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Biomedical subjects

K G Tranberg

Publications and source records attributed to K G Tranberg.

At least 91 records · Page 5Linked to original sources
PubMed1981

Disappearance of insulin in man: variation with the plasma insulin level.

Clearance rates of unlabelled insulin were studied in 45 unanaesthetized non-diabetic humans. The clearance rate, as well as the pancreatic secretion rate, of endogenous insulin was estimated from steady-state concentrations in portal and arterial blood. The clearance rate of exogenous insulin was determined after brief intraportal infusion. In the basal fasting state, the endogenous plasma insulin level varied as closely with the clearance of endogenous insulin as with the rate of pancreatic secretion. During elevation of insulin by glucose infusion, it varied predominantly with the rate of insulin secretion. Clearance of exogenous insulin did not vary with the pre-test endogenous insulin level. The clearance of endogenous insulin increased form 11 ml . min-1 . kg-1 in the basal fasting state to 17 ml . min-1. kg-1 during glucose infusion. Clearance of exogenous insulin fell progressively with increasing dose, form 35 (8 mU/kg) to 14 (43 mU/kg) ml . min-1 . kg-1 at normoglycaemia and 23 (8 mU/kg) to 17 (34 mU/kg) ml . min-1 . kg-1 at hyperglycaemia. The clearance of endogenous insulin was lower than that of exogenous insulin at normoglycaemia, but of similar size during glucose infusion. It is concluded that variation in clearance rate is partly responsible for variation in plasma insulin concentration, particularly in the basal fasting state, and that the clearance rate is lower in the basal state than otherwise. To some extent, the low clearance values for endogenous insulin in the basal state may reflect poor specificity of the insulin radioimmunoassay.

Adolescent↗
PubMed1979

Hepatic uptake of insulin in man.

The hepatic uptake of unlabeled insulin (5--50 mU/kg) was determined in 45 nondiabetic patients without hepatic disease. Thirty patients were studied at normoglycemia and 15 at moderate steady hyperglycemia, induced by intraportal infusion of 80 or 200 mg glucose per h and per kg. The first pass fractional hepatic uptake of insulin (FH) was estimated by comparing the results after a portal and a peripheral infusion of unlabeled insulin in each patient. It varied negatively with the amount of insulin given, decreasing about 50% after a tenfold increase in dose. FH was markedly smaller during steady hyperglycemia than at normoglycemia, regardless of insulin dose. For low doses (5--10 mU/kg), giving insulin concentrations within the physiological range, FH was 0.43 (5 mU/kg) and 0.40 (10 mU/kg) at normoglycemia and 0.16 (10 mU/kg) at hyperglycemia. FH did not vary with the fasting or the glucose-stimulated, endogenous insulin levels recorded before insulin infusion. It is suggested that glucose is more important than insulin in modulating the fractional hepatic uptake of insulin.

Adult↗
PubMed1979

Variation in the disappearance of unlabeled insulin from plasma: studies with portal and peripheral infusions.

One hundred and thirty brief infusions of unlabeled insulin were given to 75 unanesthetized nondiabetic human beings. The patients were examined (1) by different doses of insulin (5--50 muU/kg), (2) by intraportal and peripheral infusion, (3) in the morning and in the afternoon, and (4) during normoglycemia and moderate, steady hyperglycemia. After intraportal infusion of insulin, the non-steady state plasma clearance rate (ml min(-1)kg(-1) was lower the larger the dose (decreased about 50% by a 10-fold increase in insulin dose) and lower at hyper- than at normoglycemia (decreased about 30% after small insulin doses). It was also lower the higher the relative body weight, but this correlation was weak. After peripheral insulin infusion, none of the above relationships was demonstrated. Regardless of the route of insulin infusion, plasma clearance rate did not vary with fasting plasma insulin concentration, time of day, insulin sensitivity, or glucose tolerance. We conclude that the liver modifies the distribution and removal of pancreatically released insulin in response to acute increases in insulin or glucose. Otherwise the plasma clearance rate of insulin showed a notable lack of relationship with common indexes of metabolism and with insulin action.

Blood Glucose↗
PubMed1978

Modeling of plasma disappearance of unlabeled insulin in man.

Fifty-two portal and 68 peripheral, brief infusions of unlabeled insulin were given to ambulant, nondiabetic patients. After intraportal insulin infusion (5--50 mU/kg), plasma clearance rate (PCR, dose/area of the incremental plasma insulin concentrations) decreased with increasing dose, varying from 32 to 14 ml-min-1-kg-1 at normoglycemia. After peripheral insulin infusion (5--30 mU/kg), PCR (mean value 15 ml-min-1-kg-1) showed no certain dose-dependence, but transfer rate constants and distribution volumes did. Despite a detectable reentry of insulin from one or more extravascular pools to the plasma pool, transfer rate constants or distribution volumes could not be accurately determined. The shortcomings of conventional noncompartmental and compartmental models did not appear to be due to the dose-dependence demonstrated. Instead, the limitations of these models were caused mainly by the difficulty of defining a proper base-line concentration and, in particular, by the imprecision of the experimental data, indicating that it will be difficult to find more appropriate models from data obtained with unlabeled insulin.

Aged↗
PubMed1976

Renal artery injuries following blunt trauma.

From 1861 to 1975 fifty-three cases of blunt renal pedicle injury have been reported. Sixty-five kidneys were involved (twelve bilateral injuries) and 32 of them were removed. Reconstructive surgery was tried on 17 kidneys, of which only one healed without complication and with recovery of normal function. In addition, in 4 patients with bilateral injury, operation preserved enough kidney function to save the patients from hemodialysis, though 2 of them developed hypertension. This paper reports 4 further cases. In 2 patients with renal artery thrombosis nephrectomy was eventually performed after preceding reconstructive or conservative treatment. The third patient with thrombosis was not seen until several years after the trauma and was treated conservatively. The fourth patient had a ruptured intrarenal arterial branch with massive hematuria and finally required resection of the kidney. An early diagnosis of renal artery injury following severe abdominal trauma requires immediate aortography, sometimes with subsequent selective catheterization. If renal trauma is not strongly suspected, intravenous large dose pyelography may be indicated as the first step. Surgical repair should consist of resection of the injured artery and reconstruction with a venous graft, or autotransplantation of the kidney. If treated conservatively, the patient must be followed up at regular intervals for hypertension and other complications.

Abdominal Injuries↗
PubMed1975

Technique and complications of transumbilical catheterization of the portal vein and its tributaries.

In 120 patients who had 127 transumbilical catheterizations of the portal vein, 33 of pancreatic veins, and 15 for other portal tributaries, the surgical success rate was 91 per cent over-all, increasing to 95 per cent during the last year. Catheterization was made with the same technique as is used for arteriography. The most important complication was thrombosis of the portal vein, giving slight transient symptoms in 2 patients. Other complications were wound infection, suture granuloma, herniation in the linea alba, bleeding from the operative wound, and subintimal injections. As the technique may yield good results in studies of drug resorption, flow studies, detection of metastases, and investigation of pancreatic veins, it seems justified in suitable patients despite the complication rate. None of the complications produced lasting disability.

Adolescent↗
PubMed1975

Pancreatic glucagon response to an ordinary meal.

Glucagon concentrations in the portal and peripheral venous blood were measured in 3 patients after an ordinary meal. A brief increase in glucagon concentration was found in the portal blood but not in the peripheral blood. As the glucose concentrations rose, the glucagon levels fell. The secretion of pancreatic glucagon therefore seems to depend largely on the blood glucose level.

Blood Glucose↗