PubMed Health⌕ Search

Biomedical subjects

V Prabhakaran

Publications and source records attributed to V Prabhakaran.

29 records · Page 2Linked to original sources
PubMed1994

Mid-menstrual cycle decline in creatinine and urea clearances.

In 6 pre-menopausal and 6 post-menopausal women we compared urine volume and excretion of creatinine and urea daily from day 2 of the 1st period of menstruation to day 1 of the 2nd, along with clearances of creatinine (CCr) and urea (C-urea). Clearances were based on 7 serum samples which were taken on day 2 of the 1st menstruation and on days 8, 14, 15, 16, 21, and day 1 of the next menstruation, when 4 cycling hormones were also assayed. Mean group ages were 35 and 59 years for pre- and post-menopausal women. CCr cycled only in the pre-menopausal group, with a nadir around the time of ovulation. The mean CCr combining days 14 and 15 was lower than that for the average of the 5 other days by 22% (p < 0.003) in the pre-menopausal but not in the post-menopausal group (p = 0.99). Average CCr values fell from the peak mean of 129 ml/min on day 8 in the follicular phase to the mean nadir of 93 ml/min for days 14 and 15 and recovered to 117 ml/min by day 1 of the 2nd menstruation; the percent fall in CCr ranged from 9 to 39%. A mid-cycle nadir was also present for C-urea (p = 0.03), also found only in the pre-menopausal group. We conclude that, in pre-menopausal women, there is generally a fall in CCr and C-urea from a peak in the follicular phase to a nadir around ovulation.

Adult↗
PubMed1991

Increased calcium uptake in vascular tissue by plasma of patients with essential hypertension.

Plasma factors have been implicated in causing increased calcium uptake and cytosolic (Ca++) in vascular tissue leading to hypertension. We compared the effect of plasma from hypertensive and normotensive subjects on rat aortic calcium uptake. Plasma from hypertensive subjects was fractionated and the fractions assessed for their activity on aortic calcium uptake. Aortic calcium uptake was significantly higher in plasma from hypertensives as compared to normotensives (p less than 0.05). There was a significant positive correlation between diastolic blood pressure and aortic calcium uptake (r = 0.645; p = 0.002). There was a significant positive correlation between percentage ideal body weight and aortic calcium uptake in normotensives and hypertensives (r = 0.522; p less than 0.05). The calcium uptake stimulatory activity in plasma of hypertensives was found in nonesterified fatty acid and cholesterol ester fractions.

Adult↗
PubMed1991

Heparin lowers blood pressure and vascular calcium uptake in hypertensive rats.

Increased calcium uptake by vascular tissue, leading to elevated cytosolic calcium, has been implicated in the pathophysiology of hypertension. Heparin treatment of hypertensive rats has been known to lower blood pressure but its mechanism is not known. This study examined the effect of chronic heparin treatment on systolic blood pressure, aortic calcium and 87Rubidium (86Rb) uptake of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. Starting at 12 weeks of age SHR and WKY rats were given either sodium heparin 300 units s.c. or equal amounts of saline once a day for a period of 6 weeks. At 18 weeks, systolic blood pressure, uptakes of calcium and 86Rb by aortae were significantly higher (p less than 0.01) in saline-treated SHR compared with heparin-treated SHR and WKY. Heparin treatment lowered the elevated calcium and 86Rb Uptake and blood pressure in SHR but had no effect on WKY. The parallel increase in systolic blood pressure and vascular calcium uptake suggests that increased calcium uptake mechanisms are associated with hypertension in SHR. Heparin appears to lower elevated blood pressure in SHR by lowering elevated vascular calcium uptake.

Animals↗
PubMed1990

Deuterium oxide normalizes blood pressure and vascular calcium uptake in Dahl salt-sensitive hypertensive rats.

This study examined the effect of 25% deuterium oxide in drinking water on systolic blood pressure, uptakes of calcium, and rubidium 86 by aortas of Dahl salt-sensitive rats on 0.4% (low) and 8% (high) sodium chloride (salt) diet. Twenty-four rats were divided into four groups. Groups I and II were on the low salt diet and groups III and IV on the high salt diet from 6 weeks of age. Additionally, at 10 weeks of age groups I and III were placed on 100% water and groups II and IV on 25% deuterium oxide. At 14 weeks, systolic blood pressure, uptakes of calcium, and rubidium 86 by aortas were significantly higher (p less than 0.01) in rats on the high salt diet as compared with those on the low salt diet. Deuterium oxide intake normalized systolic blood pressure and aortic calcium uptake but not aortic rubidium 86 uptake in hypertensive rats on the high salt diet. Deuterium oxide had no effect on blood pressure or aortic calcium uptake in rats on the low salt diet. The parallel increase in systolic blood pressure and vascular calcium uptake suggests that increased calcium uptake mechanisms are associated with hypertension in salt-sensitive Dahl rats. Furthermore, deuterium oxide appears to normalize elevated blood pressure in salt-sensitive hypertensive rats by normalizing elevated vascular (aortic) calcium uptake.

Animals↗
PubMed1990

Elevated 22Na uptake in aortae of Dahl salt-sensitive rats with high salt diet.

We examined the effects of high salt intake on blood pressure and vascular 22Na uptake in Dahl salt-sensitive (DS) rats. At 6 weeks of age, one group of 6 DS rats was placed on a low (0.4%) salt diet and the second group of 6 DS rats was placed on a high (8.0%) salt diet for a period of 4 weeks. Blood pressure recordings were made weekly. At 10 weeks of age, the animals were sacrificed and aortic 22Na uptake was measured. Total and amiloride sensitive (Na(+)-H+ antiport) components of 22Na uptake were measured from which was calculated the amiloride insensitive component. Na+, K(+)-pumps were inhibited for these vascular 22Na uptake experiments with ouabain to prevent Na+ efflux. DS rats on the high salt diet demonstrated significantly (P less than 0.01) higher blood pressure when compared to DS rats on a low salt diet. Similarly, DS rats on a high salt diet demonstrated significantly (P less than 0.05) higher total, amiloride sensitive and amiloride insensitive vascular 22Na uptake as compared to DS rats on low salt diet. The parallel increase in vascular 22Na uptake and blood pressure suggests a possible, key role of Na+ influx in the mechanism of salt induced hypertension of DS rats.

Amiloride↗
PubMed1988

Evidence for an adrenal contribution to plasma digitalis-like factors.

Digitalis-like factors (DLF) were assayed on plasma collected serially using antibody to digoxin: (1) after intravenous ACTH (n = 3 patients) and (2) after 0.15 U/kg crystalline insulin, 50 micrograms gonadotropin-releasing hormone and 0.2 mg thyrotropin-releasing hormone (n = 7) as a combined pituitary function test. Patients had either hypothalamic-pituitary or ovarian problems. Mean values for DLF rose fourfold after ACTH, and by a factor of 2.3 with the combined pituitary function test. DLF rose at least 50% in all 10 subjects. In 3 dogs, adrenal vein values for DLF were on average more than double values in either adrenal artery or lower vena cava. These results suggest that certain DLFs have an adrenal origin.

Adrenal Glands↗
PubMed1979

Interaction between human IgG and human creatine kinase isoenzyme-1 in serum: a route for the intravascular catabolism of creatine kinase-1?

In vitro incubation, at 37 degrees C, of human creatine kinase isoenzyme-1 (isoenzyme BB) and human immunoglobulin G in a buffer results in the formation of a complex of high relative molecular mass (Mr approximately 825,000), which contains both proteins. This complex also forms in vitro if creatine kinase isoenzyme-1 is incubated with fresh human serum. The creatine kinase activity of the complex obtained from either incubation is extremely labile, even in the presence of a chelating agent and a thioglycerol. We present evidence for the existence of this complex in the sera of patients who have detectable serum creatine kinase isoenzyme-1 activity. Sera with high activities of creatine kinase isoenzyme-2 do not appear to have this complex. We therefore speculate that complexing of creatine kinase isoenzyme-1 with serum immunoglobulin G may be a pathway of enzyme degradation.

Creatine Kinase↗
PubMedDate not supplied

Ischemic heart disease, serum cholesterol, and apolipoproteins in CAPD.

Thirty-one patients, mean age 54 years, had been on chronic ambulatory peritoneal dialysis (CAPD) for an average of 38 months. Mean values (mg/dl) for triglycerides (567), total-C (267), LDL-C (133), and Apo-B (154) were elevated, and HDL-C (30) were low. The low values for total-C/Apo-B and LDL-C/Apo-B suggest an increase in the number of low density lipoprotein (LDL) particles, rather than in the amount of cholesterol per LDL particle. Without knowledge of lipids, ischemic heart disease for the 31 patients was categorized into five grades in the following manner. All patients were graded based on history (angina, myocardial infarction, and bypass surgery), electrocardiogram (EKG), and echocardiography. In addition, five patients underwent coronary angiography, the results of which were considered in their grading. The five grades were assigned as follows: Grade I, no evidence (n = 15); Grade II, angina with EKG ischemia (n = 4); Grade III, myocardial infarction (MI) (n = 1); Grade IV, MI with dyskinesia-akinesia on echo (n = 4); Grade V, severe three vessel disease on angiography, or multiple infarcts, or Grade IV with heart failure (n = 7). Only Apo-B (r = 0.56) and total-C/HDL-C (r = 0.57) correlated with severity of grade, with p less than 0.001. When patients with and without detectable ischemic heart disease were compared by stepwise logistic regression, Apo-B was the only variable that independently predicted heart disease (p = 0.001). However, contribution of the lipid changes induced by CAPD has not been established.

Apolipoprotein A-I↗