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Biomedical subjects

J R Henderson

Publications and source records attributed to J R Henderson.

At least 37 records · Page 2Linked to original sources
PubMed1985

A morphometric study of the endocrine and exocrine capillaries of the pancreas.

In passing from islets to the exocrine part of the gland, pancreatic capillaries change their character. Islet capillaries are significantly wider than exocrine (5.27 micrometers, diameter compared with 4.35 micrometers), thinner walled and have many more fenestrations micrometers-1 of endothelium (1.3 compared with 0.13). The point of transition at the edge of the islet is very abrupt, for capillaries that are in contact with both endocrine and exocrine tissue ('edge capillaries') have significantly more fenestrae on the side facing the endocrine cells than the side facing exocrine (1.46 fenestrae micrometers-1 compared with 0.3 micrometers-1). The structure of these edge capillaries suggests that the factors operating to induce the formation of fenestrae do so over extremely short distances. The relationship between fenestrations, the high blood flow and high water flux seen in endocrine glands is discussed.

Animals↗
PubMed1980

The arrangement of endocrine and exocrine pancreatic microcirculation observed in the living rabbit.

1. The microcirculation of the pancreas in the anaesthetized rabbit was examined by in vivo microscopy and micro-cinephotography. 2. The islets of Langerhans were identified by their appearance following the systemic injection of diphenylthiocarbazone. 3. Arterial injection of Evans blue demonstrated the arrangement of vessels within the pancreas. Blood leaving the islets passed via capillaries into the capillary meshwork; no islet was ever seen to be drained directly by a vein. 4. This significance of this portal arrangement is discussed.

Animals↗
PubMed1979

A comparative study of the portal vessels connecting the endocrine and exocrine pancreas, with a discussion of some functional implications.

We have examined the pattern of the capillaries of the pancreas in rabbits, rats, mice, guinea-pigs, cats and baboons, using arterial and venous injections of Berlin blue. In all these species we found extensive, direct connexions between the capillary beds of the islets and the exocrine tissue of the gland, forming a highly developed portal system. Some of the functional implications of these vascular connexions are discussed, particularly the influence of the islet hormones insulin, glucagon and somatostatin upon the exocrine cells.

Animals↗
PubMed1978

Portal circulations and their relation to counter-current systems.

We have reviewed the distribution of portal circulations throughout the animal body; they are commoner than is generally supposed. Most portal circulations consist of two serial capillary beds connected by one or more larger vessels. We have called these 'convergent' portal circulations: examples are hepatic portal, placental, hypophysial, renal, ovarian and testicular circulations, as are parts of the lymphatic circulation. A second type of portal circulation, which is less common, consists of two serial capillary beds that are not connected by larger vessels. These we have called 'continuous' portal circulations: adrenal and pancreatic circulations are examples of this type. When a countercurrent concentrating mechanism exists in the body it is always part of the primary or secondary bed of a convergent portal circulation, though some convergent portal circulations are not associated with countercurrent mechanisms.

Adrenal Glands↗
PubMed1976

The effect of atropine on the insulin release caused by oral and intravenous glucose in human subjects.

Oral and intravenous glucose tolerance tests were performed on normal fasting subjects, with and without atropine. Insulin release after oral glucose was significantly diminished by atropine, and this effect could not be ascribed to the drug delaying glucose absorption. However, insulin release brought about by intravenous glucose was not altered by atropine. Possible interpretations of these results are discussed.

Administration, Oral↗
PubMed1975

Congenital hypothyroidism--signs and symptoms in the newborn period.

Infants with athyrotic hypothyroidism usually manifest signs and symptoms of hypothyroidism prior to or during the period in the newborn nursery. These features are variable and include: prolonged gestation with large size at birth, large posterior fontanel, respiratory distress, hypothermia, peripheral cyanosis, hypoactivity, poor feeding, lag in onset of stooling, abdominal distension with vomiting, protracted icterus, and/or edema. Retrospective assessment of newborn nursery records of three infants from the Collaborative Perinatal Project who were subsequently found to have congenital hypothyroidism disclosed that they had six, eight, and nine, respectively, of these features while in the newborn nursery. Evaluation of newborn records on 12 other infants, often less complete, who were later found to have congenital hypothyroidism disclosed that each infant had from one to seven of these signs and symptoms, with an average of 3.2 per infant. Thus the most important period for clinical consideration of athyrotic hypothyroidism is in the newborn nursery to initiate early thyroid replacement therapy in affected infants.

Birth Weight↗
PubMed1975

The effect of atropine on insulin release caused by intravenous glucose in the rhesus monkey.

Glucose was given as a rapid intravenous injection to fasted anaesthetized rhesus monkeys, and the concentrations of blood glucose and plasma insulin were measured. Glucose caused a biphasic insulin response. The first phase (which was short) occurred 1 min after the injection; the second was longer, and occurred 17 to 30 min after the injection. Following the control glucose injection, each animal was given atropine, and the insulin response to an identical glucose stimulus was measured. This produced a mean reduction of 45% in the area under the curve of insulin release. Both phases of insulin release were inhibited by atropine. When glucose was given alone, its mean half-time of disappearance from the circulation (t1/2) was 25.4 ( plus or minus 1.9 SEM) min. After atropine the mean t1/2 was 36.6 (plus or minus 3.1 SEM) min, a significant difference. It is suggested that the delayed rate of disappearance of glucose from the circulation is the result of inhibition of insulin release by atropine.

Animals↗