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PubMed1966

The kinetics of osmotic transport through pores of molecular dimensions.

This paper presents a theoretical analysis of the kinetics of osmotic transport across a semipermeable membrane. There is a thermodynamic connection between the rate of flow under a hydrostatic pressure difference and the rate of flow due to a difference in solute concentration on the two sides. One might therefore attempt to calculate the osmotic transport coefficient by applying Poiseuille's equation to the flow produced by a difference in hydrostatic pressure. Such a procedure is, however, inappropriate if the pores in the membrane are too small to allow molecules to "overtake." It then becomes necessary to perform a statistical calculation of the transport coefficient, and such a calculation is described in this paper. The resulting expression for the number of solvent molecules passing through a pore per second is J = m D(1) deltan(1)/l(2) where m is the number of solvent molecules in the pore, l is the length of the pore, D(1) is the self-diffusion coefficient of the solute, and deltan(1) the difference in solvent mole fraction on the two sides of the membrane. This equation is used for estimating the number of pores per unit area of the squid axon membrane; the result is 6 x 10(9) pores/cm(2).

Biological Transport↗
PubMed2000

Normal saline wound dressing--is it really normal?

Gauze swabs soaked in normal saline are frequently used as dressing on open wounds. Their exact mechanism of action is not known. This study was designed to assess the hypothesis that normal saline dressings act in part as an osmotic dressing. Ten patients had skin ulcers (n = 10) dressed with normal saline soaked sponges. Acting as controls (n = 10) identical sponges were placed upon intact skin. The sponge fluid osmolarity and electrolyte concentrations were serially assayed to test our hypothesis. In the control group, the osmolarity, sodium and chloride concentrations increased with time as a result of evaporation, altering it from an isotonic to a hypertonic dressing. However, in the ulcer group, the osmolarity, sodium and chloride concentrations in the sponge fluid remained relatively isotonic with time. This result is statistically significant (P< 0.05). We postulate that, as a result of evaporation, the sponge dressing increases its tonicity. This draws fluid from the wound into the dressing so that a dynamic equilibrium occurs and the sponge dressing regains isotonicity. The dressing remains functional provided that the wound fluid is absorbed freely from the wound. This process is terminated when either the dressing completely absorbs the wound fluid or the dressing dries out. The latter often occurs prematurely in a contaminated wound or in a wound where exudate forms a non-permeable barrier which prevents osmosis and allows the remaining water in the dressing to evaporate completely. This correlates with the observation in clinical practice that for maximum efficacy the dressing should be changed regularly.

Chlorides↗
PubMed1987

Hydroosmotic responses to short pulses of vasotocin by toad bladder.

When toads, Bufo marinus, were mildly dehydrated, the permeability to water of their urinary bladders increased, but blood samples placed directly on the wall of an isolated assay bladder did not contain enough arginine vasotocin (AVT) to induce the observed response. One explanation for this discrepancy is that AVT is secreted intermittently and rapidly cleared from the blood, even though the hydroosmotic response persists. The hydroosmotic response of bladders to pulsatile secretion of AVT was simulated by dipping isolated bladders for 1 min in Ringer's fluid with AVT followed by washout of hormone. Bladders developed the characteristic increase in membrane permeability to water several minutes after AVT had been removed from the serosal bathing solution. With short periods of bladder exposure to hormone, higher concentrations were required for triggering responses equivalent to those induced with continuous stimulation. This requirement was greater for vasopressin than it was for AVT. Studies with tritium-labeled vasopressin indicated that there is a "receptor reserve" for the hydroosmotic action of vasopressin in the toad bladder. The magnitude of this reserve is reduced as the duration of stimulation with hormone is diminished. It is suggested that pulsatile exposure of the bladder to AVT increases the specificity of the hormone for hydroosmotic receptors and minimizes the development of target organ resistance. The large receptor reserve in this tissue may be required to capture short bursts of AVT secreted into blood, although this remains to be demonstrated.

Animals↗
PubMed1975

Micromanipulation of pressure in terminal lymphatics in the mesentery.

The terminal lymphatics are a network of highly previous vessels that are distributed in a loose association with the blood capillary bed, in particular along with the collecting venules. The base-line pressure in these lymphatics is close to atmospheric, but after they converge to form valved collecting channels PL is increased with a pressure differential of 1-2 cmH20 built up across each valve. This increment in lymphatic pressure is clearly related to the presence of one-way valves, the contractile activity of the collecting channels, and the comparative impermeability of these channels. The pressure differential required to draw fluid from the interstitium into the lymphatics would appear to reside in the vasomotor activity of the collecting channels, although the data do not rule out changes in Pt coincident with net capillary filtration or absorption.

Animals↗
PubMed1983

Irreversible stimulation of hydroosmotic response in toad bladder by photoaffinity labeling with [Phe2,Phe-(p-N3)3]Vasopressin.

The photoreactive analogs of vasopressin, [Phe2,Phe-(p-N3)3]AVP (3a) and [Phe-(p-N3)2]AVP (2a), and the chemically reactive analogs of vasopressin, [Phe2,Phe-(p-NHCOCH2Br)3]AVP (3b) and [Phe-(p-NHCOCH2Br)2]AVP (2c), have been tested in the toad bladder for irreversible stimulation or inhibition of the water permeability response. Analog 3a was found to be an agonist with an ED50 of 4.5 X 10(-7) M and to induce a maximal osmotic water flow across bladders equivalent to 74% of that observed with the parent hormone (AVP). Photolysis of this analog in Ringer's fluid resulted in a decrease in its biological activity, with a half-time of 7 min. However, UV irradiation of the analog in the presence of toad bladders triggered an irreversible increase in the permeability of the bladders to water. Under optimal conditions of irradiation, water permeability remained at about 60% of maximum for more than 3 h after washout of analog 3a. The addition of AVP raised the permeability of these bladders to 100%. Analog 3a did not cause irreversible stimulation without photolysis, nor did this analog induce its characteristic effect when added to the mucosal solution. Compound 2a was found to be a potent antagonist of AVP. This inhibitory action of 2a was readily reversed in both the presence and absence of UV irradiation. Compound 3b was also found to be a reversible inhibitor of AVP. Compound 2c was found to be inactive as agonist or antagonist. These studies suggest that analog 3a binds covalently at or near the toad bladder hydroosmotic receptors, resulting in a persistent increase in permeability to water of the bladder wall.

Affinity Labels↗