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Biomedical subjects

R N Roy

Publications and source records attributed to R N Roy.

At least 55 records · Page 3Linked to original sources

Timing of neonatal cerebroventricular haemorrhage with ultrasound.

Sequential real-time ultrasound examinations were performed in 174 neonates to determine the time of occurrence of cerebroventricular haemorrhage (CVH). Of the 47 infants in whom CVH was detected, in 36 (77%) CVH was present at the first examination. Of the 34 infants with CVH who were examined first within 6 hours of birth, 24 (71%) already had haemorrhage demonstrable at the initial scan. Extension of a CVH after its initial detection occurred in only 3 infants. Of 124 consecutive infants of birthweights less than 1500 g, 38 (31%) developed CVH, 56% of the outborn and 27% of the inborn babies. Our results indicate that most infants who develop CVH have done so within 6 hours of birth.

Cerebral Hemorrhage↗

Renal and tubuloglomerular feedback effects of [Sar1,Ala8]angiotensin II in the rat.

Experiments were done in normal rats to assess kidney, single nephron, and tubuloglomerular feedback responses during control conditions and during renin-angiotensin blockade with the angiotensin II (ANG II) antagonist [Sar1,Ala8]angiotensin II (saralasin, 20 micrograms.kg-1.min-1). Plasma renin activity was increased fourfold during saralasin infusion. Glomerular filtration rate (GFR) and renal blood flow increased in parallel from 1.09 +/- 0.04 to 1.26 +/- 0.05 ml/min and from 6.4 +/- 0.5 to 7.6 +/- 0.5 ml/min, respectively. Absolute and fractional sodium excretion were increased sixfold during ANG II blockade. Hydrostatic pressures in proximal tubules, peritubular capillaries, and distal tubules were unchanged. Estimates of nephron GFR (SNGFR) based on collections of distal tubular fluid were increased from 21.6 +/- 1.2 to 24.3 +/- 0.9 nl/min during ANG II blockade. Increases in SNGFR and decreases in fractional absorption at micropuncture sites beyond the late proximal tubule during saralasin administration resulted in increases of flow rate and Cl- delivery at the early distal tubule. Tubuloglomerular feedback activity, assessed by measuring changes in proximal tubule stop-flow pressure in response to alterations in orthograde microperfusion rate from late proximal tubule sites, was significantly attenuated over the range of physiological flow rates for the late proximal tubule during blockade of the renin-angiotensin system. Acute blockade of ANG II in this rat model results in attenuated tubuloglomerular feedback activity and associated changes of hemodynamic and excretory behavior by the kidney.

Angiotensin II↗

Renin-angiotensin influences on tubuloglomerular feedback activity in the rat.

We have reviewed the development of Thurau's hypothesis that angiotensin mediates the effector responses of distal tubuloglomerular feedback-induced changes of nephron function. Several studies attempting to correlate responsiveness of the tubuloglomerular feedback system with intrarenal renin or juxtaglomerular renin contents have not delineated angiotensin's role in the feedback control system. Others and our own recent studies that have assessed the effects of acute blockade of the renin-angiotensin system on the responsiveness of tubuloglomerular feedback activity suggest that the effects of angiotensin are most likely a modulating influence on the activity of the system rather than the mediator of feedback-induced changes in glomerular function.

Angiotensins↗

Impaired autoregulatory responses in contralateral kidneys of two-kidney, one-clip hypertensive rats.

1. Micropuncture and clearance experiments in two-kidney, one-clip renal vascular hypertensive rats examined the ability of the kidney contralateral to renal vascular stenosis to maintain renal function during conditions of reduced renal arterial blood pressure. 2. At their respective spontaneous blood pressures, renal vascular resistance was higher and glomerular filtration rate (GFR) and renal blood flow were not different in the contralateral kidneys of the hypertensive rats (170 +/- 5 mmHg) compared with normal animals (129 +/- 1 mmHg). Urine flow and absolute and fractional excretion of electrolyte were greater from the kidneys of the hypertensive animals. However, pressures in cortical structures were similar in the two groups. 3. As blood pressure was reduced acutely, the kidney contralateral to the renal artery stenosis achieved only small decreases in renal vascular resistance that failed to allow GFR, renal blood flow or pressures in cortical structures to be maintained. In contrast, normal rats efficiently autoregulated renal vascular resistance to allow GFR, renal blood flow and cortical pressures to be unchanged as blood pressure was altered between 130 and 115 mmHg. Urine flow and electrolyte excretion decreased to a greater extent in the hypertensive kidneys; at comparable blood pressure these indices of excretory function were not different in the two groups. 4. These observations indicate that the contralateral kidney can maintain normal haemodynamic and glomerular function only at elevated blood pressure and suggest the possibility that the impaired capacity to autoregulate renal resistances may contribute to the maintenance of hypertension observed in this model.

Animals↗

Impaired assimilation of nasojejunal feeds in healthy low-birth-weight newborn infants.

We compared nasojejunal with nasogastric tube feeding in 18 healthy low-birth-weight infants from eight to 15 days of age. NJ-fed infants had significantly more stools and excreted significantly more fat and potassium in their stools. Growth and weight gain did not differ between the groups during the study period. Future use of NJ feeding in LBW infants should take into account the possibility of malabsorption associated with this technique.

Enteral Nutrition↗

Postnatal growth of infants of less than 1.3 kg birth weight: effects of metabolic acidosis, of caloric intake, and of calcium, sodium, and phosphate supplementation.

Weekly increments of length, weight, head circumference, and skinfold thickness in response to a series of dietary changes were measured in 108 healthy infants who weighed less than 1.3 kg at birth. The serial manipulations included prevention of late metabolic acidosis, increased caloric intake, and calcium, sodium, and phosphorus supplementation. The study comprised four phases; the infants were divided into ten groups according to dietary regimen. AGA and SGA infants were studied separately. Growth in length was primarily influenced by a change to a formula providing a higher caloric intake and a 60:40 whey protein/casein ratio. Correction of late metabolic acidosis, sodium, and phosphorus supplementation had minor additive effects on growth in length. Increased caloric intake also influenced growth of head circumference, but only in AGA infants. Only the sodium intake was shown to influence body weight increments significantly with the range of caloric intake used in the study (132 to 160 calories/kg/day).

Acidosis↗

Glucose-6-phosphate dehydrogenase from brewers' yeast. The effects of pH and temperature on the steady-state kinetic parameters of the two-chain protein species.

A systematic study has been made of the pH- and temperature-dependency of the steady-state kinetic parameters of the stabilized two-subunit enzyme species of glucose-6-phosphate dehydrogenase, in the absence of superimposed association-dissociation reactions. The Vmax(app) data obtained in several buffers between pH 5 and 10 and at 18-32 degrees C lead to the postulate that at least two sets of protonic equilibria may govern the catalysis (one near pH 5.7 AT 25 DEGREES C and another near pH 9.2); furthermore, two pathways for product formation (i.e., two Vmax's) appear to be required to explain the biphasic nature of the log Vmax(app) vs. pH curves, with Vmax(basic) greater than Vmax(acidic + neutral). Of the several buffers explored, either a uniform degree of interaction or a minimal degree of buffer species interaction could be assessed from the enthalpy changes associated with the derived values for ionization constants attributed to the protonic equilibria in the enzyme-substrates ternary complexes for the case of Tris-acetate-EDTA buffers, at constant ionic strength. With the selection of this buffer at 0.1 (T/2) and at 25 and 32 degrees C, a self-consistent kinetic mechanism has emerged which allows for the random binding of the two fully ionized substrates to the enzyme via two major pathways, and product formation by both E-A--B- and HE-A--B-. As before (Kuby et al. Arch. Biochem, Biophys. 165, 153-178, 1974), a quasi-equilibrium is presumed, with rate-limiting steps (k + 5 and k + 5') at the interconversion of the ternary complexes. Values for the two sets of protonic equilibria defined by this mechanism (viz., pKk, pKH2 for the first ionizations, and pKk', pKH' for the second) could then be estimated. From their numerical values (e.g., at 25 degrees C: pKK = 5.7 PKH2 = 5.2; and pKK' = 9.1, PKH' = 8.2) and from the values for delta H degrees ioniz (e.g., delta H degrees pKK APPROXIMATELY 5.1 KCAL/MOL; DELTA H degrees pKK' APPROXIMATELY 11 KCAL/MOL), A POSTULATE IS PRESENTED WHICH ATTRIBUTES THESE Acid dissociation constants to an imidazole and epsilon-amino group, respectively.

Binding Sites↗

Late hyponatremia in very low birthweight infants. (less than 1.3 kilograms).

Late hyponatremia (plasma Na+ less than 130 mEq/liter) occurred frequently (on 54 of 159 occasions) in 46 very low virthweight (VLBW) infants (less than 1.3 kg at birth) between 2 and 6 weeks of age while receiving a sodium intake of less than or equal to 2 mEg/kg/24 hr. To elucidate possible pathogenetic mechanisms five groups of such infants were studied while receiving a commercially available formula reconstituted to give two different volumes and two different Na+ concentrations. Sodium intake in the nonsupplemented (NS) infants (n = 23) was less than 2 mEq/kg/24 hr. Supplemented (S) infants (n = 16) received approximately 3 mEq Na+/kg/24 hr. A further group of seven infants given a high volume (200 ml/kg/24 hr), high caloric (100 cal/dl) formula and Na+ supplementation (to 3 mEq/kg/24 hr) was also included. Infants were studied from age 14 days until they weighed 1.80 +/- 0.05 kg at a mean age of 47 days. At the time of start of the study, 6 of 20 NS and 6 of 19 S infants were hyponatremic. After supplementation only two episodes of hyponatremia occurred in S infants, both during the first study week, whereas the high incidence of hyponatremia in NS infants period. During baseline urine collections all infants excreted between 80 and 100 ml/kg/24 hr urine, but those receiving 150 ml/kg/24 hr formula decreased their urinary output rapidly to 50 ml/kg/24 hr, whereas infants receiving high volume feeds (200 ml/kg/24 hr) did not decrease their urinary output until the third balance at an average age of 45 days. All infants excreted between 1.0 and 1.2 mEq/kg/24 hr of sodium in their urine during the initial collection. Nonsupplemented infants reduced their urinary Na+ excretion more rapidly than supplemented babies (NS: from 1.03 to 0.55 mEq/kg/24 hr, first vs second balance; S: from 1.00 to 0.80 mEq/kg/24 hr, first vs third balance). Mean potassium excretion remained unchanged in NS and S infants during the study period and was not affected by the volume or caloric content of the formula. Extracellular volume (ECV) and total body water (TBW) were measure serially, and there were no differences between S and NS infants in the distribution of body water. The percentage of TBW and ECV decreased in all groups with increasing postnatal age.

Body Water↗

Spinal cysticercosis.

Cysticercosis of the spinal cord is rare. A case is reported in a 40-year-old Hindu. Compression of the spinal cord by the cyst which was located in the arachnoid membrane resulted in a paraplegia. Removal of the cyst resulted in marked improvement.

Adult↗

Hydration of the low birth-weight infant.

Factors relating to water balance in the perinatal and neonatal periods are reviewed. The major areas considered are changes in body water compartments, insensible water loss, and renal function. A most striking feature in all these areas is the wide variation in 'normal' values, both within the same infant with advancing postnatal age and also between infants of the same postnatal age but of different gestational ages. A second feature is the fluctuation caused by changes in environmental conditions, e.g., temperature, humidity, type of warming device, use of phototherapy. Much of the literature on water balance relates to term infants and experimental animals; only for insensible water loss are there studies on infants as small as less than 1000 gm. Because of the developmental changes occurring in these infants, many areas require further study. The last 5 to 10 years have seen marked changes in our approach to the hydration and nutrition of the low birth-weight infant. Despite much experience with new routes and types of fluids and formulas, no method has been shown to be ideal for all situations. In replacing the neonate's ongoing water losses, the clinician strives to maintain normal volume and tonicity of the body fluids, and to prevent clinical and biochemical signs of dehydration or over-hydration. In planning therapy, the clinician is presented with a wide range of possible water requirements, and with a choice of route and type of fluid administration. Each low birth-weight infant must be viewed individually, and once fluid requirements have been estimated, frequent assessment of hydration status is necessary, with appropriately frequent readjustment of the rate of fluid administration.

Adaptation, Physiological↗