PubMed Health⌕ Search

Biomedical subjects

R C Ritter

Publications and source records attributed to R C Ritter.

At least 91 records · Page 5Linked to original sources
PubMed1983

Measuring softness of inner female urethra. Part I. Simple new device.

A new device is described to measure clinically the softness of the female urethra. It is a rod-shaped urethral sound with a longitudinal groove along its surface. The sound is constructed in sizes 12 to 24 French. Each has one groove which is 2 mm wide and either 2, 2.5, or 3 mm deep. The groove is 11 cm long. When inserted into the filled female bladder per urethram, the groove will span the urethra from the bladder to the outside. If the urethral inner lining is soft and deformable, it will fill itself into the groove and prevent leakage of urine from the bladder along the groove to the outside. If the urethra is relatively rigid, urine will leak from the bladder. This instrument permits testing of women to determine urethral properties in preventing leakage when studied with a range of probe sizes.

Elasticity↗
PubMed1983

Evaluation of inner urethral softness. Part II. Clinical study using new grooved probe device.

This study, in incontinent women, evaluates the effectiveness of a new device to measure properties of urethral softness. The device is a straight sound with a longitudinal groove cut along its surface. It is inserted through the urethra and into the bladder. A soft, deformable urethra is expected to fill itself into the groove and prevent the loss of urine from the bladder along the groove to the outside. Using this instrument it is learned that (1) postmenopausal women are less able to seal the urethra than younger ones; (2) as the urethra is stretched it is less able to form a seal; and (3) the anterior urethra is the weakest link in sustaining continence when tested by methods used in this program.

Adult↗
PubMed1983

Feeding elicited by 2-deoxyglucose occurs in the absence of reduced glucose oxidation.

We have previously reported that feeding in response to either systemic or intracerebroventricular administration of 2-deoxy-D-glucose (2-DG) persists for at least 6--8 h post-2-DG injection when the sympathoadrenal hyperglycemic response to glucoprivation has abated. This delayed feeding response to 2-DG suggests either that ongoing glucoprivation is not necessary for feeding or that responses such as hyperglycemia abate while glucoprivation is still extant and able to stimulate feeding. In order to determine whether glucoprivation is still present after the sympathoadrenal hyperglycemic response to 2-DG has abated, we measured systemic 14CO2 evolution and glucose oxidation in Sprague-Dawley rats treated with 2-DG (200 mg/kg) 0.5 and 6 h earlier. In addition, we measured cerebral 14C-2-DG accumulation in rats treated with unlabelled 2-DG 6 h prior to tracer administration We found that 14CO2 evolution and glucose oxidation were reduced by 47 and 667%, respectively, during the first 3.5 h post-2-DG but were normal by 6 h post-2-DG. Furthermore, we found that the uptake of 14C-2-DG into the brain was not diminished between 6 and 7 h after administration of unlabelled 2-DG. These results suggest that ongoing reduction of systemic glucose oxidation and ongoing impairment of hexose availability to the brain need not occur during 2-DG-induced feeding.

Animals↗
PubMed1982

Area postrema lesions increase drinking to angiotensin and extracellular dehydration.

The area postrema (AP) is a circumventricular organ of the caudal medulla oblongata. This structure lacks a blood brain barrier and contains high concentrations of angiotensin II (AII) receptors. Because AII is a participant in the arousal of thirst, we have examined the effect of AP lesions upon drinking in response to exogenous AII and in response to various thirst challenges. We have found that rats with AP lesions (APL) drink more water than control rats in response to isoproterenol and polyethylene glycol. Rats with AP lesions also drank two times as much water as controls in response to subcutaneous injection of exogenous AII. Ad lib water intakes of APL and control rats were not different. Furthermore, drinking in response to 21 hr water deprivation or cell dehydration did not differ for APL and control rats. Our results suggest that AP lesions selectively enhance extracellular thirst, especially the component of that thirst mediated by AII.

Angiotensin II↗
PubMed1981

Glucoreceptors controlling feeding and blood glucose: location in the hindbrain.

Microinfusion of 5-thioglucose into either the lateral or fourth cerebral ventricle caused increased feeding and hyperglycemia in rats when the cerebral aqueduct was unobstructed. If the aqueduct was obstructed and 5-thioglucose was infused into the fourth ventricle, increased feeding and hyperglycemia persisted, whereas feeding and hyperglycemia in response to lateral ventricle infusion were abolished. Drinking in response to infusion of angiotensin II into the lateral ventricle was not diminished by aqueduct obstruction. These results indicate that glucoreceptors that mediate feeding and hyperglycemia in response to cerebral glucoprivation are located in the caudal hindbrain and not in the hypothalamus where they have previously been sought.

Animals↗
PubMed1981

Ablation of the area postrema causes exaggerated consumption of preferred foods in the rat.

The area postrema (AP) is a hindbrain circumventricular organ (CVO) with apparent chemoreceptive function. The AP has demonstrated neural and vascular connections with the nucleus of the solitary tract (SOL), a structure which receives the primary visceral afferents from the oral cavity and gastrointestinal tract. The anatomical structure and connections of the AP suggests a potential role for this CVO in the control of feeding behavior. We have found that rats with surgically produced AP lesions consumed the same amounts of pelleted food ad libitum as control rats. Lesioned and control rats also consumed equal amounts of lab chow after 21 h food deprivation. However, when presented with a preferred food (instant breakfast or cookies), AP-lesioned rats consumed at least double the amount consumed by control rats. It is possible that AP lesions impair sensitivity to satiety cues. However, lesion rats did decrease their instant breakfast intake in response to cholecystokinin injections or gastric preloads. Furthermore, overingestion by AP-lesioned rats occurred only in response to preferred (highly palatable) foods and not in response to lab chow. Lesioned rats rejected quinine-adulterated instant breakfast at the same adulterant concentration as controls. Therefore, the lesioned rats do not suffer from ageusia or from enhanced responsiveness to bitter taste. Rather, the selective overeating by AP-lesioned rats may reflect an enhanced behavioral response to the sensory qualities of normally preferred foods. The close association of the AP with the SOL provides a neuroanatomical avenue by which a putative AP-chemoreceptor could alter the quality or intensity of information arriving via the taste afferents. Such tuning of gustatory mechanisms could be an important component of ingestive control.

Animals↗
PubMed1981

Mechanical factors and tissue stresses in chronic hydronephrosis.

From 21 dogs kidneys removed at 0, 1, 2, and 4 weeks after ureteral blockage we found the expected early increase, than subsequent decrease, in pressure and the expected continuing increase in volume and thinning of the walls. However the calculated wall stress builds up continuously with time as does the elastic modulus of the wall. By the 4th week, the wall material has become approximately 3 times as resistant to stretch as the normal ureter.

Animals↗
PubMed1981

Sympathoadrenal and adrenal hormonal responses of newborn calves to hypothermia.

Seventeen newborn Holstein-Friesian bull calves were cold-stressed by total body immersion in water at 15 to 17 degrees C until the core body temperature was lowered by 10 degrees C. Nine additional calves (noncold-stressed) were immersed in water at 35 to 37 degrees C. Eight of the cold-stressed calves were euthanatized soon after removal from the water while the others (n=9) were allowed to recover in a cold room at 4 degrees C for 72 hours. Noncold-stressed calves were kept at 25 degrees C for 72 hours. Sympathoadrenal an adrenal hormonal responses of calves were determined by analysis of plasma for glucose, corticosteroids, and catecholamines. Plasma concentration of glucose and corticosteroids rapidly increased in cold-stressed calves soon after immersion and remained higher (P less than of equal to 0.05) than concentrations in noncold-stressed calves during immersion and most of recovery. There was a threefold increase (P less than or equal to 0.05) in concentration of catecholamines in plasma of cold-stressed calves and only a slight increase in noncold-stressed calves during immersion. Catecholamine concentrations remained elevated in cold-stressed calves during most of recovery. Results provide direct evidence that sympathoadrenal and adrenal hormonal responses to cold are well developed in newborn calves and that changes in concentrations of glucose, corticosteroids, and catecholamines in plasma of these animals are sensitive indicators of their ability to respond to cold stress.

Adrenal Cortex Hormones↗
PubMed1980

Increased feeding and hyperglycemia elicited by intracerebroventricular 5-thioglucose.

5-Thioglucose (5-TG) is a glucose analogue in which sulfur is substituted for the pyranose ring oxygen. Intracerebroventricular infusion of 5-TG caused prompt initiation of feeding and a marked rise in plasma glucose concentration at doses as low as 0.54 mumol (106 microgram). 5-TG is, therefore, more potent for eliciting feeding than any other previously tested glucose antimetabolite. The potency of 5-TG for eliciting feeding should make 5-TG a useful tool for localizing brain glucoreceptors which participate in the control of food intake.

Animals↗
PubMed1980

Intracerebroventricular 2-DG causes feeding in the absence of other signs of glucoprivation.

Intracerebroventricular (ICV) infusions of 2-deoxy-D-glucose (2-DG) elicited hyperglycemia and increased feeding at short latencies. If access to food was prevented for 6 h post-2-DG infusion, when blood glucose levels were normal and brain 2-DG concentrations were virtually zero, the rats still ate significantly more food than they did 6 h after control infusions. These data indicate that activation of brain glucoreceptors may mediate increased feeding even after other signs of cerebral glucoprivation have disappeared.

Animals↗
PubMed1980

Role of inner urethral softness in urinary continence.

Given adequate external squeeze upon suitable urethral geometry, continence depends on the mechanical properties of the outflow tract wall. Evidence indicates that these mechanical properties include an ability to deform and behave in a fluid-like manner.

Humans↗
PubMed1980

5-Thio-D-glucose causes increased feeding and hyperglycemia in the rat.

5-Thio-D-glucose (5TG) is a novel antimetabolic glucose analogue in which sulfur is substituted for the pyranose ring oxygen. Intracardiac infusion of 5TG caused dose-dependent increases in feeding and blood glucose concentrations. Increased food intake was reliably elicited by molar doses of 5TG that were one-third those necessary to reliably elicit feeding using 2-deoxy-D-glucose (2DG). 5TG also caused marked dose-related hyperglycemia. Plasma glucose concentrations after 5TG rose to levels 3 to 4.6 times as high as those measured after equimolar 2DG. 5TG-induced hyperglycemia was reduced by only 40% after adrenalectomy. These results, taken together with known differences in the biochemical modes of action for 2DG and 5TG, suggest that feeding elicited by 5TG may result from interference with metabolic events different from or additional to those affected by 2DG. 5TG should be a useful new tool for investigation of the physiology of feeding behavior.

Animals↗
PubMed1980

The effects of cold stress on neonatal calves. I. Clinical condition and pathological lesions.

Newborn Holstein-Friesian calves were cold stressed by immersion in water at 15 to 17 degrees C until the core body temperature was lowered by 10 degrees C. Non-cold stressed calves were immersed in water at thermoneutral temperature (35 to 37 degrees C). The time required to lower the core body temperature of the cold stressed calves by 10 degrees C was 172 +/- 87 minutes (mean +/- SD). The time required for the core body temperature of the cold stressed calves to return to normal after immersion was 400 +/- 140 minutes (mean +/- SD). Differences were observed between cold and noncold stressed calves in the shivering response during immersion and the clinical condition after immersion. Cold-induced pathological lesions were confined to tissues located peripherally, particularly in the hind legs. Significant differences were observed between cold and noncold stressed calves in the incidence of subcutaneous edema in the ventral sternum (P less than or equal to 0.025), subcutaneous hemorrhage in the hind legs (P less than or equal to 0.025), synovitis (P less than or equal to 0.025) and hemorrhage (P less than or equal to 0.05) of the synovial membranes of the hock joints and hemorrhage (P less than or equal to 0.05) into the hock joint cavities.

Animals↗
PubMed1980

The effects of cold stress on neonatal calves. II. Absorption of colostral immunoglobulins.

Newborn calves were subjected to cold stress and made hypothermic by immersion in water at 15 to 17 degrees C. Cold stress delayed the onset and significantly decreased (P less than 0.05) the rate of absorption of immunoglobulins (IgM, IgG1 and IgG2) up to 15 hours after first feeding of pooled colostrum. However, the net absorption of colostral immunoglobulins was not affected. The possible deleterious effect of cold stress on absorption of colostral immunoglobulins by newborn calves under range conditions is discussed.

Animals↗
PubMed1978

Absence of glucoprivic feeding after stress suggest impairment of noradrenergic neuron function.

Feeding in response to 2-deoxy-D-glucose (2DG), a quantifiable behavior which appears to depend on noradrenergic (NE) neuron function, was used in these experiments to evaluate the functional capabilities of NE neurons after stress exposure. Depletion of hypothalamic NE after footshock or hypothermic stress was directly correlated with impairment of glucoprivic feeding. When NE depletion was prevented by prior exposure to chronic stress, no impairment of feeding was observed. After hypothermic stress, repletion of NE proceeded more rapidly in the telencephalon than in the hypothalamus and reappearance of a normal feeding response precisely paralleled the time course of repletion in the hypothalamus. Drinking in response to cell dehydration, a behavior not directly dependent on brain catecholamines, was not impaired after either footshock or hypothermic stress, despite similar NE depletions. Presence of a normal drinking response assured that deficits observed in the 2DG test were not due to nonspecific behavioral suppression resulting from stress. These data suggest that NE neuron function may be impaired or temporarily abolished after severe stress exposure. In addition, these results demonstrate that behavioral pathology need not be the result of massive neurotransmitter depletion but may result from relatively subtle alterations of specific neurotransmitter pools.

Animals↗