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Biomedical subjects

R Schulz

Publications and source records attributed to R Schulz.

At least 415 records · Page 23Linked to original sources
PubMed1991

Thyrotropin-releasing hormone has stimulatory effects on ventilation in humans.

Thyrotropin-releasing hormone (TRH) stimulates pituitary thyrotropin synthesis and release and also regulates autonomic nervous system functions by acting as a neuromodulator and neurotransmitter. In experimental animals a stimulation of ventilation by thyrotropin-releasing hormone was shown when applied at central nervous system sites that affect respiratory motor output. It was the goal of our study to investigate the respiratory properties of thyrotropin-releasing hormone on basal and stimulated (i.e. CO2-rebreathing) conditions following systemic thyrotropin-releasing hormone application in healthy humans. Thyrotropin-releasing hormone (200 micrograms, 400 micrograms intravenous) initiated a rapid short lasting rise of minute volume, ventilatory air-flow and alveolar oxygen tension under steady state breathing (P less than 0.001). Breathing frequency was less affected, heart rate rose concomitantly (P less than 0.001). While breathing with increasing concentrations of carbon dioxide, minute volume was higher under thyrotropin-releasing hormone than under placebo alone. Further effects (e.g. nausea, dizziness, palpitations) mostly appeared later than respiratory changes and thus may not be responsible for their initiation. Our findings prove systemic thyrotropin-releasing hormone to be a strong respiratory stimulant in man. Response in respiratory output was also accompanied by central nervous system-effects (e.g. dizziness, restlessness, augmented vigilance). The mode of thyrotropin-releasing hormone effects on respiration after peripheral administration is still speculative. An augmented sympathetic output or a direct receptor mediated action at central nervous system sites may be responsible, while a peripheral effect cannot be excluded.

Adolescent↗
PubMed1991

Heart rate reduction improves myocardial ischemia in swine: role of interventricular blood flow redistribution.

Regional myocardial blood flow (MBF) distribution and function upon slowing the heart rate (HR) during ischemia were studied in anesthetized swine, a species without coronary collaterals. Perfusion of the left anterior descending artery by a pump allowed controlled production of regional ischemia. Slowing tachycardia by electrical pacing (127 to 87 beats/min) caused marked improvement of regional dysfunction [% wall thickening (WTh) from 9 to 27%] and increased subendocardial MBF [from 0.31 to 0.55 ml.min-1.g-1 (P less than 0.001)] without change of subepicardial MBF. Total left ventricular (LV) MBF increased, whereas right ventricular (RV) MBF fell by 18% (P less than 0.02). The mechanism of MBF changes during slowed HR was assessed by surgically excluding the RV and comparing findings with previous experiments with RV intact when HR was slowed from 96 to 60 beats/min. A similar improvement of regional LV function occurred (8% vs. 30% WTh) with the RV excluded, but without a change in total flow to the LV bed, whereas subendocardial MBF increased and subepicardial MBF fell, indicating transmural redistribution only. These findings show that the RV vascular bed can contribute to LV perfusion in swine during ischemia, and they document the potential for "reverse RV steal" during slowed heart rate in this setting.

Animals↗
PubMed1991

Measurement of regional myocardial blood flow with multiple colored microspheres.

BACKGROUND: The use of radioactive microspheres (RM) for the measurement of regional myocardial blood flow (RMBF) is limited and inaccessible to many investigators due to radiation safety concerns and radioactive waste disposal problems. Therefore, a new method for the measurement of RMBF using colored microspheres (CM) was developed. METHODS AND RESULTS: Polystyrene spheres (diameter, 15 +/- 0.1 [SD] micron; density, 1.09 g/ml) were dyed with one of five colors. With the injection of CM into the left atrium or into a coronary perfusion line, RMBF and its distribution can be determined. CM are extracted from the myocardium and blood by digestion with potassium hydroxide and subsequent microfiltration. The dyes are then recovered from the CM within a defined volume of a solvent, and their concentrations are determined by spectrophotometry. The separation of composite absorbance spectra by spectrophotometry with the CM technique was as good as the separation of energy spectra by a gamma-counter using the RM technique. Leaching of dye from the CM was less than 0.1% during a 2-month period in vitro. Significant leaching of dye from the microspheres also did not occur during 8 hours in the blood and myocardium of four anesthetized dogs in vivo. For further validation of this method, pairs of CM and RM (15.5 +/- 0.1 [SD] microns) were simultaneously injected under five different RMBF conditions (range, 0-10 ml/[min.g]) into the left anterior descending coronary artery of four anesthetized pigs, with coronary inflow as a flow reference, or into the left atrium of four anesthetized dogs using aortic blood withdrawal as a reference. The relation between RMBF determined by CM and RM was CM = 0.01 + 1.00.RM (r = 0.98, n = 1,080 data points) in the pigs, and CM = -0.19 + 0.92.RM (r = 0.97, n = 1,813 data points) in the dogs. CONCLUSIONS: Measurement of RMBF with CM yields values very similar to those of RM. Their use is less expensive and avoids all the disadvantages related to radioactivity, thus offering an alternative method for as many as five RMBF measurements in a single experiment.

Animals↗
PubMed1991

No effect of coronary perfusion on regional myocardial function within the autoregulatory range in pigs. Evidence against the Gregg phenomenon.

BACKGROUND: The hypothesis that increases in coronary perfusion increase ventricular performance independently from providing enhanced oxygen supply ("Gregg phenomenon") remains controversial. METHODS AND RESULTS: To study the physiological significance of changes in coronary perfusion on global and regional myocardial function in situ, the left anterior descending coronary artery of isoflurane-anesthetized swine was cannulated, and perfusion was varied. In one group of swine (n = 5), coronary arterial pressure was increased in four steps from 88 +/- 11 to 186 +/- 11 mm Hg by increasing the speed of the pump circuit providing coronary blood flow. No changes in left ventricular end-diastolic pressure, peak pressure, or maximum left ventricular dP/dt were observed. Subendocardial blood flow (by radiolabeled microspheres) increased from 0.96 +/- 0.27 to 2.04 +/- 0.73 ml/min/g without any increase in systolic wall thickening (by sonomicrometry) or myocardial oxygen consumption of the anterior myocardium. In a second group of swine (n = 8), coronary arterial pressure was kept constant and coronary blood flow was increased stepwise by intracoronary adenosine infusion. End-diastolic pressure, peak pressure, and maximum left ventricular dP/dt remained unchanged when coronary blood flow increased from 21.7 +/- 9.8 to 93.8 +/- 34.1 ml/min. Subendocardial blood flow increased from 0.89 +/- 0.26 to 3.28 +/- 1.02 ml/min/g, again without any increase in systolic wall thickening (45.6 +/- 8.6 versus 42.6 +/- 9.8%) and myocardial oxygen consumption (5.75 +/- 1.18 versus 5.87 +/- 1.67 ml/min/100 g). In a third group of swine (n = 10), coronary arterial pressure was lowered by intracoronary adenosine infusion during constant coronary inflow. Left ventricular hemodynamics remained unchanged. With a decrease in coronary arterial pressure from 130 +/- 25 to 71 +/- 14 mm Hg, no decreases in subendocardial blood flow and systolic wall thickening were observed. Only when coronary arterial pressure was further reduced to 57 +/- 13 mm Hg did systolic wall thickening fall to 25.7 +/- 9.9% (control, 31.1 +/- 11.1%), associated with a decrease in subendocardial blood flow from 1.17 +/- 0.39 to 0.87 +/- 0.52 ml/min/g. CONCLUSIONS: Thus, the Gregg phenomenon plays no significant role within or above the autoregulatory pressure-flow range normally seen in anesthetized swine in situ.

Animals↗
PubMed1991

Characterisation of neutral endopeptidase 3.4.24.11 (NEP) in the kidney: comparison between normotensive, genetically hypertensive and experimentally hypertensive rats.

Neutral endopeptidase 3.4.24.11 (NEP) has been identified as the major atrial natriuretic factor (ANF) degrading enzyme in rat kidney, therefore, suggesting a possible role for this enzyme in blood volume and pressure regulation. Various experimentally induced and genetically hypertensive rat models have been used to test NEP inhibitors. The presence of different isoforms of NEP in the various hypertensive rat models would have relevance when searching for novel NEP inhibitors. Therefore, we compared the properties of NEP in kidney cortex homogenates in order to test for possible differences in the following hypertensive rat models and their appropriate controls: spontaneously hypertensive rats (SHR), Wistar Kyoto strain (WKY), DOCA-salt hypertensive rats, and Sprague Dawley control rats (SD). No relevant differences were found when comparing the following parameters: (1) specific activity (mean: 204 U/mg protein), (2) Michaelis constant (mean: 280 microM), (3) IC50 of thiorphan (mean: 6.5 nM) and phosphoramidon (mean: 54 nM), (4) pH profiles (optimum at pH 8.0), (5) heat inactivation profiles (half-life 20 min at 65 degrees C), (6) immunotitration of kidney cortex homogenates, (7) molecular weight as determined by gel filtration (92,000 Dalton) and (8) affinity chromatography with concanavalin A. Without evidence for the presence of different NEP isoforms, it is unlikely that divergent findings in DOCA-salt rats and SHR using a given NEP inhibitor are due to isoforms of NEP.

Animals↗
PubMed1991

Regulation of G proteins by chronic opiate and clonidine treatment in the guinea pig myenteric plexus.

G proteins have been implicated in the development of opioid dependence of the guinea pig myenteric plexus as chronic fentanyl elevates G0/i alpha and pertussis toxin prevents this phenomenon. Therefore, the present study investigates G proteins more closely in this peripheral nerve plexus after chronic exposure to addictive drugs of the opiate and nonopiate type. After 6 days of treatment with either the mu receptor ligand fentanyl, the kappa- agonist U-50,488H or the alpha-2 adrenergic receptor ligand clonidine, at doses which render the myenteric plexus tolerant and dependent, the G protein subunits Go alpha and G beta were quantified by immunoblot analysis by using polyclonal antisera. Regardless of the drug used, these G proteins were found to be significantly increased in particulate membrane preparations linked to nerve somata and nerve terminals. This increase in G protein subunits is developed maximally after 6 days, is dose-dependent and reversible upon termination of the drug supply. The concentrations found elevated return to control levels within 4 to 5 days after commencing withdrawal. The common increase of Go alpha and G beta subunits observed after chronic opiate or clonidine exposure is associated with the phenomenon of cross-dependence among all drugs studied. The findings may suggest that in the guinea pig myenteric plexus multiple inhibitory receptor types make use of a common pool of G proteins.

Adrenergic alpha-Agonists↗
PubMed1991

Atrial natriuretic peptide concentration in dogs with congestive heart failure, chronic renal failure, and hyperadrenocorticism.

The function of atrial natriuretic peptide (ANP) is claimed to be control of salt and water homeostasis, and thus, the hormone may be involved in the pathogenesis of certain diseases with impaired volume regulation. We, therefore, studied plasma ANP concentration in dogs with chronic renal failure, congestive heart failure, and hyperadrenocorticism. Dogs with chronic renal failure had twofold higher plasma ANP concentration (16.2 +/- 5.8 fmol/ml), compared with healthy dogs (8.3 +/- 3.5 fmol/ml). An even more distinct increase (sixfold) of plasma ANP concentration was found in dogs with congestive heart failure (52.9 +/- 29.7 fmol/ml). In contrast, dogs with hyperadrenocorticism did not have high ANP plasma concentration (5.5 +/- 2.0 fmol/ml). High-performance liquid chromatographic analysis of plasma from dogs with congestive heart failure indicated that, in addition to the normal circulating form of ANP (99-126), the unprocessed precursor ANP (1-126) is detectable in the circulation. These qualitative and quantitative alterations of plasma ANP concentration in dogs further suggest involvement of this peptide in the development and/or maintenance of diseases associated with impaired volume regulation.

Adrenocortical Hyperfunction↗
PubMed1991

[A two-stage regulatory system for pressure-constant perfusion of coronary vessels].

This paper describes a double-loop servo-controlled pump system for the constant-pressure perfusion of a coronary artery. Due to the transient nature of changes in coronary vasomotor tone, such a perfusion system must have a fast regulatory response. In the first stage, a servo-controlled pump primes a windkessel having a volume of 35 ml with blood. The pumping rate is electronically controlled to maintain a constant pressure within the windkessel max. 700 mmHg. The maximal flow rate is 300 ml/min. To reduce the high pressure in the windkessel to the desired coronary perfusion pressure, a variable flow resistance, comprising a clamped thin-walled silicone tube, is provided in the output line of the system. A fast servo-motor drives the clamp and is controlled by an electronic regulator, using a second feedback loop from the pressure signal measured at the tip of the perfusion cannula. The system stabilizes the coronary perfusion pressure within 300 ms. An additional modulation of the setpoint signal in synchrony with the cardiac cycle improves the phasic pattern of the blood flow, and thus prevents changes in transmural blood flow distribution. The dead volume of the overall system is about 60 ml. Hemolysis caused by this system during five hours of perfusion in vivo is negligible.

Animals↗
PubMed1991

[Studies on the influence of releasing hormones TRH and CRH on respiratory regulation].

Patterns of neuroanatomical distribution of Thyrotropin-releasing hormone (TRH) and Corticotropin-releasing hormone (CRH) and of their receptors in brain areas of humans and of animals suppose a regulating function of both peptides on regulation of respiration. In experimental animals TRH induces rhythmical and synchronous firing of defined neurons of nucleus tractus solitarii. In fetal sheep, endogenous and exogenous CRH promotes maturation of breathing rhythm genesis. In own human studies we demonstrated a modulation of respiration in healthy test-subjects - predominantly a stimulation of respiration - by systemic TRH and CRH. This effect persists also during hypercapnia, as we showed in patients and in 12 healthy test subjects while re-breathing CO2: when compared to placebo, CRH i.v. (200 micrograms. Bissendorf, Hannover, FRG) induces a significant (p less than 0.0001) shift of the ventilatory response curve to the left (petCO2 vs minute volume). Stimulation of respiration by CRH is independent of activation of the pituitary-adrenal axis. At present two analogues of CRH are available for application in humans (as a diagnostic of endocrinological disorders): human CRH and ovine CRH. Both analogues are comparably effective in stimulation of ventilation although sequence of effects is different in both analogues. We also evaluated the effect of CRH in 10 aged patients who were under prolonged respirator therapy after major abdominal surgery; both human and ovine CRH (100-200 micrograms i.v.) induced a profound and long lasting stimulation of ventilation under assisted respirator therapy. Vigilance was also markedly increased in all patients and thus was of therapeutic value. CRH also has a potential to alter sleep architecture in healthy and in diseased persons.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Intrarenal actions of the new adenosine agonist CGS 21680A, selective for the A2 receptor.

The purpose of this study was to define the direct intrarenal actions of the new adenosine agonist CGS 21680A (hydrochloride "A" salt of (2-[p-2-carboxyethyl)phenethylamino]5'-N-ethyl-carboxamido adenosine), which is selective for the A2 receptor. CGS 21680A was infused into the left renal artery, while simultaneously measuring blood pressure (BP) and parameters of renal function from both the left and right kidneys. At doses higher than 0.05 micrograms/kg/min, CGS 21680A appeared to leak from the circulation of the infused kidney in pharmacologically significant quantities, inasmuch as BP fell and renal blood flow was increased and renal vascular resistance decreased in the noninfused contralateral kidney. At doses of 0.025 to 0.05 micrograms/kg/min, CGS 21680A appeared localized to the renal circulation, because neither BP nor any measured parameter of contralateral renal function was altered. Intrarenal infusion of 0.025 to 0.05 micrograms/kg/min of CGS 21680A increased renal blood flow but not glomerular filtration rate leading to a fall in the filtration fraction. Urine volume and urinary sodium excretion were unaffected by selective intrarenal infusion of CGS 21680A. Plasma renin activity and renin secretion rate were also not altered significantly by intrarenal infusion of 0.05 micrograms/kg/min of CGS 21680A. In contrast plasma renin activity increased significantly in response to the intrarenal infusion of 0.075 micrograms/kg/min of CGS 21680A, a dose which leaked from the kidney and lowered BP. The results presented suggest that the new adenosine agonist CGS 21680A exerts a direct intrarenal effect on renal hemodynamics, but does not affect urine volume or sodium excretion or directly influence renin release.

Adenosine↗
PubMed1990

Immunologic methods for quantitative estimation of small peptides and their application to bradykinin.

A simple strategy was developed for the immunologic quantitative determination of small, biologically active peptides utilizing bradykinin (BK) as the model peptide prototype. Methods were developed for the preparation of a peptide-carrier complex suitable for immunization and for immobilization of peptides onto the plastic surface of enzyme-linked immunosorbent assay (ELISA) plates. An avidin-bound biotinylated peptide complex was used for raising peptide antibodies with high titers (1:4000) in the rabbit. The peptide BK was coupled to synthetic polymeric carriers poly-D-lysine (PL) and poly-D-lysine-succinylated (PLS) via the BK carboxy and amino terminus, respectively, with the aid of a water soluble carbodiimide. These carriers with antigen peptide side chains as well as avidin-biotinyl-peptide complexes were efficient surface immobilizing reagents for microwell plastic plates used in the detection of kinins by ELISA. Monoclonal antibodies reacted competitively with kinins in plates coated with either PL-BK or PLS-BK. In contrast, rabbit (polyclonal) antibodies reacted specifically in the plates coated with PLS-BK but only a non-specific reaction could be obtained with the PL-BK coated plates (i.e., could not be displaced with BK). Based on results using synthetic BK analogues, the carboxy terminal half of the BK molecule appears to be the stronger antigenic determinant in both mouse and rabbit systems. The polyclonal antibodies demonstrated a greater affinity to bradykinin compared to the monoclonal antibodies. Their use improved the sensitivity of the ELISA for kinin determination by one order of magnitude. Kinin levels determined in plasma tryptic digests by ELISA with the polyclonal antibodies and PLS-BK system were in agreement with published values.

Amines↗
PubMed1990

No impairment of sympathetic neurotransmission in stunned myocardium.

Reversibly injured myocardium after short periods of ischemia is characterized by a prolonged depression of contractile function which can, however, be enhanced by inotropic interventions. Thus, a lack of inotropic stimulation due to ischemic damage of cardiac sympathetic nerves has been suggested as a mechanism underlying postischemic myocardial dysfunction. We tested this hypothesis in nine anesthetized, vagotomized dogs with left cardiac sympathetic nerve stimulation (CSNS) at 1, 2, 5, 10, and 20 Hz and compared this response to that of intravenous norepinephrine infusion (NE, 0.5-1 microgram/kg.min). Regional myocardial wall thickness was measured using sonomicrometry, and mean systolic wall thickening velocity (MSTV) was determined. CSNS was performed before and at 0, 1, 2, 3, 4, 8, 12, 16, 20, and 24 h after release of a 15 min occlusion of a left circumflex coronary artery branch. Before coronary artery occlusion MSTV was increased in a frequency-dependent way from 7.5 +/- 2.7 (S.D.) (rest) to 8.1 +/- 3.1 (1 Hz), 9.4 +/- 3.2 (2 Hz), 11.4 +/- 2.7 (5 Hz), 13.4 +/- 2.4 (10 Hz), and 16.8 +/- 2.1 (20 Hz) by CSNS, and to 12.6 +/- 3.4 mm/s by NE. Immediately upon reperfusion CSNS increased MSTV from 2.9 +/- 2.0 to 2.9 +/- 2.8, 4.1 +/- 3.0, 5.4 +/- 4.6, 6.9 +/- 4.5 and 9.4 +/- 5.9, and NE increased MSTV to 7.8 +/- 1.9 mm/s. Baseline function recovered over 24 h, as did the response to CSNS and NE. Since the recovery of baseline function paralleled the increases in regional contractile function achieved by CSNS or NE, we conclude that there is no impairment of sympathetic neurotransmission in the stunned myocardium.

Animals↗
PubMed1990

Minimal alpha 1- and alpha 2-adrenoceptor-mediated coronary vasoconstriction in the anaesthetized swine.

alpha-Adrenoceptor-mediated coronary vasoconstriction contributes to the initiation and aggravation of experimental and clinical myocardial ischaemia. However, the extent of alpha 1- and alpha 2-adrenoceptor-mediated constriction has not been characterized in the porcine coronary circulation despite the frequent use of this experimental model. Fifteen swine were anaesthetized with either alpha-chloralose, enflurane or isoflurane to determine the amount of alpha-adrenoceptor-mediated coronary constriction elicited by either the selective alpha 1-adrenoceptor agonist methoxamine or the selective alpha 2-adrenoceptor agonist azepexole. The left anterior descending coronary artery was cannulated and perfused by an external pump delivering constant blood flow from the carotid artery. Following bilateral cervical vagotomy and beta-adrenoceptor blockade with propranolol (2 mg kg-1), graded dosages of either one of the alpha-adrenoceptor agonists (9-45 micrograms kg-1 min-1) were infused into the coronary perfusion line while coronary arterial pressure (CAP) was measured through a distal side arm of the cannula to detect changes in coronary vascular resistance. Infusion of the alpha-adrenoceptor agonists was terminated when systemic arterial pressure increased. Sonomicrometers were used to measure anterior left ventricular wall thickening for the assessment of regional contractile function. During methoxamine infusion, no increase in vascular resistance was observed during alpha-chloralose, enflurane or isoflurane anaesthesia, whereas the infusion of azepexole increased CAP from 103 +/- 31 mmHg to 120 +/- 35 mmHg (alpha-chloralose), from 101 +/- 16 mmHg to 122 +/- 11 mmHg (enflurane) and from 84 +/- 20 mmHg to 94 +/- 19 mmHg (isoflurane), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1990

Seasonal changes in and effect of castration/androgen replacement on the plasma levels of five androgens in the male three-spined stickleback, Gasterosteus aculeatus L.

The seasonal changes in plasma levels of the androgens 11-ketotestosterone (OT), testosterone (T), 11 beta-hydroxytestosterone (OHT), 11-ketoandrostenedione (OA), and 11 beta-hydroxyandrostenedione (OHA) were measured in the male three-spined stickleback (Gasterosteus aculeatus L). OT was the dominant plasma androgen in the breeding season in summer and was the only androgen that peaked during this period. The levels of OT correlated closely with the development of male secondary sexual characters and reproductive behavior. T and OHT were low in all seasons, whereas OHA and OA displayed the highest levels in early winter. During the postbreeding period, the time of active spermatogenesis, all measured steroids were low. Castration resulted in an almost complete loss of plasma OT and reduced T, whereas OHT, OHA, and OA were not reliably influenced. Androstenedione implants in castrated fish increased plasma T and OA implants increased plasma OT, suggesting a nontesticular site of conversion.

Androgens↗
PubMed1990

Steroid secretion of rainbow trout testis in vitro: variation during the reproductive cycle.

Testicular tissue collected at different stages of gonadal development was incubated with a pituitary extract (PE) from mature salmon. Three androgens (11-ketotestosterone, OT; 11 beta-hydroxytestosterone, OHT; and testosterone, T) and 17 alpha,20 beta-dihydroxyprogesterone (17-20 beta P) were quantified by radioimmunoassay in incubation media. OHT and OT were secreted in larger quantities than T and 17-20 beta P. The PE dose that evoked a half-maximal response (ED50), the ratios of maximum stimulated vs baseline secretion, and total testicular steroid output all changed during the reproductive cycle. Androgen secretion in response to PE was low in immature and spent fish, both in terms of ED50 and the ratio of maximum stimulated vs baseline secretion. This ratio increased in testes showing the first signs of maturation and remained elevated during rapid testicular growth, before reaching maximum values at full maturity. The lowest ED50 values were found at the end of spermatogenesis and during the peak spawning period. 17-20 beta P secretion could not be stimulated noticeably until the fish had entered the spawning period and, as opposed to androgens, remained stimulable in spent fish. ED50 values for 17-20 beta P ranged, without showing clear-cut variations, above those calculated for androgens. The changes in PE reactivity and steroid secretion capacity during the reproductive cycle are likely to contribute to the changes in circulating steroid concentrations and may allow modulations of testicular steroid production without large changes in circulating GTH levels.

Androgens↗
PubMed1990

Conversion of 11-ketoandrostenedione to 11-ketotestosterone by blood cells of six fish species.

Blood cells from Baltic salmon, Salmo salar, three-spined stickleback, Gasterosteus aculeatus, eel pout, Zoarces viviparus, crucian carp, Carassius carassius, African catfish, Clarias gariepinus, and reedfish, Calamoichthys calabaricus, were incubated with tritiated 11 beta-hydroxyandrostenedione (OHA) or 11-ketoandrostenedione (OA). In all fish there was conversion of OA to 11-ketotestosterone (OT), indicating that 17 beta-hydroxysteroid dehydrogenase activity was present in the blood cells. On the other hand, OHA was not converted to 11 beta-hydroxytestosterone in any fish. The addition of serum to the incubates largely prevented the OA-OT conversion by salmon blood cells.

Androstenes↗