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Biomedical subjects

B C Wang

Publications and source records attributed to B C Wang.

At least 163 records · Page 9Linked to original sources
PubMed1979

Effects of lumen volume transit time and pressure on loop of Henle function.

Experiments on Henle's loops were designed to demonstrate the relationships of absorption to distal pressure, transit time, and luminal diameter. Loops of superficial nephrons in hydropenic rats, isolated from the rest of the nephron by oil or solid paraffin blocks, were microperfused at 13.6--20 nl/min. Two samples of fluid were collected from the early distal tubule--one with suction in order to lower distal pressure and reduce luminal volume, the other without suction so that the lumen was distended. Transit times were 30 +/- 2 s without and 19 +/- 2 s with suction. Proximal tubule pressure and perfusion rate were not altered by collection with suction. Absolute absorption, however, descreased from 10.6 +/- 0.4 to 8.4 +/- 0.4 nl/min (P less than 0.001). When salt transport was inhibited by 10(-4) M furosemide in the perfusate, water absorption was 7.8 +/- 0.7 nl/min without suction and 6.1 +/- 0.8 nl/min with suction (P less than 0.01). Computer simulation of Henle's loop shows that these observations cannot be explained by changes in transit time, hydrostatic pressure, or unstirred layers. The observations are simulated when radial fluxes depend on wall thickness and surface area in the descending thin limb.

Animals↗
PubMed1977

Effect of dipivalyl derivatives of catecholamines on cardiovascular function in the conscious dog.

Dipivalyl derivatives of epinephrine, norepinephrine and isoproterenol were injected intravenously into conscious dogs while cardiovascular variables were monitored. The dipivalyl compounds produced cardiovascular effects that were comparable to those produced by their respective parent catecholamines except that the responses had a delayed onset and a prolonged duration. The catecholamines were more potent than their derivatives; norepinephrine was 28 times, epinephrine 15 times and isoproterenol 1.7 times as effective as their respective dipivalyl derivatives. Alpha or beta adrenergic responses to the dipivalyl compounds were attenuated or abolished after alpha adrenergic blockade (phenoxybenzamine or phentolamine), or beta adrenergic blockade (propranolol), respectively, or combined alpha and beta blockade. Since other evidence indicates that the dipivalyl derivatives themselves are inactive, our results suggest that these compounds act as prodrugs that exert their cardiovascular effects only after they are biotransformed to catecholamines.

Adrenergic alpha-Antagonists↗
PubMed1976

Intracellular buffering of heart and skeletal muscles during the onset of hypercapnia.

Changes in the total CO2 content of tissues were determined in order to characterize variations in intracellular acid-base parameters during the onset of hypercapnia. Within two minutes after an increasement in the CO2 tension of the inspired air of rats, there were large increases in the intracellular bicarbonate concentrations of both cardiac and skeletal muscles. Greater changes occurred in the heart, and its intracellular pH remained near normal during the first hour of hypercapnia; whereas there was an intracellular acidosis in skeletal muscle. This greater capacity of the heart to buffer excess CO2 has been linked to an increased movement of bicarbonate ions into and/or hydrogen ions out of cardiac cells during hypercapnia (Lai et al., 1973c). Yet, the buffer capacity of the heart was not compromised by metabolic acidosis during which there was a greatly reduced extracellular bicarbonate ion concentration and a greatly increased extracellular hydrogen ion concentration. The intracellular pH of the cardiac ventricle was stable following the imposition of a noncarbonic acid load on normocapnic rats.

Acid-Base Equilibrium↗
PubMed1976

Intracellular and extracellular acid-base changes in hemorrhagic shock.

Each of 21 dogs was bled until mean arterial blood pressure fell to 50 torr; this hemorrhagic shock state was then maintained for two hours. During hemorrhagic shock, the blood lactate concentration increased sixfold. The severe metabolic acidosis in arterial blood was partially compensated by a decreased PCO2 caused by increased ventilation. However, in mixed venous blood, the metabolic acidosis was combined with a respiratory acidosis. This hypercapnia in venous blood was indicative of the increased PCO2 in tissues poorly perfused following hemorrhage. The increase in the PCO2 of the femoral venous blood was greater than that in mixed venous blood, suggesting that some tissue beds were better perfused than those of the hind limb during shock. The intracellular lactate concentration of hind limb skeletal muscle was greatly increased in the shock state, and tissue PCO2 rose. Intracellular pH of skeletal muscle was only slightly decreased and bicarbonate concentration was unchanged during this combined metabolic and respiratory acidosis. This capacity of skeletal muscle to maintain a high HCO-3 concentration in intracellular fluid during metabolic acidosis may be an enhanced response of the mechanism responsible for maintaining (HCO-3)i normally at a level approximately ten times that which would be expected if HCO-3 were distributed passively.

Acid-Base Equilibrium↗
PubMed1975

Anesthetic hazards for patients who have undergone bilateral thoracolumbar sympathectomy.

Abrupt and serious circulatory changes may take place during and after operations under general anesthesia in patients who have had extensive thoracolumbar sympathectomy performed previously. These changes should be anticipated and treated promptly and vigorously, if prevention is not possible. Experiences with 23 such cases are presented.

Anesthesia, General↗
PubMedDate not supplied

Kinked DNA in crystalline complex with EcoRI endonuclease.

The 3 A electron density map of a co-crystalline recognition complex between EcoRI endonuclease and the oligonucleotide TCGCGAATTCGCG reveals that a tight, complementary interface between the enzyme and the major groove of the DNA is the major determinant of sequence specificity. The DNA contains a torsional kink and other departures from the B conformation which unwind the DNA and thereby widen the major groove in the recognition site.

Base Sequence↗
PubMedDate not supplied

Pressor responsiveness to vasopressin in the rat with DOC-salt hypertension.

To further characterize the role of vasopressin in DOC-salt hypertension, four groups of unilaterally nephrectomized rats were studied: control rats given no further treatment, rats treated with DOC and given 1% saline to drink, or rats treated with only DIC or 1% saline had similar pressor responses to exogenous vasopressin and angiotensin II. Within the DOC-salt group, two populations of rats were identified: one with normal pressor responsiveness to vasopressin, and one with markedly enhanced pressor responsiveness to vasopressin. Incidence of enhanced responsiveness increased with duration of treatment. Urinary excretion of vasopressin was elevated in the 1% saline and DOC-salt groups after 1 week of treatment, and in the DOC group after 4 weeks. However, the plasma vasopressin concentration was elevated only in the rats treated with both DOC and saline. It is suggested that vasopressin is essential for the expansion of blood volume in the early stages of DOC-salt hypertension, and functions as a direct pressor agent only in the later stages.

Angiotensin II↗
PubMedDate not supplied

Effect of intracerebroventricular captopril on vasopressin and blood pressure in spontaneously hypertensive rats.

In conscious, unrestrained spontaneously hypertensive rats (SHR), mean arterial blood pressure (MAP) increased from a pretreatment value of 150 +/- 4 to 179 +/- 7mm Hg within 10 min (p less than 0.01) following an intracerebroventricular (i.c.v.) injection of captopril (2 mg/kg body weight), and the plasma vasopressin concentration was increased eightfold (p less than 0.01). MAP than fell to 131 +/- 5 mm Hg at 120 minutes (p less than 0.01), and plasma vasopressin concentration returned to pretreatment levels. The initial increase in MAP was due in large part to increased plasma vasopressin levels since this increase was reduced 50% by pre-treatment with a specific antagonist of the pressor action of vasopressin. The reduction in MAP at 120 minutes in captopril-treated rats may been nonspecific, since a similar effect was observed in SHR given an i.c.v. injection of a control solution. In (Wistar-Kyoto) WKY rats, i.c.v. captopril was without a statistically significant effect on MAP, but the plasma vasopressin concentration increased three-fold (p less than 0.01). These findings may reflect an increased sensitivity of the control system for vasopressin release in the SHR.

Animals↗