Biomedical subjects

C J Mathias

Publications and source records attributed to C J Mathias.

At least 199 records · Page 11Linked to original sources

PubMed1989

Cardiovascular, biochemical and hormonal changes during food-induced hypotension in chronic autonomic failure.

The cardiovascular, biochemical and hormonal responses to a standard test meal have been investigated in patients with chronic autonomic failure and normal subjects. In autonomic failure there was a rapid (within 15 min), substantial and prolonged fall in blood pressure after the meal. A marked fall in blood pressure also occurred after a liquid meal of similar composition and caloric content, with no change in blood pressure in age-matched subjects with normal autonomic function. In autonomic failure after the test meal the blood pressure reached its nadir (45% fall) after 60 min, and had not returned to pre-meal levels after 3 h. There were no changes in cutaneous and forearm blood flow. In the normal subjects there were no changes in blood pressure after the meal; forearm blood flow fell and cardiac output increased. In autonomic failure there were no changes in plasma noradrenaline levels, unlike the normal subjects. Plasma adrenaline levels were unchanged in both groups. There was a similar rise in levels of plasma renin activity in both groups. The haematocrit and plasma osmolality did not change in either group. Changes in plasma glucose and plasma insulin levels were similar in both groups. The responses of 3 pancreatic gut peptides, neurotensin, pancreatic polypeptide and enteroglucagon, were greater in autonomic failure. Basal levels and responses of vasoactive intestinal polypeptide, cholecystokinin-8 and somatostatin were similar in both groups. The motilin response was greater in normal subjects. We conclude that in patients with autonomic failure there was a rapid, substantial and prolonged fall in blood pressure after a meal. This reduction in blood pressure was not counteracted by an increase in sympathetic nervous activity and other compensatory changes, as occur normally. It was unlikely that osmotic effects of the meal or gut secretions resulted in a significant loss of intravascular fluid into the gut. The fall in blood pressure probably results from vasodilatation within the splanchnic circulation, to which pancreatic and gastrointestinal hormones with vasodilatory actions may contribute.

Adult↗

PubMed1989

Differentiation in vivo of the sequential blood cell invasion following ureter obstruction of the rabbit kidney.

Inflammatory cellular changes occurring during renal injury as a consequence of unilateral ureter obstruction were studied in vivo using 111In-labeled leukocytes and 111In-labeled platelets. The radiolabeled cells were administered at various times after induction of hydronephrosis by unilateral ureter ligation in New Zealand rabbits. The contralateral kidney (CLK) served as the control. The migration and accumulation of the radiolabeled cells was monitored by dual isotope scintigraphic imaging (i.e. 99mTc-labeled red blood cell subtraction) and confirmed by direct analysis of removed epsilateral hydronephrotic kidney (HNK) and CLK at the time of sacrifice. When 111In platelets were administered, significantly greater uptake in the hydronephrotic kidney was observed within 15 min of ureter ligation. Furthermore, the HNK accumulated twice the amount of 111In radioactivity than the CLK, when either the polymorphonuclear neutrophils (PMN) or monocytes were injected at the time of ureter obstruction. The differences between HNK and CLK were scintigraphically detectable between 6 and 12 h after hydronephrosis respectively; and 111In-labeled monocytes selectively accumulated in HNK if administered during the first 48 h after ureter ligation. These data suggest that inflammatory cells sequentially accumulate following ureter obstruction and are derived from circulating white blood cells.

Animals↗

PubMed1989

Evidence that intravenous morphine stimulates central opiate receptors to increase sympatho-adrenal outflow and cause hypertension in conscious rabbits.

1. In conscious rabbits, intravenous morphine caused hypertension, bradycardia, hyperglycaemia and increased plasma adrenaline and noradrenaline. These effects were prevented by ganglionic blockade with pentolinium. 2. The cardiovascular responses to morphine were not altered by pretreatment with a vasopressin V1-receptor antagonist. 3. After bilateral adrenalectomy morphine caused a similar rise in noradrenaline but no increase in adrenaline. The rise in blood pressure was attenuated and the hyperglycaemia was abolished. 4. Adrenaline infused intravenously to mimic the levels that occurred after morphine caused a similar degree of hyperglycaemia but only a small increase in blood pressure. 5. Pretreatment with intracerebroventricular naloxone prevented the morphine-induced hypertension, hyperglycaemia, increase in plasma catecholamines, respiratory depression and sedation. 6. These results demonstrate that, in conscious rabbits, intravenous morphine causes hypertension by increasing sympathetic vasoconstrictor nerve activity and elevating plasma adrenaline levels; the latter alone produces the hyperglycaemia. Vasopressin release is not involved in the hypertensive response to morphine. The effects of morphine appear to result from stimulation of central opiate receptors leading to enhanced sympathoadrenal outflow.

Adrenalectomy↗

PubMed1989

Differential blood pressure and hormonal effects after glucose and xylose ingestion in chronic autonomic failure.

1. To investigate whether carbohydrate contributes to postprandial hypotension in autonomic failure, the cardiovascular, biochemical and hormonal effects of oral glucose and an iso-osmotic solution of oral xylose were studied on separate occasions in six patients with chronic autonomic failure. The effects of oral glucose were also studied in eight normal subjects. 2. In the patients oral glucose lowered blood pressure substantially (-34 +/- 7% at 60 min, area under curve -24.9 +/- 3.5%, P less than 0.001) and for a prolonged period (-25 +/- 4% at 120 min). Plasma noradrenaline levels did not change. In the normal subjects blood pressure was unchanged and plasma noradrenaline rose, suggesting a compensatory increase in sympathetic nervous activity. 3. In the patients xylose caused a smaller and more transient fall in blood pressure (-15 +/- 6% at 90 min, area under curve -8.9 +/- 4%, P less than 0.05) with a non-significant elevation in packed cell volume (36.7 +/- 1.8 to 38.2 +/- 1.8). It was therefore unclear if xylose was exerting osmotic effects within the bowel which contributed to the small blood pressure fall. Packed cell volume did not change in either the patients or normal subjects after glucose. 4. In the patients and normal subjects plasma insulin rose after glucose. Insulin levels were unchanged after xylose. Levels of pancreatic polypeptide and neurotensin, a potential vasodilator, rose in the patients only. The latter rose to a similar extent after both glucose and xylose, making it unlikely that neurotensin alone accounted for the hypotension. 5. These studies indicate that the carbohydrate components of a meal, and in particular those causing insulin release, contribute to postprandial hypotension in patients with autonomic failure.

Administration, Oral↗

PubMed1989

Prevention of glucose-induced hypotension by the somatostatin analogue octreotide (SMS 201-995) in chronic autonomic failure: haemodynamic and hormonal changes.

1. The haemodynamic and hormonal changes following glucose ingestion (1 g/kg) were determined before and after pretreatment with either placebo or the somatostatin analogue, octreotide (SMS 201-995, 50 micrograms subcutaneously), in seven patients with chronic autonomic failure. 2. In the placebo phase, after glucose, there was a marked and prolonged fall in blood pressure with no change in cardiac index and peripheral blood flow. Plasma insulin and neurotensin levels increased, whereas glucagon, vasoactive intestinal polypeptide, noradrenaline and adrenaline levels were unchanged. 3. Octreotide transiently raised blood pressure and prevented glucose-induced hypotension. There were no changes in cardiac index or peripheral blood flow. Plasma insulin and neurotensin levels did not rise. Plasma glucose levels increased more slowly but reached a similar level to the placebo phase. 4. We conclude that in autonomic failure patients, glucose-induced hypotension was not accompanied by changes in cardiac index or peripheral blood flow, indicating a lack of compensation to probable splanchnic vasodilatation. The hypotension was prevented by the peptide release inhibitor, octreotide, with no change in cardiac index or in peripheral blood flow, suggesting an effect on the splanchnic vasculature, probably through inhibiting release of vasodilatatory pancreatic and gut peptides.

Adult↗

PubMed1989

Relationship between splanchnic vasodilation and postprandial hypotension in patients with primary autonomic failure.

The haemodynamic responses to a standard liquid meal were measured in patients with autonomic failure and in normal subjects. Resting superior mesenteric artery blood flow was similar in both groups, but mean supine arterial pressure and the superior mesenteric artery vascular resistance were higher in the patients with autonomic failure than in the normal subjects. After the meal there was a rise in superior mesenteric artery blood flow and a fall in superior mesenteric artery vascular resistance in both groups. Mean arterial blood pressure fell substantially after food in the patients with autonomic failure but not in the normal subjects. The basal heart rate, stroke distance and cardiac index were higher in the patients with autonomic failure, and rose significantly after the meal only in the normal subjects. Forearm blood flow fell and the vascular resistance rose after the meal in the normal subjects but not in the patients with autonomic failure. We conclude that superior mesenteric artery blood flow rose and superior mesenteric artery vascular resistance fell after the meal in the normal subjects and in the patients with autonomic failure. However, in the normal subjects the blood pressure was maintained by factors which include a rise in the heart rate and cardiac output. The lack of such compensatory changes probably accounts for postprandial hypotension in patients with autonomic failure.

Adult↗

PubMed1989

Angiotensin converting enzyme inhibition lowers blood pressure in patients with primary autonomic failure independently of plasma renin levels and sympathetic nervous activity.

The haemodynamic and neurohormonal responses to the angiotensin converting enzyme (ACE) inhibitor captopril were studied in 12 patients with primary autonomic failure; seven had multiple system atrophy and five had pure autonomic failure. Basal supine mean arterial blood pressure was higher in the patients with multiple system atrophy than in those with pure autonomic failure and the normal subjects. Basal plasma noradrenaline levels were normal in the patients with multiple system atrophy, but lower in those with pure autonomic failure. Captopril lowered the mean arterial pressure in the patients with multiple system atrophy and pure autonomic failure but not in the normal subjects. In the patients with multiple system atrophy and pure autonomic failure, captopril lowered the cardiac output and the stroke volume. Forearm vascular resistance was unchanged. No significant changes occurred in the normal subjects. Plasma renin activity was unchanged after captopril in the patients with autonomic failure, but rose in the normal subjects. Plasma noradrenaline was unchanged in all groups after the administration of captopril. We conclude that captopril lowers the mean arterial pressure in patients with multiple system atrophy and pure autonomic failure. After the administration of captopril there is a reduction in cardiac output, secondary to a fall in stroke volume. The vasodepressor response to captopril in patients with autonomic failure is not related to the basal level of plasma renin activity or sympathetic nervous activity, indicating that the hypotensive effects of bradykinin or prostaglandins, or both, may contribute.

Adult↗

PubMed1989

The haemodynamic and hormonal responses after clonidine occur independently of sedation in essential hypertension.

1. To investigate the contribution of sedation to the cardiovascular effects induced by clonidine, we studied patients with essential hypertension on two separate occasions when similar levels of sedation were induced by clonidine and nitrazepam. 2. After clonidine, there was a fall in blood pressure, heart rate, digital skin vascular resistance and plasma noradrenaline which is consistent with its ability to reduce sympathetic outflow. Dissociation of the circulatory/neurohormonal and sedative responses after clonidine indicated that sedation alone is not an important factor in the blood pressure lowering effect of clonidine. 3. The absence of a fall in blood pressure, heart rate, digital skin vascular resistance and plasma noradrenaline after nitrazepam further suggest that sedation did not influence the hypotensive response in essential hypertension.

Adult↗

PubMed1989

Investigation of the central sites at which morphine acts to cause hypertension in conscious rabbits.

1. In conscious rabbits intracerebroventricular (i.c.v.) morphine (10 and 50 micrograms kg-1) caused a dose-related increase in plasma noradrenaline and adrenaline, respiratory depression and sedation. The increase in sympatho-adrenal outflow resulted in hypertension accompanied by bradycardia and the increase in adrenaline secretion caused hyperglycaemia. Morphine (1 microgram kg-1 i.c.v.) and i.c.v. saline had no effect. 2. The same doses of morphine given intracisternally (i.c.) caused bradycardia and a similar degree of respiratory depression to i.c.v. morphine, but no significant increase in blood pressure and only a small, gradual rise in plasma adrenaline. 3. Intravenous naloxone (1 mg kg-1) did not block the hypertension, hyperglycaemia or increase in plasma catecholamines that followed i.c.v. morphine, but prevented the respiratory depression and sedation. 4. Ganglionic blockade with pentolinium prevented the rise in plasma catecholamines, blood pressure and plasma glucose induced by i.c.v. morphine. 5. These findings demonstrate that the increased sympathoadrenal outflow following i.c.v. morphine results from an action on periventricular structures. The resultant increase in plasma catecholamines, which is largely naloxone resistant, accounts for the hypertension and hyperglycaemia. The bradycardia is probably partly baroflex mediated and partly due to an increase in vagal tone as a result of stimulation of brainstem opioid receptors. The respiratory depression is probably due to an action of morphine on brainstem opioid receptors.

Animals↗

PubMed1989

Differential cardiovascular and respiratory responses to central administration of selective opioid agonists in conscious rabbits: correlation with receptor distribution.

1. The effects of intracerebroventricular (i.c.v.) and intracisternal (i.c.) administration of a range of doses (0.01, 0.1 and 1.0 nmol kg-1) of specific mu- delta- and kappa-opioid agonists on cardiovascular and respiratory function and on plasma catecholamines have been studied in conscious rabbits. The distribution of mu- delta- and kappa-opioid receptors was localized in rabbit brain by in vitro autoradiography. 2. The mu-agonist [D-Ala2, MePhe4-Gly5-ol]enkephalin (DAGOL) given i.c.v. caused a large rise in plasma noradrenaline and adrenaline, hypertension accompanied by an initial bradycardia followed by tachycardia, respiratory depression and sedation. After i.c. administration there were similar changes in heart rate (HR) and respiration, but no significant changes in mean arterial pressure (MAP) or plasma catecholamines. 3. The delta-agonist [D-Pen2.5]enkephalin (DPDPE) increased MAP and HR after both i.c.v. and i.c. administration, caused a small increase in noradrenaline but had no effect on adrenaline and did not alter respiration rate or blood gases. After i.c.v. DPDPE the rabbits became more alert and active. 4. The kappa-agonist U69593 given i.c.v. or i.c. had no effect on MAP or HR. After i.c.v. U69593, PaCO2 fell, but there were no other respiratory effects. The responses to dynorphin 1-13, an endogenous kappa-agonist, were similar to those of U69593. 5. The opioid antagonist naloxone (30 nmol kg-1) given intravenously (i.v.) blocked the effects of i.c.v. DAGOL (1 nmol kg-1). A 100 fold higher dose of i.v. naloxone (3 mumol kg-1) was required to abolish the effects of i.c.v. DPDPE (1 nmol kg-1). 6. Autoradiographic studies demonstrated a high density of mu- and delta-opioid receptors in hypothalamic sites. In the brainstem mu-receptors were demonstrated in the nucleus tractus solitarius (NTS) and delta-receptors in the dorsal motor nucleus of the vagus. kappa-Receptors were not detected in either the hypothalamus or brainstem. 7. These findings demonstrate that DAGOL increases sympatho-adrenal outflow, probably by stimulation of hypothalamic mu-receptors. The effects on HR are probably partly through a baroreflex and partly through an action of DAGOL on mu-receptors in the dorsal motor nucleus of the vagus. DPDPE probably acts on delta-receptors in the NTS to increase MAP and HR. Respiratory depression resulted from stimulation of mu-receptors in the brainstem with no evidence of delta- or kappa-receptors being involved.

Animals↗

PubMed1989

The peptide release inhibitor, Octreotide (SMS 201-995), prevents the haemodynamic changes following food ingestion in normal human subjects.

We have determined the haemodynamic responses to a balanced liquid meal in eight normal subjects, before and after administration of the somatostatin analogue, Octreotide (SMS 201-995), which inhibits the release of gastrointestinal peptides. In the absence of Octreotide ingestion of the meal caused a marked increase in superior mesenteric artery (SMA) blood flow. Blood pressure was maintained, presumably by a compensatory rise in cardiac output and forearm vascular resistance. After Octreotide there was a fall in SMA blood flow alone, with no further changes after food ingestion. We conclude that Octreotide prevents the haemodynamic changes following food ingestion, probably by inhibiting the release of those gastrointestinal peptides that induce splanchnic vasodilatation.

Adult↗

PubMed1989

The effect of orthostatic hypotension on cerebral blood flow and middle cerebral artery velocity in autonomic failure, with observations on the action of ephedrine.

Cerebral blood flow (CBF) and middle cerebral artery velocity (MCAv) have been measured using 133xenon washout and transcranial Doppler in ten patients with autonomic failure. Four pure autonomic failure and four multiple system atrophy patients behaved similarly: tilting them sufficiently to induce significant orthostatic hypotension without causing syncopal symptoms led to a significant fall in their mean MCAv, but no change in their mean CBF. These findings suggest that cerebral autoregulation is preserved in autonomic failure, orthostatic hypotension resulting in a reactive vasodilatation which lowers MCAv, reduces vascular resistance, and maintains CBF. Ephedrine helped to correct the orthostatic hypotension, but had no direct effect on CBF. Two siblings with orthostatic hypotension secondary to dopamine-beta-hydroxylase deficiency also had preserved cerebral autoregulation, but ephedrine led to paradoxical hypotension in these patients.

Adult↗

PubMed1989

N-3-[18F]fluoropropylputrescine as potential PET imaging agent for prostate and prostate derived tumors.

A potential PET imagining agent for prostate and prostate derived tumors, N-3-[18F]fluoropropylputrescine, has been prepared. The radiochemical yield was 7-10% at end-of-synthesis (EOS) and the specific activity was greater than 1.1 Ci/mumol (overall synthesis time was 1.5 hr). In vivo biodistribution in mature male rats showed high prostate uptake. In rats that were pretreated with alpha-difluoromethylornithine and dihydrotestosterone propionate, the prostate to muscle ratio and prostate to blood ratio increased significantly. This high target uptake and target to nontarget ratio indicates the potential of this compound as a prostate imaging agent.

Animals↗

PubMed1989

Pharmacodynamics and pharmacokinetics of the oral antispastic agent tizanidine in patients with spinal cord injury.

The efficiency and duration of action of a single oral dose (8 mg) of tizanidine in patients with spinal cord injuries were determined by studying its antispastic, cardiovascular and sedative effects along with its pharmacokinetic profile in five tetraplegic and five paraplegic patients. After the administration of tizanidine, there was a reduction in spasticity in both groups within half an hour, with the effects lasting for 3 to 4 hours. There was no rebound increase in blood pressure. There was a greater increase in sedation in the tetraplegics than in the paraplegics. Plasma tizanidine levels rose within half an hour after dosing and peaked at one hour. The levels had fallen to 15 percent by 6 hours. The plasma half-life was 2.7 +/- 0.06 hours. We conclude that oral tizanidine has antispastic effects in patients with spinal cord injuries without affecting the power of non-involved muscle groups. It has minimal effects on blood pressure and it lowers heart rate. Side effects include sedation and dryness of mouth.

Administration, Oral↗

PubMed1989

Kinetics of copper-PTSM in isolated hearts: a novel tracer for measuring blood flow with positron emission tomography.

Copper(II) pyruvaldehyde bis(N4-methylthiosemicarbazone) ([Cu]PTSM) has shown potential as a flow tracer and can be labeled with the generator-produced positron emitting radionuclide 62Cu as well as with other copper radioisotopes. To define the myocardial handling of [Cu]PTSM, the externally detected single pass extraction and retention of [67Cu]PTSM was characterized after bolus administration in 12 isolated rabbit hearts perfused with erythrocyte-enriched modified Krebs-Henseleit buffer which permitted physiologic flow rates. The myocardial residual (extraction) fraction at control flow rates (approximately 1.5 ml/g/min) was 45 +/- 7(s.d.)% (n = 12), and was invariate with ischemia (flow = 0.15 ml/g/min, n = 4), hyperemia (flow = 3 ml/g/min, n = 4) or with hypoxia induced by perfusion at control flow rates with hypoxic buffer (n = 4) (residual fraction 45 +/- 20, 43 +/- 8, and 49 +/- 8%, respectively, p = N.S.). Once extracted, the tracer was retained with a biologic t1/2 of greater than 3600 min in all groups. The high single-pass extraction, which is not influenced by flow, and the prolonged retention of this tracer under diverse conditions indicate that [Cu]PTSM could be a useful tracer for measuring blood flow with positron emission tomography.

Animals↗

PubMed1988

Targeting radiopharmaceuticals: comparative biodistribution studies of gallium and indium complexes of multidentate ligands.

New multidentate ligands with structures similar to N,N'-bis[2-hydroxybenzyl]ethylenediamine-N,N'-diacetic acid (HBED) and N,N'-bis(pyridoxyl)ethylenediamine-N,N'-diacetic acid (PLED) were synthesized. The in vitro lipophilicity, electrophoretic behavior, and the in vitro biodistribution were studied for the 111In- and 67, 68Ga-complexes of N,N'-bis(2-hydroxy-3,5-dimethylbenzyl)ethylenediamine-N,N'-diacetic acid (Me4HBED); N,N'-bis(5-t-butyl-2-hydroxy-3-methylbenzyl)ethylenediamine-N,N'-diac eti c acid (t-butyl HBED); N,N'-bis[2-hydroxy-5-sulfobenzyl)ethylenediamine-N,N'-diacetic acid (SHBED); N,N'-bis(2-hydroxy-3,5-dimethylbenzyl)ethylenediamine-N-(2-hydroxyethyl) -N'-acetic acid (HBMA); and N,N'-bis(5-deoxypyridoxyl)ethylenediamine-N,N'-diacetic acid (DPLED). The biodistribution of the radiometal complexes were carried out in rats and an imaging study was performed in a non-human primate. The rapid clearance of the lipophilic complexes from blood and through the hepatobiliary system was easily demonstrated; as well, the hydrophilic complexes were cleared rapidly through the urinary tract. Positron emission tomographic images were generated from a study in a primate after administration of 68Ga-t-butyl HBED. These images well demonstrate the efficient liver accumulation and rapid hepatobiliary clearance (less than 1 h) and well differentiate images of the liver and gall bladder.

Animals↗

PubMed1988

N-(3-[18F]fluoropropyl)-spiperone: the preferred 18F labeled spiperone analog for positron emission tomographic studies of the dopamine receptor.

The ligands currently used for PET studies of the dopamine receptor are fluorine-18-labeled spiperone (FSp) and carbon-11 or fluorine-18-labeled N-methyl-spiperone. All three of these ligands have drawbacks in either their chemical preparation or their biological behavior. We have previously prepared a series of N-fluoroalkyl-spiperone derivatives which are simple to prepare in high radiochemical yield. N-[18F]fluoropropyl-spiperone (3-F-Pr-Sp) and N-[18F]fluoroethyl-spiperone (2-F-Et-Sp) were the most promising ligands. In vitro competitive binding studies showed affinities for the dopamine receptor of 3-F-Pr-Sp greater than FSp greater than 2-F-Et-Sp. Brain extraction studies in a primate model showed that FSp, 2-F-Et-Sp, and 3-F-Pr-Sp were not completely extracted by the brain. High bone uptake and kidney clearance was observed with 3-F-Pr-Sp, while 2-F-Et-Sp cleared through the intestine in rats. This is in contrast to FSp where clearance is through the kidney. Studies to evaluate the extraction of metabolites in the brain were carried out by administering large doses (10 mCi) of FSp, 2-F-Et-Sp and 3-F-Pr-Sp to rats and reinjecting the metabolites in blood into other rats. These experiments showed that less than 0.02% of the metabolites from FSp and 3-F-Pr-Sp entered the brain, while 0.5% of the metabolites from 2-F-Et-Sp entered the brain. The majority of the activity present in the cerebellum after the administration of 2-F-Et-Sp is metabolites; therefore 2-F-Et-Sp is unsuitable for PET imaging studies. PET imaging studies in baboons and in one normal human volunteer with 3-F-Pr-Sp showed a high striatum-to-cerebellum ratio, showing that 3-F-Pr-Sp can replace ligands currently in use to study dopamine receptors.

Animals↗

PubMed1988

21-[18F]fluoro-16 alpha-ethyl-19-norprogesterone: synthesis and target tissue selective uptake of a progestin receptor based radiotracer for positron emission tomography.

We have synthesized 21-[18F]fluoro-16 alpha-ethyl-19-norprogesterone (FENP), a high affinity ligand for the progesterone receptor, labeled with the positron-emitting radionuclide fluorine-18 (t1/2 = 110 min). The synthesis proceeds in two steps from 21-hydroxy-16 alpha-ethyl-19-norprogesterone and involves [18F]fluoride ion displacement of the 21-trifluoromethanesulfonate (21-triflate). This material is purified by HPLC and is obtained in 4-30% overall yield (decay corrected) within 40 min after the end of bombardment to produce [18F]fluoride ion. The effective specific activity, determined by competitive radioreceptor binding assays, is 700-1400 Ci/mmol. In vivo, [18F]FENP demonstrates highly selective, receptor-mediated uptake by the uterus of estrogen-primed rats; the uterus to blood and uterus to muscle ratios were respectively 26 and 16 at 1 h and 71 and 41 at 3 h after injection. The high target tissue selectivity of this uptake suggests that this compound may be useful for the in vivo imaging of progestin target tissues and receptor-rich tumors (such as human breast tumors) by positron emission tomography.

Animals↗