PubMed Health⌕ Search

Biomedical subjects

C M Cottrill

Publications and source records attributed to C M Cottrill.

At least 19 recordsLinked to original sources
PubMed1991

Effects of placental pathology on maternal plasma progestagen and mammary secretion calcium concentrations and on neonatal adrenocortical function in the horse.

Between 1985 and 1990, 25 Thoroughbred mares were classified as having an abnormal pregnancy on the basis of precocious signs of impending parturition. Throughout the remainder of their pregnancies, plasma progestagen and mammary secretion calcium concentrations were monitored. After parturition, evidence of placental pathology was recorded and their foals were assessed with regard to adrenocortical function and behaviour. Seven pony mares were used to establish a model of placental pathology and, following induced placental separation, were subjected to the same protocol. Control animals consisted of 35 Thoroughbred mares and 39 pony mares, all considered to have normal pregnancies. Of the 25 abnormal mares, 16 had precociously increased plasma progestagen concentrations, 17 had precociously increased mammary calcium concentrations and 24 had an abnormal placenta. Eighteen live foals resulted, of which 11 appeared abnormal on the basis of behaviour. Adrenocortical function was assessed in 13; 4 had normo- and 3 hypofunction and 6 were intermediate. These results were independent of gestational age at delivery. Of 13 foals examined for plasma progestagens, 7 had normal and 6 abnormal concentrations. Following placental separation in the pony mares, maternal plasma progestagen concentrations increased in 4 of the 7 mares within 4-11 days and in 1 after 42 days; there was placental pathology in 3 of these mares, 1 of which aborted at 287 days gestation. There was no increment in progestagens in the remaining 2 mares, which aborted at 240 days and 271 days. It was concluded that placental dysfunction may be diagnosed from early plasma progestagen increments prior to 308 days gestation; and that foals that survive birth in these circumstances may be physiologically immature but often have normal or intermediate adrenocortical function, irrespective of gestational age. This is in contrast to foals born prematurely without maternal plasma progestagen or mammary secretion calcium increments.

Adrenocorticotropic Hormone↗
PubMed1991

The placenta as a determinant of fetal well-being in normal and abnormal equine pregnancies.

One hundred twenty-four horse placentas were evaluated according to gross appearance, weight and surface area. Grossly abnormal placentas were photographed, and histological sections were taken from abnormal appearing areas, and from representative areas (pregnant horn, non-pregnant horn, body and cervical pole) in both normal and abnormal placentas. Information about the resulting foals was obtained and correlations examined. Histological sections were reviewed and related to the resulting foals. Four normal fresh placentas were infused with dyes to ascertain the blood supply to various areas. Foal weight was statistically related to both allantochorionic surface area and allantochorionic weight. When normal placental surface area was divided by foal weight and related to gestational age, a statistical (P less than 0.0001 and r = 0.829) relationship emerged. Long cords were seen frequently with fetal demise. Histological abnormalities in the placenta were highly associated with fetal demise or fetal abnormalities, with only 2 normal Thoroughbred foals resulted from the 23 placentas exhibiting abnormal histology. Among the ponies, the same relationship held, with 3 normal ponies delivered from 9 abnormal placentas. Normal placentas were associated with normal offspring in most cases. Perfusion studies indicated that, in the four placentas studied, one umbilical artery supplied the cervical area and the non-pregnant horn, whereas the other supplied the pregnant horn. The body had a mixed supply from both arteries. This study evaluated the feto-placental unit in terms of normal and abnormal measurements and histology related to foal outcome. The presence of abnormal histological appearance of the placenta appeared to be more closely associated with foal abnormality than the percentage of placental area involved in the abnormal process. More information is needed before placental blood supply can be related to abnormal processes.

Animals↗
PubMed1990

Iodine-123-HIPDM lung imaging in pulmonary vein-banded pulmonary hypertension.

To evaluate the use of N,N,N'-trimethyl-N,-[2-hydroxy-3-methyl-5 iodobenzyl-1, 3 propanediamine iodine-123 (HIPDM) in lung imagings for the diagnosis of individual pulmonary vein stenosis, 14 single-pulmonary vein-banded rats underwent lung imaging. After i.v. injection of 250-300 microCi [123I]HIPDM lung images were recorded at 2 min by a gamma camera interfaced with a PDP computer. Banded lung demonstrated higher [123I]HIPDM radioactivity than that of nonbanded lungs. The activity ratio of banded-to-nonbanded lungs ranged from 4.0 to 1.22 (average 1.62). Technetium-99m-macroaggregated albumin (MAA) lung images showed decreased perfusion in banded lung, and normal perfusion in the nonbanded lung. Postmortem microscopic changes in pulmonary arteries and veins were compatible with the elevated pulmonary artery and venous pressure in vein-banded lung. Whether the high uptake of [123I]HIPDM in banded lungs relates to endothelial receptors for HIPDM is unknown. Nevertheless, the finding of high lung uptake in banded lung in [123I]HIPDM lung imaging may be potentially used to diagnose individual pulmonary vein stenosis.

Animals↗
PubMed1988

Ventriculocoronary connections in hypoplastic right heart syndrome: autopsy serial section study of six cases.

Myocardial sinusoids communicating with the coronary systems occur in pulmonary atresia with intact ventricular septum. To test the hypothesis that the extent of ventriculocoronary connections correlates with the degree of right ventricular outflow obstruction as evidenced by clinical, angiographic and gross anatomic findings, a serial section study of six human autopsy hearts representing a spectrum of hypoplastic right heart was undertaken. Slides were evaluated for the presence and extent of ventriculocoronary connections, associated developmental abnormalities and secondary changes in the ventricular walls. Whereas extensive blind-ended deep sinusoids were a feature of all five cases with unrelieved obstruction, ventriculocoronary connections were identified in three. Changes that suggested ongoing remodeling provide new evidence for the postnatal temporal evolution of these anomalous communications. The regional distribution of myofiber disarray in hypoplastic right heart supports the concept that vascularization parallels myocardial organization in the developing human heart.

Coronary Vessels↗
PubMed1988

Echocardiographic detection of pulmonary hypertension in anesthetized rats.

Evaluation of pulmonary arterial pressure in small laboratory animals requires surgical catheter implantation. However, even this modest surgical procedure is known to retard weight gain, alter various biochemical parameters and may exert other deleterious actions which could complicate data interpretation. To obviate these adverse effects of surgery and to permit better staging of experimental procedures, a method for non-invasive detection of pulmonary hypertension would be desirable. The present study examined the utility of m-mode echocardiography to detect increased pulmonary arterial pressure and right ventricular hypertrophy in rats with monocrotaline-induced pulmonary hypertension. At various times after administration of monocrotaline (105 mg/kg), rats were anesthetized lightly with sodium pentobarbital (30 mg/kg) and m-mode echocardiograms were generated using a 7 mHz transducer with the animals in the supine position. Mean pulmonary arterial pressure was then determined by closed-chest catheterization of the pulmonary artery. At sacrifice, the extent of right ventricular hypertrophy was determined as the ratio of the weight of the right ventricular free wall to that of the left ventricle plus septum. Right ventricular systolic time intervals, determined from the echocardiogram, correlated significantly with the extent of right ventricular hypertrophy (p = 0.05; r2 = 0.39) but not with mean pulmonary arterial pressure (p = 0.2; r2 = 0.14). Echocardiography may provide a simple, non-invasive means to detect cardiopulmonary abnormalities in rats and may thus be useful in staging subsequent experimental procedures without need for prior surgical catheter implantation.

Animals↗
PubMed1987

Parental genetic contribution to mode of presentation in Pompe disease.

Echocardiograms were performed on parents of five infants with Pompe disease (glycogen storage disease, type II). Three of the infants had presented with congestive cardiomyopathy and two with dynamic muscular subaortic stenosis. No heart murmurs were audible in any of the parents of the five infants. The parents of the three infants without left ventricular outflow tract obstruction had normal echocardiographic results, whereas one parent of each of the infants with left ventricular outflow obstruction had asymmetric septal hypertrophy. The association between left ventricular outflow obstruction and parental asymmetric septal hypertrophy suggests that both septal hypertrophy and glycogen storage disease were inherited by these two infants.

Cardiomyopathy, Hypertrophic↗
PubMed1986

Ventricular septal defect with mobile tricuspid valve pouch mimicking tetralogy of Fallot.

A newborn with partial deletion of the long arm of chromosome six presented with cyanosis at birth. Initial studies suggested the diagnosis of tetralogy of Fallot and the infant underwent a Waterston shunt procedure with subsequent clinical improvement. The infant subsequently died of unrelated causes. Autopsy revealed a ventricular septal defect and a dysplastic pouchlike structure related to an anomalous tricuspid valve leaflet which obstructed right ventricular outflow. Classical anatomic findings of tetralogy of Fallot were absent. Clinical and echocardiographic findings that would be expected to aid early diagnosis of future cases are presented.

Cardiac Catheterization↗
PubMed1985

Anomalous left coronary artery from the pulmonary artery: significance of associated intracardiac defects.

Two patients with anomalous origin of the left main coronary artery from the pulmonary artery had an associated defect (one, critical pulmonary stenosis; the other, ventricular septal defect). They presented with signs and symptoms of the associated defect and the coronary anomaly was unrecognized. Both cases at autopsy lacked the usual large right coronary artery seen with this anomaly. The pathophysiologic features of the combined defects are described, their differences from the isolated anomaly are noted and their relation to surgery is discussed.

Abnormalities, Multiple↗
PubMed1985

Supravalvular aortic stenosis. Clinical and pathologic observations in six patients.

Supravalvular aortic stenosis with a mean pressure gradient of 101 mm Hg was encountered in six patients aged 1 1/2 to 12 years. Three patients had Williams syndrome. In two other patients the stenosis was familial. The angiographic/anatomic subtype of deformity was hourglass in four patients, diffuse in one, and membranous in one. Four patients are alive following successful surgical repair; the other two died without surgery. Microscopically, disorganized medial elements with fibrotic intima sometimes containing lacunae were observed in five cases; the one other had valvelike tissue only. Ultrastructurally, thick irregular elastic fibers, abundant swirling collagen, hypertrophied smooth-muscle cells, and scant ground substance characterized the medial tissue defect. Although hemodynamics during intrauterine development may predispose to localization of the stenosis to the supra-aortic valvar region, the cause for the mural dysplasia remains uncertain.

Adult↗
PubMed1977

Propranolol therapy during pregnancy, labor, and delivery: evidence for transplacental drug transfer and impaired neonatal drug disposition.

The administration of 160 mg of propranolol during pregnancy, labor, and delivery was associated with profound hypoglycemia and respiratory depression in a newborn infant. The neonate's plasma propranolol level rose from 40 ng/ml at the time of birth to 90 ng/ml four hours later. This increase in plasma propranolol concentration might be due to redistribution of the drug in the neonate as well as to different elimination mechanisms than in adults. The elevated propranolol level four hours after delivery was not associated with any signs or symptoms of drug toxicity, but drug effect was apparent on the electrocardiogram. The administration of propranolol during pregnancy in doses capable of producing therapeutic maternal blood levels may be dangerous to the neonate.

Adult↗