We present a tutorial on the mechanisms of and connections among osmosis, diffusion, and convection. For simplicity, we consider only two-component nonelectrolyte solutions under isothermal conditions. Further, we confine our attention to laminar convection with application to the case of flow through narrow channels, as might occur in membranes containing pores or slits. The application of equilibrium and near-equilibrium thermodynamics to flow processes is just like considerations of mechanics with friction, or hydrodynamics. The description of flow processes of more than two atomistic components, either solutions or suspensions, is identical in the dilute limit to the description we give, except possibly when the curvature of the flow field (at the velocity profile) is significant. Flow fields, therefore, naturally divide into three regimes: 1) "one-dimensional" flow fields, e.g., solutions or suspensions in extended regions, whose velocity profile is macroscopically flat (compared to the atomistic curvature); 2) flow fields with significant curvature, e.g., Poiseuille or turbulent fields; and 3) high curvature fields, e.g., narrow flow channels.

Studies were carried out in rats to evaluate the release of iron from monoferric and diferric transferrin. Isoelectric focusing was carried out on plasma tagged at low and high saturations, and it was shown that these represented primarily monoferric and diferric transferrin, respectively. In vivo studies with these tagged plasmas were carried out on normal, iron-deficient, and hypertransfused rats. In all three groups there was a greater in vivo uptake of iron from diferric transferrin by all tissues monitored. Though the amount varied in different animals, the ratio of uptake between diferric and monoferric transferrin iron varied between 1.56 and 2.10 in the erythron and between 2.38 and 2.65 in the liver. These studies indicate that changes in transferrin saturation, by changing the proportion of monoferric to diferric transferrin iron, changed the amount of iron released to tissues.

Six adult rabbits were maintained on an 18 h fast, 6 h feeding schedule. At the end of the fast either 0.5-40 Ivy dog units (IDU)/kg cholecystokinin (CCK) or 0.9% NaCl were injected intravenously. Feed intake was then measured for 15 min. Significant depression of intake was found at 1 IDU/kg, a 50% depression of intake after 5.5 IDU/kg, and no intake after 40 IDU/kg. Caerulein in similar experiments gave significant depression of intake at 0.125 microgram/kg, a 50% depression after 0.28 microgram/kg, and no intake after 5.0 microgram/kg. In three of these rabbits subdiaphragmatic vagotomy did not abolish the satiety effects of CCK and caerulein. The synthetic octapeptide of CCK was less potent in causing satiety. After CCK or caerulein the rabbits showed typical postprandial behavior. Taste aversion tests failed to demonstrate a strong aversion to flavors associated with the compounds used. These results indicate that exogenous CCK can act as a satiety agent at levels of the same order as the physiological range.

In seven male monkeys, Macaca mulatta, the infusion of nutrients into the stomach just prior to or 20 h before a 4-h feeding period reduced the feeding by an amount comparable to the calories infused. Pure carbohydrates, fat, protein, and mixtures were employed as infusions and given in a random fashion over a caloric range of 75-300 kcal. In a second series of experiments, monkeys were partially fasted on 1 day and in this way deprived of 75, 150, 300, or 450 kcal. On successive days, they overate to compensate for this deprivation. The smaller deprivations (75 and 150 kcal) were corrected on the first recovery day. The 300-kcal deprivation required 2 days to be corrected while the 450-kcal deficit was only partially restored. These experiments demonstrate the capacities of the monkey to respond with precision to caloric supply and deprivation so as to maintain a constant caloric intake.

Freshwater bivalves maintain a Na steady state in artificial pondwater: JiNa = 1.2 +/- 0.1 mumol/g dry tissue per h. Na uptake is Cl independent. The affinity (KS) of the Na transport system is 0.15-0.23 mmol Na/1. Sodium influx is coupled to H and/or NH4 exchange. Salt depletion stimulates JiNa 300% relative to nondepleted animals with no change in Ks. Injected ammonium ion stimulates JiNa. Sodium transport is inhibited 84% by 0.5 mM amiloride but is not affected by 4 mM NH4 or 1 mM furosemide in the bathing solution or injection of acetazolamide (0.26 mumol/ml blood).

Elevating serotonin (5-HT) contents in brain with 5-hydroxytryptophan (5-HTP) reduced rectal temperature (Tre) in rabbits after peripheral decarboxylase inhibition with the aromatic-L-amino-acid decarboxylase inhibitor R04-4602 at two ambient temperatures (Ta), 2 and 22 degrees C. The hypothermia was brought about by both an increase in respiratory evaporative heat loss (Eres) and a decrease in metabolic rate (MR) in the cold. At a Ta of 22 degrees C, the hypothermia was achieved solely due to an increase in heat loss. Depleting brain contents of 5-HT with intraventricular, 5,7-dihydroxytryptamine (5,7-DHT) produced an increased Eres and ear blood flow even at Ta of 2 degrees C. Also, MR increased at all but the Ta of 32 degrees C. However, depleting the central and peripheral contents of 5-HT with p-chlorophenylalanine (pCPA) produced lower MR accompanied by lower Eres in the cold compared to the untreated control. Both groups of pCPA-treated and 5,7-DHT-treated animals maintained their Tre within normal limits. The data suggest that changes in 5-HT content in brain affects the MR of rabbits in the cold. Elevating brain content of 5-HT tends to depress the MR response to cold, while depleting brain content of 5-HT tends to enhance the MR response to cold.

Six female adult rhesus monkeys and baboons with exteriorized enterohepatic circulations were simultaneously assessed following [26-14C]cholesterol pulse labeling by 14CO2 breath analysis and combined isotopic and chromatographic sterol balance during metabolic steady state. Bile acid synthesis and/or secretion were compared with 14CO2 breath analysis of cholesterol oxidation during short term physiological changes, and with total bile acid diversion and feedback inhibition, and biliary tract obstruction. Cholesterol oxidation by breath analysis compared closely with acidic sterol losses during steady-state conditions (145.6 +/- 23.9 vs 144.6 +/- 24.4 mg/24 h) and was sensitive enough to detect changes resulting from diurnal variation and fasting. The 14CO2 test detected inhibition of bile acid synthesis consequent to bile acid feedback (355 +/- 32 to 88 +/- 31 mg/24 h, P less than 0.001) or biliary tract obstruction (158 +/- 27 to 60 +/- 28 mg/24 h, P less than 0.05) but underestimated increased synthesis induced by acute bile diversion (245 +/- 24 vs. 868 +/- 104 mg/24 h, P less than 0.01 at 24 h). Insignificant 14C was detected by carcass analysis following cessation of exhaled 14CO2.

The velocity and magnitude of neurally elicited renal vasoconstrictions decrease with reduction of renal arterial pressure. We investigated the relative roles of humoral and mechanical factors in this decrease. Cats were anesthetized with chloralose. Renal arterial pressure was controlled with an aortic cuff. Vasoconstrictions were elicited by electrical stimulation of the renal nerves until renal vascular resistance stabilized. Renal blood flow autoregulation was maintained during stimulation. Competitive blockade of angiotensin II did not affect the decrease in renal vascular responsiveness to neural input at reduced renal arterial pressure. A mathematical model suggested that a major portion of the decrease in the velocity of vasoconstrictions was a mechanical consequence of autoregulatory vasodilation. However, the model was only able to account for the experimental findings after the blockade of prostaglandin synthesis, and this blockade significantly increased the velocity of vasoconstrictions at renal arterial pressures of 75 Torr or below. These results suggested that prostaglandins as well as mechanical factors played a role in the autoregulatory decrease in responsiveness to sympathetic input.

Cholinomimetics (pilocarpine, carbachol, physostigmine, acetylcholine, acetyl-beta-methylcholine) and sympathomimetics (dopamine, epinephrine), when injected into the hemolymph, provoked salivary fluid secretion in the female ixodid tick Amblyomma hebraeum Koch. Atropine, but not tubocurarine or toxiferine, abolished pilocarpine-induced secretion without reducing the response to dopamine. Reserpine and guanethidine likewise selectively attenuated pilocarpine-induced secretion. Following extirpation of the synganglion, pilocarpine no longer provoked a secretory response whereas dopamine did. Thus, the salivary gland appears to be innervated directly by catecholaminergic rather than cholinergic secretory nerves. It is suggested that pilocarpine elicits salivation by interacting with muscarinic-type cholinergic receptors situated either on the cell bodies of the secretory nerves, or alternatively in the integrative or sensory pathway.

Cardiac output, renal and hepatic blood flows, arterial lactate concentration, and minute volume were measured before, during, and after 40 min of rest induced either by the practice known as "transcendental meditation" (TM) or by an ordinary eyes-closed rest-relaxation period. Two groups of normal young adults were studied: one group consisted of regular practitioners of TM and the other of similar individuals studied prior to learning this technique. Marked declines of renal blood flow were noted in both groups. Decline of hepatic blood flow, increased cardiac output, decreased arterial lactate, and minute volume were also recorded in the TM-induced rest period. These changes imply a considerable increase of nonrenal, nonhepatic blood flow during TM (44%) and, to a lesser extent, during rest (12%). Increased cerebral and/or skin blood flow is hypothesized to account for part of the redistributed blood flow in the practitioner.

Numerical parameters for a compartmental model of a neuron can be chosen to conform both to the neuron's structure and to its measured steady-state electrical properties. A systematic procedure for assigning parameters is described that makes use of the matrix of coefficients of the set of differential equations that embodies the compartmental model. The inverse of this matrix furnishes input resistances and voltage attenuation factors for the model, and an interactive modification of the original matrix and its inverse may be used to fit the model to anatomic and electrical measurements.