Search PubMed⌕ Search

Biomedical subjects

R C Ritter

Publications and source records attributed to R C Ritter.

At least 109 records · Page 6Linked to original sources
PubMed1978

Feeding in response to insulin but not to 2-deoxy-D-glucose in the hamster.

Adult hamsters did not increase their food intake in response to subcutaneous injection of 2-deoxy-D-glucose (2DG) at doses of 50, 200, 350, 500, 750, 1,000, or 1,500 mg/kg. The failure to feed in response to 2DG was apparent regardless of time of testing and length of test. Hamsters did display marked hyperglycemia after 2DG treatment. Therefore, hamsters do detect and form neural responses to 2DG. In contrast to 2DG, injection of regular insulin, 2, 4, or 8 U/animal, caused hamsters to significantly increase their food intake over a 5-h test period. Furthermore, injection of 4 U of protamine zinc insulin twice daily also caused pronounced increases in food intake and weight gain by hamsters. Because hamsters do not seem to posses a feeding response to 2DG-induced glucoprivation, it seems unlikely that insulin elicits feeding via the glucoprivic control in this species. The results suggest that 1) hamsters lack the glucoprivic control of feeding behavior as exercised by 2DG, 2) 2DG and insulin treatments are not equivalent ingestive challenges, and 3) insulin-induced feeding may result in part from activation of a nonglucoprivic control of food intake.

Animals↗
PubMed1978

Glucoprivic feeding behavior in absence of other signs of glucoprivation.

When rats were denied immediate access to food after subcutaneous injection of 2-deoxy-D-glucose (2DG), the glucoprivically induced sympathoadrenal hyperglycemia subsided spontaneously within 6 h. However, if food was returned to the rats 6 h after 2DG injection, they still ate significantly more than after saline control injections. Rats injected with insulin also increased their feeding even when food was withheld until the animals had returned to normoglycemia. Injections of exogenous glucose sufficient to elevate blood glucose concentrations above normal failed to inhibit increased feeding observed when food was returned 6 h after injection of regular insulin. These data show that 2DG and insulin-induced feeding can occur in the absence of overt signs of glucoprivation and suggest that the glucoprivic control may be operable in the day-to-day control of feeding when other signs of glucoprivation are not readily observable.

Animals↗
PubMed1977

The physical basis of some urodynamic measurements.

This report concerns certain principles of physics that are relevant to the clinical practice of Urology as well as the research urodynamicist. Supplemental material is available in previous publications for the physiologist, cardiovascular, dynamicist, anesthesiologist and the like. The material is fairly recent only in its application to the lower urinary tract. Pressure-volume relationships were applied to be cardiovascular system more than 20 years age. Indeed, for those interested in urodynamic methods, there is a vast fund of useful pertinent information in the literature on vascular dynamics. The problems of steady and unsteady flow in flexible structures are common to both specialties. It would be unfortunate if urodynamicists were required to learn of the phenomena and their implications by the drudgery of repeated measurements rather than taking guidance from previous work. This report is intended to serve as an introduction to the approach and, hopefully, will stimulate those who are interested in urodynamic methods to seek out this information and to interpret their measurements in the light of fundamental physical phenomena that have been described and analyzed.

Biomechanical Phenomena↗
PubMed1977

Physical information in the external urinary stream of the normal and obstructed adult male.

The qualitative status of physical information contained in the stream of the male lower urinary tract is traced from the bladder to the broken-up external stream. The progression of modifications of this information is discussed and it is argued that information remains in the drops. Electro-optical measurements of the drops leads to pulses which can be analysed for various types of information content. These confirms that there is potential clinical value in some aspects of the information.

Humans↗
PubMed1975

Megestrol acetate in treatment of benign prostatic hypertrophy.

In this study we found no significant effect on benign prostatic hypertrophy due to megestrol using standard clinical criteria. However, there is evidence using urinary drop spectrometer data which makes one suspect that megestrol does have a positive effect. If there is an effect, it is apparently so small as to be undetectable using the clinical protocol of this investigation. Since the urodynamic evidence does indicate a possibility of a positive effect, it appears reasonable to investigate further using a different protocol - perhaps a higher dosage and/or a more controlled test population.

Clinical Trials as Topic↗
PubMed1975

Control of meal size by central noradrenergic action.

Previous investigations of central noradrenergic effects on food intake have concentrated on the use of high doses of noradrenaline (two to 200 times brain noradrenaline content). In this work we examined the effect of low doses of noradrenaline (not exceeding brain noradrenaline content) on the parameters of spontaneous ingestive behavior. By arranging for rats to trigger remote infusions of noradrenaline into their own anterior forebrains at the beginning of spontaneously initiated meals, meal size was very reliably increased more than 200% by doses of 0.015--0.37 nmol (2.5--62 ng of noradrenaline base) (n = 12). The effect was alpha-adrenergic. It was blocked by phentolamine but not by propranolol. Infusions of noradrenaline at the above doses, which nearly triple meal size, did not elicit eating when made during an intermeal interval, nor did they influence the length of the intermeal interval when made 60 min after the termination of an uninfused meal. These results show that noradrenaline increased food intake at doses less than 1% of the brain's endogenous noradrenaline content. Meal size is more susceptible to alteration by noradrenaline manipulations than is meal frequency. The brain's own noradrenergic system may function to sustain food intake once feeding is initiated. This function of brain noradrenaline may control spontaneous meal size.

Animals↗
PubMedDate not supplied

Cholecystokinin-induced suppression of locomotion is attenuated in capsaicin pretreated rats.

Cholecystokinin (CCK), a peptide found in both gastrointestinal endocrine cells and neurons, suppresses food intake and reduces locomotor behavior when injected systemically. Both the locomotor and ingestive effects of CCK are abolished by subdiaphragmatic vagotomy. Pretreatment of adult rats with capsaicin attenuates the reduced locomotor activity and reduced food intake which normally occurs following injection of exogenous cholecystokinin. Since capsaicin damages or destroys small-diameter, unmyelinated, sensory neurons, including vagal sensory fibers, these data support the interpretation that both CCK-induced suppression of food intake and CCK-induced reduction of locomotion are mediated by fine, unmyelinated sensory neurons.

Animals↗
PubMedDate not supplied

Capsaicin application to central or peripheral vagal fibers attenuates CCK satiety.

Capsaicin treatment destroys small primary sensory neurons including a subpopulation of vagal afferents. Intraperitoneal, fourth ventricular or perivagal application of capsaicin attenuated or abolished cholecystokinin (CCK)-induced suppression of food intake. Capsaicin applied to the thoracolumbar spinal cord or to the pyloric region of the stomach did not alter CCK-induced reductions of food intake. Intraperitoneal capsaicin treatment reduced substance P-like immunoreactivity (SPLI) in the spinal dorsal horn and parts of the dorsal hindbrain. SPLI depletion, therefore, served as a histochemical indicator of the spread of capsaicin from its site of application. Capsaicin applied directly to the vagal trunks did not reduce SPLI in the spinal cord or hindbrain. Intraventricular capsaicin reduced SPLI in the hindbrain but not in the spinal cord. These data indicate that localized capsaicin application attenuates CCK-induced suppression of food intake by impairing the function of either central or peripheral portions of vagal afferent neurons. The data also support the conclusion that intraperitoneal capsaicin attenuates CCK-induced suppression of feeding by impairing vagal sensory function.

Afferent Pathways↗