: insulin-mediated glucose disposal in vivo in relation to insulin binding and action in adipocytes in vitro.

To evaluate the mechanism of insulin resistance in type 1 diabetes mellitus, we measured insulin sensitivity in vivo and insulin action in adipocytes in vitro. The study groups consisted of 18 insulin-treated type 1 diabetic patients and 14 matched normal subjects. In each subject, insulin-mediated glucose disposal in vivo was measured by the euglycemic clamp technique. An open surgical biopsy was performed in 9 diabetic and 7 healthy subjects to obtain abdominal sc adipose tissue for the measurement of [125I]insulin binding, D-[14C]-glucose transport, oxidation, and lipogenesis. During the euglycemic clamp studies, similar steady state plasma glucose (4.8 mmol/liter) and insulin (80 mU/liter = 700 pM) levels were maintained in both groups. The rate of glucose metabolism (M) was 43% lower in the diabetic patients (4.75 +/- 0.34 mg/kg X min) than in the normal subjects (8.27 +/- 0.43 mg/kg X min; P less than 0.001). [125I]Insulin binding to adipocytes was reduced in the diabetic patients (26% reduction in tracer binding; P less than 0.05) due to a reduction in receptor number. Insulin binding was not related to the M value at any insulin concentration. Basal and insulin-stimulated rates of glucose transport were not significantly different in diabetic and normal subjects. The basal glucose oxidation rate was reduced by 50% (P less than 0.02), and maximal glucose oxidation was reduced by 49% (P less than 0.03) in the diabetic patients (237 +/- 30 vs. 359 +/- 49 pmol/30,000 cells X 90 min, basal vs. maximal glucose oxidation, respectively) compared to those in normal subjects (513 +/- 101 vs. 700 +/- 133 pmol/30,000 cells X 90 min). The percentage responses of glucose oxidation and glucose transport to insulin were similar in both groups. Glucose oxidation rates at basal (r = 0.68; P less than 0.01), half-maximally (ED50; r = 0.70; P less than 0.01), and maximally (r = 0.64; P less than 0.05) effective insulin concentrations were positively related to the M value. Basal and insulin-stimulated rates of lipogenesis were comparable between the diabetic and normal subjects. In conclusion, insulin-mediated glucose disposal in vivo is reduced in conventionally treated type 1 diabetic patients. In vitro, adipocytes from diabetes bound slightly less insulin at tracer insulin concentrations, but the magnitude of this reduction was not related to impairment of glucose metabolism in vivo. Of the pathways of glucose metabolism studied, the rate of glucose oxidation was most affected. A significant relationship was found between the M value and the rate of in vitro glucose oxidation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adipose Tissue↗

Elective operations in chronic alcohol induced pancreatitis.

The role of surgical treatment in the management of chronic pancreatitis has increased, mainly because of improved diagnostic methods. In the present study, 83 consecutive patients who were operated upon for chronic alcohol induced pancreatitis between 1970 and 1980 are reviewed. The results indicate that the best results with regard to pain relief were achieved with lateral drainage operation in patients with dilated pancreatic ducts. A sufficient pancreatic resection gives satisfactory results in patients with nondilated ducts. Patients with severe pancreatic changes and a long history of alcoholism are best treated by extended pancreatic resections with regard to pain relief; however, most of the patients are still unable to work after the operation. A constant follow-up and active surgical attitude at the early stage of the disease before the circulus vitiosus of pain, drugs, inability to work and disturbances in social life are of paramount importance.

Adult↗

Acute haemorrhage associated with pancreatic pseudocyst and chronic pancreatitis.

The present study reports 18 patients operated on for chronic pancreatitis complicated by bleeding in the upper gastrointestinal tract, the peritoneal cavity or the retroperitoneal space. Damage to the splenic artery by a pancreatic pseudocyst was the most common reason for the bleeding (10 patients, 56%) and the most common site was the duodenum (10 patients, 56%). Eleven patients were treated by transcystic multiple suture ligations combined with external drainage of the pseudocyst, and seven by pancreatic resection or total pancreatectomy. Hospital mortality was 33% (6 patients); two patients had undergone transcystic suture ligation, and four pancreatic resection. Five patients needed a reoperation because of further bleeding, four of them having been treated initially by transcystic suture ligation. Our results suggest that haemostasis by suture ligation is a method to be recommended if the patient's condition has been exacerbated by severe haemorrhage.

Adult↗

A case report of biliary cystadenoma and cystadenocarcinoma.

Three cases of intrahepatic biliary cystadenoma with mesenchymal stroma and one case of biliary cystadenocarcinoma are presented. Their immunohistochemical features and the surgical treatment are discussed together with a brief review of the literature. The benign cystadenomas stained positive for cytokeratin and CA 19-9 in the epithelium of the cyst wall. Mesenchymal stromal cells were strongly positive for a-SMA and moderately positive for desmin. The epithelium of the cystadenocarcinoma, however, was positive only for cytokeratin and the stroma only for a-SMA. Our findings indicate that biliary cystadenomas seem to be of primitive hepatobiliary origin. Furthermore, the malignant variant cystadenocarcinoma may loose its immunoreactivity for CA 19-9 and desmin.

Adenoma, Bile Duct↗