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Biomedical subjects

H H Parving

Publications and source records attributed to H H Parving.

At least 253 records · Page 14Linked to original sources
PubMed1982

Acid glycosaminoglycans in myxoedema.

Acid glycosaminoglycans were measured in the tissues of a virtually untreated 83-year-old woman with myxoedema. Intercellular oedema was demonstrated histologically in the tongue, myocardium, striated muscles, and in the skin. Tissue oedema was absent in two female control patients. All tissues from the patient with myxoedema, apart from the stomach, showed high concentrations of hyaluronic acid, but there was no consistent elevation of chondroitin-4,6-sulphate, heparan sulphate or dermatan sulphate. The accumulation of hyaluronic acid might contribute to the oedema formation in myxoedema.

Aged↗
PubMed1982

Myxoedema and Raynaud's phenomenon.

Cold hands is a common complaint in myxoedema and were reported by 15 of 17 patients before treatment of myxoedema with 4 having Raynaud's phenomenon. An increased cold sensitivity of the digital arteries could be demonstrated during finger cooling in about half of the patients and Raynaud's phenomenon was verified in the 4 patients as digital arterial closure. The cold sensitivity decreased significantly after treatment with L-thyroxine. The increased cold sensitivity in untreated myxoedema is probably due to an increased sympathetic discharge to the hands that might disclose a predisposition for Raynaud's phenomenon.

Adult↗
PubMed1982

Increased transvascular escape rate and lymph drainage of albumin in pigs during intravenous diuretic medication. Relations to treatment in man and transport mechanisms.

Transvascular escape rate of albumin (TERalb, i.e. the fraction of intravascular mass of albumin (IVMalb) passing to (or during steady state returning from) the extravascular space per unit time) was determined from the initial disappearance rate of i.v. injected radioiodinated serum albumin in anaesthetized pigs during control conditions and during diuretic medication (furosemide i.v. 20 mg/15 min, total 160-200 mg). During diuretic medication TERalb (mean 17.1% IVMalb X h-1, range 11.5-21, n = 6) increased significantly above the control period (mean 12.3% IVMalb X h-1, range 9.5-16.5, P less than 0.05). Pressures in artery, right atrium, hepatic and portal veins did not change significantly from control to diuretic period. TERalb equals the lymphatic return rate of albumin provided the transport mechanisms are filtrative-convective (i.e. no local back transport). Additional measurements in five pigs with proteins of different molecular size confirmed a dominating filtrative-convective transport. The increased TERalb during diuretic medication is best explained by an increased lymph drainage, which may decrease interstitial fluid pressure and thereby increase the transmural capillary pressure difference being essential for a filtrative-convective transvascular albumin transport. Increased lymph drainage may contribute to the therapeutic effect of diuretic treatment in oedema and ascites.

Albumins↗
PubMed1981

Effect of intravenous glucose infusion on renal function in normal man and in insulin-dependent diabetics.

The effect of intravenous glucose infusion on glomerular filtration rate and renal plasma flow (constant infusion technique using 125I-iothalamate and 131I-hippuran) and on urinary excretion of albumin and beta-2-microglobulin were studied in ten normal subjects and seven metabolically well-controlled insulin-dependent diabetics. Following glucose infusion in normal subjects (n = 10) blood glucose increased from 4.7 +/- 0.1 to 10.9 +/- 0.4 mmol/l (SEM) (p less than or equal to 0.01). Glomerular filtration rate increased from 116 +/- 2 to 123 +/- 3 ml/mi x 1.73 m2 (p less than or equal to 0.01), while no change in renal plasma flow was seen - 552 +/- 11 versus 553 +/- 18 ml/min x 1.73 m2. Volume expansion with intravenous saline infusion in six of the normal subjects induced no changes in blood glucose or kidney function. In seven strictly controlled insulin-dependent diabetics, blood glucose values were raised from 4.6 +/- 0.4 to 16.0 +/- 0.6 mmol/l and clamped by means of an 'artificial beta cell'. Glomerular filtration rate increased in all patients, from 133 +/- 5 to 140 +/- 6 ml/min x 1.73 m2 (p less than or equal to 0.02), as did renal plasma flow from 576 +/- 26 to 623 +/- 38 ml/min x 1.73 m2 (p less than or equal to 0.02). Urinary albumin excretion remained unchanged in both normal subjects and diabetics. beta-2-microglobulin excretion rate increased significantly in the diabetics following glucose infusion, while no significant change was seen in the normal subjects. Our results show that hyperglycaemia per se contributes to the increased glomerular filtration rate and renal plasma flow in insulin-dependent diabetes.

Adult↗
PubMed1981

Increased kidney size, glomerular filtration rate and renal plasma flow in short-term insulin-dependent diabetics.

Glomerular filtration rate (GFR), renal plasma flow (RPF) and kidney volume were measured in thirteen male subjects (mean age 30 years) with short-term insulin-dependent diabetes (mean duration of disease 2.4 years) and fourteen normal male subjects (mean age 29 years). GFR and RPF were measured by constant infusion technique using I125-iothalamate and 131I-hippuran. Kidney size was determined by means of ultrasound. GFR, RPF and kidney volume were increased in the diabetic patients compared to the normal controls, 144 versus 113 ml/min X 1.73 m2 (p less than 0.0005), 627 versus 523 ml/min X 1.73 m2 (p less than 0.0025) and 278 versus 224 ml/1.73 m2 (p less than 0.0005) respectively. Combining results from diabetic patients and controls revealed a positive correlation between kidney size and GFR (r = 0.70, p less than 0.001) and between kidney size and RPF (r = 0.61, p less than 0.001). Within the groups kidney size and RPF correlated significantly in the diabetics (p less than 0.01) and the same was found for kidney size and GFR (0.025 less than p less than 0.05), while no correlations were found in the normal group. GFR and RPF correlated in the diabetics when evaluated separately (r = 0.81, p less than 0.001) and in the controls (r = 0.73, p less than 0.001). The previous and present data suggest that the mechanisms of the elevated GFR in insulin-dependent diabetics are enhanced RPF, increased transglomerular hydrostatic pressure gradient and increased glomerular ultrafiltration coefficient. The increased kidney size is probably the main cause of the above alterations in the GFR determinants.

Adult↗
PubMed1981

A prospective study of glomerular filtration rate and arterial blood pressure in insulin-dependent diabetics with diabetic nephropathy.

Glomerular filtration rate (GFR, single bolus 51Cr-EDTA technique), serum creatinine, proteinuria and arterial blood pressure have been measured prospectively in 14 young onset insulin-dependent diabetics selected by of persistent proteinuria (greater than 0.5 g/day) secondary to diabetic nephropathy. Twelve of the 14 patients had normal serum creatinine levels. None of the patients received antihypertensive treatment. During the mean observation period of 26 months (range 23 to 33 months) GFR decreased from 107 to 87 ml/min/1.73 m2 (p less than 0.001), serum creatinine remained unchanged: 107 and 112/mumol/l (NS), proteinuria increased from 1.8 to 3.3 g/day (p less than 0.001) and arterial blood pressure rose from 132/88 to 153/101 mmHg (p less than 0.001). Glomerular filtration rate decreased linearly with time (slope = -0.75, r = 0.99, p less than 0.001) by a mean of 0.75 ml/min/month (range 0.1 to 1.5 ml/min/month). The decrease in GFR did not correlate wih sex, age at onset, duration of diabetes, arterial blood pressure, proteinuria, insulin requirement, postprandial blood glucose or the initial GFR in each individual was constant, but varied considerably between patients. Increase in arterial blood pressure to a hypertensive level is an early feature of diabetic nephropathy in young insulin-dependent diabetics.

Adult↗
PubMed1981

Increased transvascular escape rate of albumin during experimental portal and hepatic venous hypertension in the pig. Relation to findings in patients with cirrhosis of the liver.

Transvascular escape rate of albumin [TERalb, i.e. the fraction of the intravascular mass of albumin (IVMalb) passing to the extravascular space per unit time] was determined from the disappearance of i.v. injected radioiodinated serum albumin in anaesthetized pigs during control conditions and during regional venous congestion in the infradiaphragmatic area. Balloon catheters were placed in the portal vein (infrahepatic portal congestion) and in the inferior vena cava above (suprahepatic caval congestion) and below (infrahepatic caval congestion) the outlets of the hepatic veins. TERalb was on the average 13% IVMalb.h-1 under basal pressure conditions. TERalb rose significantly (p less than 0.01) during suprahepatic caval and infrahepatic portal congestion to an average of 29 and 19% IVMalb.h-1, respectively. TERalb was positively correlated to the portal pressure (r = 0.75, P less than 0.001). Only a minor increment in TERalb was found during infrahepatic caval congestion. The hepatic share of the increased TERalb during stasis above the hepatic veins was estimated to be threefold that of the extrahepatic splanchnic area. Our results point to filtration of protein, predominantely through the lining of the sinusoids and perisinusoidal space of the liver into the interstitial space around the portal vessels and further into the lymphatics, as the main mechanism of the previously demonstrated marked increase in TERalb in patients with portal venous hypertension due to cirrhosis of the liver.

Animals↗
PubMed1981

Plasma and interstitial fluid volume in extensive skin disease.

Plasma volume and extracellular fluid volume were determined simultaneously in 17 patients with extensive skin disease and 18 matched normal subjects after an intravenous bolus injection of 131I-labeled human serum albumin and inulin. The patients had a decrease in plasma volume (-6%), which, however, was statistically significant only when related tao body weight or surface area. There was a concomitant increase in extracellular fluid volume (+7%) and interstitial fluid volume (+12%). These deviations from control data were statistically significant neither in absolute values nor when related to body size. Interstitial fluid volume was calculated as the difference between extracellular fluid volume and plasma volume. The mean plasma volume: interstitial fluid volume ratio was significantly lower in the patients (0.35 +/- 0.05 SD) than in the control group (0.42 +/0 0.05 SD) (p < 0.001). These results show that a shift of fluid from the intra- to the extracellular spaces is present in patients with extensive skin disease. Elevated microvascular water filtration in the skin is suggested as a major mechanism of this abnormal fluid distribution.

Body Water↗
PubMed1981

Distribution and degradation of albumin in extensive skin disease.

The distribution and degradation of albumin were determined in twelve patients with extensive skin disease and in ten control subjects by measuring the metabolic turnover and transcapillary escape of 132 I-labelled albumin. The ratio of intravascular to total mass of albumin was normal. Thus the observed hypoalbuminaemia and the low intravascular mass reflect a reduced mass of total body albumin. The rate of synthesis was normal, but the transcapillary escape rate reflecting the microvascular leakiness to macromolecules, and the fractional disappearance rate were significantly higher in the patients than in the controls (P less than 0.001). It is concluded that the hypoalbuminaemia in these patients is the result of an increased endogenous catabolism of albumin without significant loss via urine, stools or skin. A positive correlation between the transcapillary escape rate and fractional catabolic rate of albumin supports the concept of a causal relationship between these parameters.

Adult↗
PubMed1981

Kidney function and size in normal subjects before and during growth hormone administration for one week.

Kidney function and size were studied in seven normal male subjects before and after administration of highly purified human growth hormone for 1 week. Glomerular filtration rate, renal plasma flow (steady-state infusion technique with urinary collections using 125I-iothalamate and 131I-hippuran) kidney size (ultrasonic scanning) and urinary excretion rates of albumin and beta 2-microglobulin (radioimmunoassays) were measured. Highly purified growth hormone was injected subcutaneously, 2 IU in the morning and 4 IU in the evening. Glomerular filtration rate increased from (mean +/- SEM) 114 +/- 5 to 125 +/- 4 ml/min x 1.73 m2 (P less than 0.01) and renal plasma flow increased from 554 +/- 30 to 601 +/- 36 ml/min x 1.73 m2 (P less than 0.01). Kidney size and urinary excretion rates of albumin and beta 2-microglobulin did not change significantly. Our results show that raising plasma growth hormone into a range similar to that found in insulin-dependent diabetics enhances glomerular filtration rate and renal plasma flow, while kidney size remains unchanged. Increased renal plasma flow is the major determinant of growth hormone induced elevation in glomerular filtration rate. Growth hormone may thus contribute to the enhancement of glomerular filtration rate and renal plasma flow typically found in insulin-dependent diabetics.

Adult↗
PubMed1981

Hemodynamics in diabetic orthostatic hypotension.

Hemodynamic variables (blood pressure, cardiac output, heart rate, plasma volume, splanchnic blood flow, and peripheral subcutaneous blood flow) and plasma concentrations of norepinephrine, epinephrine, and renin were measured in the supine position and after 30 min of quiet standing. This was done in normal subjects (n = 7) and in juvenile-onset diabetic patients without neuropathy (n = 8), with slight neuropathy (decreased beat-to-beat variation in heart rate during hyperventilation) (n = 8), and with severe neuropathy including orthostatic hypotension (n = 7). Blood pressure decreased precipitously in the standing position in the diabetics with orthostatic hypotension, whereas moderate decreases were found in the other three groups. Upon standing, heart rate rose and cardiac output and plasma volume decreased similarly in the four groups. The increases in total peripheral resistance, splanchnic vascular resistance and subcutaneous vascular resistance were all significantly lower (P less than 0.025) in the patients with orthostatic hypotension compared with the other three groups. The increase in plasma norepinephrine concentrations in the patients with orthostatic hypotension was significantly lower (P less than 0.025) than in the patients without neuropathy, whereas plasma renin responses to standing were similar in the four groups. We conclude that in diabetic hypoadrenergic orthostatic hypotension the basic pathophysiological defect is lack of ability to increase vascular resistance, probably due to impaired sympathetic activity in the autonomic nerves innervating resistance vessels; cardiac output and plasma volume responses to standing are similar to those found in normal subjects and in diabetics without neuropathy.

Adult↗
PubMed1981

The effect of ascitic fluid hydrostatic pressure on albumin extravasation rate in patients with cirrhosis of the liver.

Overall transvascular escape rate of albumin [TERalb, i.e. the fraction of intravascular mass of albumin (IVMalb) passing to the extravascular space per unit time] was determined from the disappearance of i.v. injected radioiodinated serum albumin. Patients with tense ascites due to liver cirrhosis and pigs with posthepatic portal hypertension and intraperitoneally instilled fluid were studied before and after abdominal paracentesis in order to evaluate the effect of ascitic fluid hydrostatic pressure on the transvascular escape rate of albumin. TERalb of the ascitic patients (n = 6) were on average 7.8% IVMalb.h-1, which is somewhat higher but not significantly above normal (mean 5.6% IVMalb.h-1). After paracentesis and removal of the ascitic fluid, TERalb rose significantly to an average of 11.9% IVMalb.h-1 (P less than 0.05). The fraction of IVMalb passing into the peritoneal cavity was on average 0.21 and 0.38% IVMalb.h-1 before and after paracentesis, respectively (n = 4). In ascitic, posthepatic portal-hypertensive pigs (n = 6), TERalb averaged 15.1% IVMalb.h-1, a value not being significantly different from non-ascitic, normotensive controls (mean 16.1% IVMalb.h-1). After paracentesis, TERalb rose significantly to an average of 24.3% IVMalb.h-1. The increased albumin extravasation rate after removal of ascites is best explained by an increased sinusoidal-tissue pressure difference caused by a decreased hydrostatic fluid pressure in the liver interstitium (portal and subcapsular spaces) due to the hydrostatic effect of the removed ascitic fluid.

Abdomen↗
PubMed1981

Renal function in streptozotocin-diabetic rats.

Renal function was examined with micropuncture methods in the insulin-treated streptozotocin-diabetic rat. Kidney glomerular filtration rate was significantly higher in the diabetic rats (1.21 ml/min) than in the control group (0.84 ml/min) Nephron glomerular filtration rate increased in proportion to the rise in kidney glomerular filtration rate (diabetic rats: 37.0 nl/min; control rats: 27.9 nl/min). Likewise renal plasma flow was significantly higher in the diabetic rats (4.1 ml/min) than in the control group (3.0 ml/min). Glomerular capillary pressure was identical in both groups (56.0 and 56.0 mmHg, respectively). The proximal intratubular pressure was significantly reduced in the diabetic rats (10.4 mmHg; control value: 12.5 mmHg). The effective glomerular ultrafiltration coefficient was slightly but not significantly higher in the diabetic rats (0.027 nl s-1mmHg-1) than in the control group (0.023 nl s-1mmHg-1). Kidney weight was significantly higher in the diabetic rats (1.15 g; control rats: 0.96 g) while body weight was similar in both groups (diabetic rats: 232 g; control rats: 238 g). Calculations indicate that the increases in transglomerular hydraulic pressure, renal plasma flow and ultrafiltration coefficient of the glomerular membrane contribute about equally to the rise in glomerular filtration rate. The increases in the values of the determinants of glomerular filtration rate may be the result of renal hypertrophy. These studies suggest that this model provides a useful method for investigating kidney function in diabetes, which may have relevance for our understanding of the kidney abnormalities in human diabetes.

Animals↗