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At least 343 records · Page 19Linked to original sources
PubMedDate not supplied

Effect of organ perfusion on renal drug transport. Application to furosemide in the isolated perfused rat kidney.

Angiotensin II was used as a probe to study the effect of changes in perfusate flow rate on the renal clearance parameters of furosemide in the isolated perfused rat kidney. Drug studies were performed in three rats with no angiotensin II present in the perfusate (treatment I) and in three rats with a 2.7 ng/min infusion of angiotensin II into the perfusate (treatment II). Furosemide was introduced into the recirculating perfusate at an initial concentration of 3.5 micrograms/ml and was assayed using HPLC. The protein binding of furosemide in perfusate was determined by equilibrium dialysis. Angiotensin II was found to have a dramatic effect on the renal hemodynamics, resulting in a 42% decrease in perfusate flow, a 27% decrease in GFR, and a 25% increase in filtration fraction. Values for the fractional excretion of glucose were very low and consistent, with or without angiotensin II (3.0-3.5%). Although the fraction unbound of furosemide was unchanged between treatments (0.770 for treatment I vs. 0.695% for treatment II), the renal and secretion clearances of furosemide were reduced by about 30% in the presence of angiotensin II. However, if the renal clearance (CLr) was corrected for free fraction (fu) and glomerular filtration rate (GFR) [ER = CLr/(fu.GFR)], there was no difference between the excretion ratio (ER) values of furosemide after the two treatments (29.0 for treatment I vs. 29.6 for treatment II). These results imply that the altered clearance parameters of furosemide are more likely the consequence of a reduction in functional nephron mass rather than a change in intrinsic secretory transport per unit mass of nephron.

Angiotensin II↗
PubMedDate not supplied

Identification of glucuronide metabolites of benzomorphan narcotic analgesic drugs in bile from the isolated perfused rat liver by gas chromatography and mass spectrometry.

The metabolism of four benzomorphan compounds was studied in the isolated perfused rat liver, and glucuronide metabolites were identified by combined gas chromatography-mass spectrometry (GC/MS). Cyclazocine, ketocyclazocine, volazocine, and pantazocine were each added to the perfusate of the isolated perfused rat liver and the bile collected for 3 hours. The residue from evaporation of the bile was derivatized with the dimethylsulfoxide anion and methyl iodide, and the permethylated glucuronide metabolites were identified by GC/MS. The four compounds were hydroxylated by the liver and excreted in the bile as phenolic glucuronides. For example, permethylated hydroxycyclazocine glucuronide had a mass spectrum with a molecular ion at m/e 533 and fragment ions at m/e 301 (aglycone), m/e 260 (loss of cyclopropyl group) and prominent ions at m/e 232, 201, 169, 141, and 101 caused by fragmentation of the permethylated glucuronic acid moiety. Perdeuteriomethylation demonstrated that pentazocine, volazocine, and cyclazocine were further metabolized by methylation of one hydroxy substituent and glucuronidation on the other. Pentazocine, cyclazocine, and ketocyclazocine were also metabolized to phenolic glucuronides of the parent drugs. N-deakylated metabolites of pentazocine, volazocine, and cyclazocine were identified both as permethylated glucuronic acid conjugates and as the trimethylsilyl derivatives of the aglycones, obtained by enzymatic hydrolysis on the conjugates in bile.

Analgesics, Opioid↗
PubMed1977

Thyroid calorigenesis in isolated, perfused rat liver: minor role of active sodium-potassium transport.

1. The effects of ouabain on hepatic oxygen uptake, cell membrane potential, and Na-K transport were examined at 37 degrees C during non-recirculating perfusion of isolated livers from fasted normal rats and rats treated with triiodothyronine (T3). The perfusate was Krebs-Ringer bicarbonate buffer containing albumin and bovine erythrocytes. 2. Treatment with T3 increased the rate of hepatic oxygen uptake by 30% (i.e. by 0-83 (micromole/min) per gram liver). 3. After shifting to perfusate containing 2-5 mM ouabain, a 4-5 mV depolarization and maximal rates of net hepatic K release and Na uptake occurred within 2 min in both thyroid states. These changes were not accompanied by any significant change in the rates of hepatic oxygen uptake. 4. T3-treatment increased the maximal, post-ouabain net flux of K by 29% (i.e. by 0-52 (muequiv/min) per gram liver). The T3-indlced increase in the net flux of Na (19%) did not achieve statistical significance. 5. In either thyroid state, the observed passive fluxes of Na and K were calculated to be balanced by active vluxes at the expense of 5-6% of the observed rate of hepatic oxygen uptake. 6. The results indicate that hyperthyroidism may enhance the rate of hepatic Na-K transport, but the energy expenditure due to this process appears to be too small to make any important contribution to thyroid calorigenesis in perfused rat liver.

Animals↗
PubMed1979

Modification of intramuscular pH oscillations in the isolated perfused rat heart by different interventions.

Changes in the intramuscular pH oscillations were examined by the use of an antimony electrode upon perfusing the isolated rat heart under different experimental conditions. The pH oscillations were decreased upon perfusing the hearts with Na+- or Ca2+-free medium and increased upon perfusing with K+-free medium. Increasing the temperature of perfusion medium from 25 to 40 degrees C or omitting glucose from the perfusing medium decreased the magnitude of oscillations. On the other hand, complete interruption of the perfusion flow resulted in an increase in the amplitude of pH oscillation. An initial increase followed by a decrease in the pH oscillation was seen when hearts were perfused with medium containing lactic acid at pH 6.6. These results suggest that pH oscillations reflect fluctuations in myocardial metabolism.

Animals↗
PubMedDate not supplied

Intraislet somatostatin inhibits insulin (via a subtype-2 somatostatin receptor) but not islet amyloid polypeptide secretion in the isolated perfused human pancreas.

It is our hypothesis that intraislet somatostatin regulates beta cell secretion in the isolated perfused human pancreas. The present study was designed to determine the relative influence of intraislet somatostatin on the regulation of islet amyloid polypeptide (IAPP) and insulin secretion, and to determine the effect of specific somatostatin receptor (SSTR) agonists on beta cell secretion during immunoneutralization of endogenous somatostatin in the isolated perfused human pancreas. Single-pass perfusion was performed in pancreata obtained from seven cadaveric organ donors using a modified Krebs medium with 3.9 mmol/L glucose. Sequential test periods were separated by basal periods and experiments were performed by infusion of any of the following: (1) somatostatin monoclonal antibody (S-Ab); (2) S-Ab + SSTR2 agonist (DC32-87); or (3) S-Ab + SSTR5 agonist (DC32-92). The changes in insulin and IAPP secretion from basal levels during each stimulation were calculated. Infusion of S-Ab resulted in a significant increase in insulin secretion (2033 +/- 429 pmol/L; P <0.05) but not IAPP. In the presence of S-Ab, infusion of the SSTR2 agonist resulted in a significant inhibition of insulin secretion (-1128 +/- 457 pmol/L; P <0.05) but not IAPP. In the presence of S-Ab, infusion of the SSTR5 agonist had no significant effect on insulin or IAPP secretion. We conclude that intraislet somatostatin inhibits insulin secretion via SSTR2, but not IAPP secretion, in the isolated perfused human pancreas model and that this effect occurs via SSTR2. These results also suggest that insulin and IAPP secretion are regulated by different mechanisms despite being co-localized to the beta cell.

Adolescent↗
PubMed1990

Study of tachyphylaxis to the vasoconstrictor effect of arachidonic acid in the isolated perfused kidney of the rat.

The isolated perfused kidney of the rat was used to address the development of tachyphylaxis to the vasoconstrictor effects of arachidonic acid. Repeated administration of arachidonic acid (3 micrograms at 10-min intervals) to the isolated kidney of the rat, perfused in situ with Krebs-Henseleit solution, led to the development of tachyphylaxis to the renal vasoconstrictor effects of arachidonic acid, using perfusion pressure changes as an index. Vasoconstrictor responses to either angiotensin or the endoperoxide analog, U46619, were unaffected by repeated administration of arachidonic acid. Associated with progressively reduced renal vasoconstrictor responses to arachidonic acid were parallel decrements in the renal venous release of prostanoids, measured by radioimmunoassay. In contrast, the release of prostanoids from the kidney stimulated by angiotensin II was increased after repeated administrations of arachidonic acid. These data suggest that the sequential reduction in renal vasoconstrictor responses to arachidonic acid is due to diminished conversion to prostaglandins, possibly due to inactivation of cyclooxygenase, decreased entry of arachidonic acid into the cell or its increased esterification into phospholipids.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1995

An apical permeability barrier to NH3/NH4+ in isolated, perfused colonic crypts.

Fermentation of nonabsorbed nutrients in the colon generates high concentrations of NH3/NH4+ in the colonic lumen. NH3 is a small, lipophilic neutral weak base that readily permeates almost all cell membranes, whereas its conjugate weak acid NH4+ generally crosses membranes much more slowly. It is not known how colonocytes maintain intracellular pH in the unusual acid-base environment of the colon, where permeant acid-base products of fermentation exist in high concentration. To address this issue, we hand dissected and perfused single, isolated crypts from rabbit proximal colon, adapting techniques from renal-tubule microperfusion. Crypt perfusion permits control of solutions at the apical (luminal) and basolateral (serosal) surfaces of crypt cells. We assessed apical- vs. basolateral-membrane transport of NH3/NH4+ by using fluorescent dyes and digital imaging to monitor intracellular pH of microvacuolated crypt cells as well as luminal pH. We found that, although the basolateral membranes have normal NH3/NH4+ permeability properties, there is no evidence for transport of either NH3 or NH4+ across the apical borders of these crypt cells. Disaggregating luminal mucus did not increase the transport of NH3/NH4+ across the apical border. We conclude that, compared to the basolateral membrane, the apical border of crypt colonocytes has a very low permeability-area product for NH3/NH4+. This barrier may represent an important adaptation for the survival of crypt cells in the environment of the colon.

Absorption↗
PubMed1989

Diltiazem (0.5 mg/l) decreases coronary vascular resistance during reperfusion, but not during low flow ischemia, in the isolated perfused rat heart.

Isolated rat hearts underwent low flow perfusion with a perfusion pressure of 15 mmHg for two hours followed by reperfusion at a perfusion pressure of 80 mmHg for two hours. In these severely damaged hearts we tested whether diltiazem (0.5 mg/l) administered during ischemia or during reperfusion had vasodilatory effects. Ischemia-induced progressive vasoconstriction was not influenced by the presence of diltiazem: during ischemia coronary vascular resistance (CVR) rose from 3.3 +/- 0.1 to 46.4 +/- 17.6 mmHg.ml-1.min in the diltiazem group and from 3.5 +/- 0.1 to 42.4 +/- 5.3 mmHg.ml-1.min in the control group (n.s.). If diltiazem was administered during reperfusion only CVR dropped from 45.7 +/- 9.2 to 4.4 +/- 1.1 mmHg.ml-1.min in the presence of diltiazem, and from 47.1 +/- 11.6 to 9.3 +/- 1.5 mmHg.ml-1.min in the control group (P less than 0.025). The disparity between diltiazem's effects during ischemia and reperfusion suggests a different mechanism of Ca2+-influx in vascular smooth muscle cells in ischemic and reperfused hearts: in reperfusion through the Ca2+-channels which are sensitive to calcium antagonists, and in ischemia through other channels, like the Na+/Ca2+ exchanger, or from intracellular calcium stores.

Animals↗
PubMed1995

Corticosteroid metabolism in isolated perfused rat liver and kidney. Experimental studies with emphasis on aldosterone.

The metabolism of corticosteroids, especially of aldosterone, the most important mineralocorticoid, and of prednisone, a synthetic glucocorticoid, was studied in the isolated perfused liver (IPL) and in the isolated perfused kidney (IPK) of the rat. In IPL, the elimination of aldosterone at 10(-9)-10(-6) M exhibited first order kinetics. Aldosterone was converted to tetrahydroaldosterone (THA), and dihydroaldosterone (DHA) (reduced metabolites), a metabolite less polar than THA, and predominantly to more polar metabolites. These consisted of conjugated reduced metabolites, and of greater amounts of unconjugated polar metabolites. Aldosterone metabolite accumulated rapidly in the circulation. Only the polar metabolites were later excreted in the bile. The elimination of prednisone at 10(-6) M also exhibited first order kinetics, but the clearance of aldosterone was 80% higher than the clearance of prednisone, indicating that different hepatic enzymes are involved in the metabolism of these corticosteroids. In IPK, the clearance of aldosterone was only about 2% of the hepatic clearance, and amounted to 39% of the renal glomerular filtration rate. The excretory and metabolic clearance in the kidney amounted to 26% and 74%, respectively. In the combined isolated perfused liver and kidney (CIPLK) hepatic polar, both unconjugated and conjugated reduced, and less polar reduced, aldosterone metabolites accumulated in the perfusate. Only polar metabolites were excreted in bile, while all circulating metabolites were isolated from urine within 90 minutes. This indicated, that the aldosterone metabolites, which are found in the kidney are formed predominantly in the liver. The presence of the kidney in the perfusion circuit seemed to inhibit the hepatic metabolism of aldosterone, as the total clearance of aldosterone in CIPLK was 23% lower than in the single perfused liver. Furthermore, addition of aldosterone 10(-9) M to CIPLK, but not to IPK without a liver, resulted in an increasing kaliuresis in 3 subsequent periods of 30 minutes, without any concomitant antinatriuresis. The hepatic aldosterone metabolites, which were released to the perfusate in the combined experiments, thus, seemed to possess kaliuretic effect. The metabolism of aldosterone in IPL was sex dependent. In female rat liver a 75% higher clearance of aldosterone per gram of liver was found, compared to that of male rat liver obtained from rats with a similar age. And the total hepatic clearance of aldosterone was 33% higher in female rats than in younger male rats with a similar body weight. The formation of free and conjugated THA and DHA was only observed in male rat liver, while a metabolite less polar than THA was only observed in female rat liver. The predominating polar metabolites in female rat liver consisted of at least 3 polar peaks, which were neither glucuronides nor sulfates of reduced less polar aldosterone metabolites. The sex dependence of the hepatic metabolism of aldosterone was into some extend neonatally determined. Administration of a diet with a high sodium content to salt sensitive Dahl (S) rats with elevated blood pressure, resulted, in IPL, in a 28% and 35% higher clearance of aldosterone than in s rats on a normal diet, and salt resistant normotensive Dahl rats on high sodium diet, respectively. (ABSTRACT TRUNCATED)

Adrenal Cortex Hormones↗
PubMed1989

Effects of perfusion flow rate, prostaglandin F2 alpha, phenylephrine, and serotonin on isolated, perfused brains of spontaneously hypertensive rats.

Effects of perfusion flow rate and three vasoconstrictors, phenylephrine, prostaglandin F2 alpha (PGF2 alpha) and serotonin, on isolated, perfused brain preparations of spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto rats (WKY) were investigated. The basal perfusion pressure of the cerebral vascular beds at a flow rate of 2.5 ml/min was 48 +/- 3 mm Hg (n = 11) in SHR and 32 +/- 2 mm Hg (n = 12) in WKY (P less than 0.005). The perfusion pressures at all flow rates tested (2.5-6.5 ml/min) in SHR were significantly greater than those in WKY. Concentration-perfusion pressure curves for the vasoconstrictors showed that the brain vascular bed was much more reactive to serotonin compared with phenylephrine and PGF2 alpha. EC50 values (-logM) for serotonin in the perfused brains of SHR and WKY were 7.0 +/- 0.06 (n = 10) and 6.5 +/- 0.06 (n = 11), respectively (P less than 0.01). There were no differences in EC50 values for phenylephrine or PGF2 alpha between SHR and WKY. Exogenous serotonin and phenylephrine caused significantly greater maximal vasoconstrictor responses in SHR compared with WKY, while the pressor response to PGF2 alpha was very weak and no significant difference between SHR and WKY preparations was observed. These results indicate that cerebral vascular beds in SHR exhibit higher cerebrovascular resistance than those in WKY. and that reactivity and sensitivity to serotonin and reactivity to phenylephrine in SHR rats are enhanced to a greater extent compared to WKY.

Animals↗
PubMed1985

A method for the evaluation of calcitonin secretion using the isolated perfused porcine thyroid.

A method for the in vitro perfusion of isolated porcine thyroid glands was developed. The intact glands were placed in a chamber and perfused at a rate of 2.5 ml/min with an oxygenated Tris-balanced salt solution maintained at 37 degrees C. Perfusate fractions were collected at 5-min intervals and analyzed for immunoreactive porcine calcitonin (CT). Calcitonin secretion increased in a dose-related manner with the level of calcium ion (2.5-6.25 mM) in the perfusion solution to a level of 7.5-fold greater than baseline levels. Other established CT secretagogues, such as theophylline (5 mM) and pentagastrin (4 microM), were found to stimulate calcitonin secretion. The CT secretory responsiveness of this system appears to mimic, both quantitatively and qualitatively, the secretory pattern observed in vivo in the pig. Therefore, this perfusion method should provide a valid in vitro model for the study of the process of CT secretion in the mammalian thyroid.

Animals↗
PubMedDate not supplied

Biotransformation of nitrosobenzene, phenylhydroxylamine, and aniline in the isolated perfused rat liver.

1. Haemoglobin-free single-pass perfusion of isolated rat liver with [14C]aniline, [14C]phenylhydroxylamine, and [14C]nitrosobenzene was carried out. 2. Perfusion with aniline revealed apparent enzyme kinetics for 4-aminophenol formation with Km = 144 microM, Vmax = 51 nmol/min per g liver wet; for 2-aminophenol Km = 144 microM, Vmax = 16 nmol/min per g; for acetanilide Km = 33 microM, Vmax = 25 nmol/min per g. Formation of phenylhydroxylamine and nitrosobenzene was observed at a rate of 1.5 nmol/min per g provided that these metabolites had been trapped within red cells. 3. Perfusion with phenylhydroxylamine displayed a metabolic pattern similar to aniline with apparent phenylhydroxylamine reduction kinetics of Km = 260 microM and Vmax = 600 nmol/min per g. In addition an acid-labile phenylhydroxylamine glucuronide was formed. 4. Perfusion with nitrosobenzene showed very rapid reduction to phenylhydroxylamine and to the metabolites observed with phenylhydroxylamine. In postmicrosomal supernatant, enzymic reduction of nitrobenzene by NADH and NADPH showed Km = 12 microM nitrosobenzene and Vmax = 5000 nmol/min per g. 5. Three per cent of nitrosobenzene was irreversibly bound to liver proteins. After 20 min perfusion with nitrosobenzene, 0.95 mumol of liver glutathione was lost per 10 mumol nitrosobenzene infused; 0.16 mumol of glutathione was released with effusate and bile, 0.46 mumol of glutathionesulphinanilide was produced, the rest, 0.33 mumol, may have formed mixed disulphides.

Aniline Compounds↗
PubMed1989

Zonal distribution of paracetamol glucuronidation in the isolated perfused rat liver.

1. The lobular distribution of paracetamol conjugation was studied using antegrade and retrograde perfusion of isolated rat liver. After addition of 25 mg of paracetamol, recovery of sulphate from antegrade perfusions was greater than from retrograde perfusions indicating periportal predominance of this metabolic pathway. 2. Recovery of sulphate was greater than recovery of glucuronide after addition of 25 mg of paracetamol during both antegrade and retrograde perfusions. Recovery of sulphate was similar after addition of 25 or 100 mg of paracetamol, whereas recovery of the glucuronide was increased at the higher dose, indicating a higher capacity for glucuronidation than for sulphation, but a higher affinity for sulphation. 3. Recovery of glucuronide from antegrade and retrograde perfusions was similar after addition of 25 mg of paracetamol, but was greater from antegrade perfusions after addition of 100 mg. This indicates that drug concentration may be an important determinant of the zonal distribution of drug metabolism. Factors other than localization of drug-metabolizing enzymes, such as competition with other metabolic pathways or availability of cofactors, may also influence the apparent zonal distribution of drug metabolism.

Acetaminophen↗
PubMed1991

19-nor-DOC biosynthesis in the isolated perfused rat kidney.

19-nor-deoxycorticosterone (19-nor-DOC) is a potent salt retaining and hypertensinogenic mineralocorticoid that is excreted in the urine. While the precursor of 19-nor-DOC, 19-oxo-DOC, is produced by the adrenal cortex, conversion to 19-nor-DOC does not occur in the adrenal gland. We have examined the hypothesis that 19-nor-DOC is synthesized from precursors in the kidney. 19-oxo-DOC was added to the perfusate of isolated rat kidney preparations (n = 5) at a concentration of 10 microM. During 1 h of perfusion following addition of 19-oxo-DOC, 71 +/- 6% of the precursor was converted to 19-oic-DOC, an immediate precursor of 19-nor-DOC, and 8.3 +/- 1.8% was converted to 19-nor-DOC. This represents the first definitive evidence that 19-nor-DOC is produced in the kidney from adrenal precursors.

Animals↗
PubMed1989

Release of VIP and substance P from isolated perfused canine ileum.

Basal release of vasoactive intestinal polypeptide (VIP) was 100-fold higher than substance P (SP) release from the vascularly perfused, neurally isolated canine small intestine. High-frequency field stimulation increased SP release but decreased VIP release. VIP release was markedly reduced by tetrodotoxin, perfusion with Ca-free medium, or by hexamethonium but not by atropine. Acetylcholine increased VIP output by an atropine-sensitive mechanism. Methionine-enkephalin or dynorphin (at 10-fold higher concentrations) markedly reduced VIP output; the actions of both these were abolished by naloxone. BHT-920, an alpha 2-adrenoceptor agonist, reduced VIP output markedly by a rauwolscine-sensitive mechanism. Isoproterenol and phenylephrine were without effect. Motilin produced persistent inhibition of VIP output. Thus VIP neurons of isolated canine small intestine were continuously active, driven by intrinsic cholinergic nerves, and subject to presynaptic inhibition by opioid agonists, alpha 2-adrenoceptor agonists, and motilin. This intrinsic neural system may provide tonic inhibitory control to the small intestinal circular muscle and provide a mechanism by which agents may modulate intestinal motor function.

Animals↗
PubMed1983

In vitro studies of ovarian function in the isolated perfused rabbit ovary.

An in vitro model for studies of preovulatory follicle and ovulation is described, using a recirculating system for perfusion of isolated rabbit ovaries. The preovulatory follicle was studied by addition of human chorionic gonadotropin (hCG) to the perfusion medium 1.5 h after the start of perfusion. Ovulations occurred approximately 13 h after in vivo hCG injection to the animal and 5-10 h after the start of perfusion. The ultrastructural changes during the perfusion were similar to in vivo conditions. The release of estradiol and progesterone into the medium are consistent with in vivo measurements. This in vitro model is probably useful for further studies of the biochemistry and morphology of ovarian function.

Animals↗
PubMed1997

Platelet-activating factor mediates angiotensin II-induced proteinuria in isolated perfused rat kidney.

Isolated kidney preparations (IPK) from male Sprague Dawley rats perfused at constant pressure were used to evaluate the effect of angiotensin II (AII) and platelet-activating factor (PAF) on renal function and urinary protein excretion. Compared with basal, intrarenal infusion of AII at 8 ng/min caused a progressive increase in protein excretion (11 +/- 6 versus 73 +/- 21 micrograms/min) in parallel with a decline in renal perfusate flow (RPF) (29 +/- 3 versus 18 +/- 3 ml/min). Addition to the perfusate of PAF at 50 nM final concentration also induced proteinuria (9 +/- 4 versus 55 +/- 14 micrograms/min) but did not change RPF (29 +/- 3 versus 30 +/- 3 ml/min). Preexposure of isolated kidneys to the PAF receptor antagonist WEB 2086 prevented the increase in urinary protein excretion induced by AII infusion (basal: 13 +/- 6; post-AII: 12 +/- 7 micrograms/min) but failed to prevent the vasoactive effect of AII (RPF, basal: 30 +/- 2; post-AII: 21 +/- 3 ml/min). In additional experiments, dexamethasone reduced the proteinuric effect of PAF remarkably. These results indicate that in isolated kidney preparation: (1) AII infusion induced proteinuria and decreased RPF; and (2) the effect of AII in enhancing urinary protein excretion was completely prevented by a specific PAF receptor antagonist, which, however, did not influence the AII-induced fall in RPF. It is suggested that PAF plays a major role in AII-induced changes in the permselective function of the glomerular capillary barrier.

Angiotensin II↗
PubMed1998

The Isolated Perfused Heart and Its Pioneers.

In 1866, Carl Ludwig together with Elias Cyon created the first isolated perfused frog heart preparation. Perfusion systems for the isolated mammalian heart were developed by H. Newell Martin in 1883 and by Oscar Langendorff in 1895. In its working mode, the isolated perfused rat heart was established in the 1960s.

Journal Article↗