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Biomedical subjects

A Stella

Publications and source records attributed to A Stella.

At least 163 records · Page 9Linked to original sources
PubMed1984

Effects of afferent renal nerve stimulation on renal hemodynamic and excretory functions.

In anesthetized cats (n = 9) renal afferent fibers were electrically stimulated for 11 min, and the response of the contralateral innervated kidney was compared with that of the ipsilateral denervated one. Before stimulation, renal blood flow, glomerular filtration rate, and water and sodium excretions were significantly lower in the innervated kidney than in the denervated one. Afferent renal nerve stimulation augmented arterial pressure and also increased sodium and water excretions from both kidneys without concomitant changes in glomerular filtration rates and renal blood flows. Absolute and percent changes in sodium and water excretions from the innervated kidney were similar to those observed in the denervated one. The same results were obtained in cats (n = 4) which underwent bilateral adrenalectomy to avoid the effect of circulating catecholamines. In another group of cats (n = 5), the increase in renal perfusion pressure due to the stimulation was prevented by an aortic snare: this resulted in a slight but equal decrease of all variables in both kidneys. These experiments do not show a reflex control of renal function from renal afferents.

Afferent Pathways↗
PubMed1984

Elastic modulus in young diabetic patients (ultrasound measurements of pulse wave velocity).

Aim of this study is to confirm the validity of non-invasive evaluation with Doppler C.W. in the study of arterial diseases and in the identification of pre-clinical arterial lesions. We studied twenty-eight children suffering from diabetes mellitus, and dependent on insulin and a control group composed of twenty-eight healthy persons. All subjects were studied using the methodology of the transit time for the determination of the elastic modulus of the lower limb arterial wall and results were analysed according to a statistical method. Although the groups were small, an increase in pulse wave velocity was noted in diabetic children and a significative correlation was found between the elastic modulus and duration of diabetes.

Adolescent↗
PubMed1984

Neural control of the kidney--are there reno-renal reflexes?

Circulatory, secretory (renin release) and excretory (tubular sodium and water reabsorption) renal functions are known to be under neural control exerted by sympathetic fibers. Influences on circulatory and secretory functions are modulated by vagally mediated reflexes originated from low pressure (or volume) receptors in the cardiopulmonary area. The possibility that reno-renal reflexes may also exist has raised interest recently. Mechanoreceptors and chemoreceptors have been described in the kidney, and electrophysiological evidence of reno-renal reflexes is available. However, electrical stimulation of afferent renal nerves has failed to reflexly influence circulatory, secretory and excretory functions of the contralateral kidney. Deafferentation studies have been more successful, however. Transient denervation of one kidney by renal nerve cooling is accompanied by reduction of sodium and water excretion from the contralateral kidney with negligible changes in blood flow and glomerular filtration rate. The contralateral antidiuretic activity is prevented either by denervation of the contralateral kidney or by interruption of the afferent fibers running in the spinal dorsal roots. This definitely shows that a reno-renal reflex exists, consisting in a tonic inhibition of contralateral sympathetic activity controlling tubular reabsorption of sodium and water, and renin release.

Afferent Pathways↗
PubMed1983

A placebo-controlled trial of thymic hormone treatment of recurrent herpes simplex labialis infection in immunodeficient hosts.

Twenty-one immunodeficient patients with recurrent herpes simplex labialis (HSL) were randomly allocated to either saline or the bovine thymus extract thymostimulin (TS) and treated for a period of 6 months. An impressive reduction in both number and severity of the recurrences of the infection was observed in TS-treated patients during the trial and for up to 3 months afterward. A significant increase in total WBC, lymphocyte count, and T cells was detected in the TS group after 6 months. In vitro lymphoproliferative responses to herpes simplex virus antigen and natural killer cell activity were also significantly higher in the TS group, whereas no significant difference in antibody titers to herpes simplex could be detected between the two groups. TS can therefore help prevent viral reactivation in immunocompromised hosts by potentiating cell-mediated immune responses and should be considered for use in prophylaxis of infection in patients at risk and also in apparently normal subjects with recurrent HSL.

Adolescent↗
PubMed1983

Do renal afferent fibres modulate the function of the contralateral kidney?

Denervation of one kidney has been shown to induce a prompt decrease in sodium and water excretion from the contralateral kidney. The present study was designed to clarify whether this response is due to suppression of a tonic inhibitory renorenal reflex. Experiments were performed in anaesthetized cats in which the renal nerves of the left kidney were transiently blocked by cooling and the effects of this blockade on either kidney were studied in three different groups of animals. The decrease in sodium and water excretion from the contralateral (right) kidney observed in the sham-operated group (intact dorsal roots) was still present, and substantially unchanged, in the second group of animals in which the ipsilateral (left) dorsal roots from T9 to L4 were cut. In the third group of cats, bilateral dorsal root section entirely abolished the response of the contralateral kidney to renal nerve cooling. These experiments demonstrate that the contralateral decrease in sodium and water excretion is due to the block of afferent renal nerve fibres which project bilaterally to the spinal cord.

Afferent Pathways↗
PubMed1982

Cardiovascular lesions in chronic pancreatitis: a prospective study.

We prospectively investigated fifty-four consecutive patients with proven chronic pancreatitis and 54 control subjects for the presence of cardiovascular lesions. Clinical and laboratory evidence of arterial involvement was found in 18 patients (33%) and in five controls (9%) (P less than 0.01). Electrocardiographic alterations indicating coronary heart disease were found in eight patients and in three controls, and peripheral symptoms and signs indicating obliterative atherosclerotic disease of the lower extremities were found in 12 patients (two had associated electrocardiographic changes) and in two controls. No significant differences in the prevalence of the major vascular risk factors were observed between patients with vascular lesions and those without, and between patients and control subjects. It is concluded that patients with chronic pancreatitis have more frequent cardiovascular lesions which tent to develop at an earlier age, compared to the general population. The possibility that chronic pancreatitis may favor the development of these lesions is discussed.

Adolescent↗
PubMed1979

Vagal and sinoaortic reflexes in postural control of circulation and renin release.

Anesthetized cats were subjected to two 10-min trials of head-up tilting spaced 60 min apart. Bilateral cervical vagotomy, performed after the first tilting episode, did not affect the hemodynamic response to the change in posture, but significantyly and markedly reduced the increase in renin release from the innervated kidney. After sinoaortic denervation a marked and sustained arterial hypotension occurred during tilting, and the postural increase in renin release, though still limited to the innervated kidney, was even greater. When pressure homeostasis to tilting was disturbed, the renin release response was seen to be independent of the vagi, as it occurred after combined vagotomy and sinoaortic denervation. Maintenance of arterial pressure during tilting is mainly due to sinoaortic reflexes, whereas vagal reflexes are mostly responsible for the postural increase in renin release. The vagally independent release of renin observed when the cardiovascular response to tilting is impaired, is probably due to a direct action of arterial hypotension on intrarenal receptors, an action occurring only in innervated kidneys.

Animals↗
PubMed1978

Differences in reflex control of arterial pressure and renin release during head-up tilting in the cat.

1. Anaesthetized cats were subjected to two 10 min trials of head-up tilting spaced 30 min. Arterial pressure, heart rate, blood flow to an innervated kidney and to the contralateral denervated one, and renin release from both kidneys were measured. 2. The same haemodynamic changes and comparable increases in renin release from innervated kidneys occurred during both episodes of tilting when cats were subjected to sham cervical vagotomy between the two tilting trials. 3. Bilateral cervical vagotomy, performed after the first episode of head-up tilting, did not affect the haemodynamic response to the change in posture, but significantly and markedly reduced the increase in renin release from the innervated kidney. 4. After sino-aortic denervation a marked and sustained arterial hypotension occurred during tilting, and the postural increase in renin release from the innervated kidney was even greater. 5. In no condition, even during the marked fall in blood pressure in sino-aortic denervated cats, did head-up tilting increase renin release from the denervated kidney. 6. It is concluded that maintenance of arterial pressure during tilting is mainly due to sino-aortic reflexes, whereas vagal reflexes are mostly responsible for the postural increase in renin release.

Afferent Pathways↗
PubMed1977

Effects of renal denervation on renin release in response to tilting and furosemide.

In anesthetized cats head-up tilting for 30 min and infusion of furosemide at 0.75 mg/kg in 30 min significantly raised renin release from the innervated kidney (increments of 90.7 +/- 21.4 ng/min on tilting and 105.4 +/- 26.4 ng/min after furosemide); a small and inconstant increase from the contralateral denervated kidney (increments of 16.8 +/- 16.0 and 16.3 +/- 17.7 ng/min, respectively) was abolished by acute bilateral adrenalectomy. Larger doses of furosemide (6.0 mg/kg) could release renin from the denervated kidney also, but the response was still more marked on the innervated side especially in the early period of infusion (increments of 132.7 +/- 23.8 and 33.7 +/- 23.8 ng/min of innervated and denervated sides at 10 min). The response of the denervated kidney to 6.0 mg furosemide/kg was not affected by adrenalectomy. Stimulation of juxtaglomerular cells by tilting is entirely due to sympathoadrenergic activation; stimulation by furosemide is also entirely neural when the diuretic drug is given in moderate doses, but is partly independent of innervation when larger doses are administered.

Adrenalectomy↗
PubMed1976

Control of renin release: a review of experimental evidence and clinical implications.

Present knowledge of the mechanisms regulating release of renin is reviewed with particular emphasis on neural factors. Evidence is given for a direct effect of renal innervation on beta adrenergic receptors in juxtaglomerular cells, and for the involvement of reflex release of renin in conditions such as tilting and acute salt depletion. Participation of neural and nonneural mechanisms of control is also shown to occur in other conditions, such as aortic constriction and hemorrhage. The view is held that neural sympathetic factors might explain some of the renin disturbances found in essential hypertension. First, in patients with high renin hypertension part of the hypertension is renin-dependent, and these pressor levels of renin seem to be neurally induced since they can commonly be suppressed by beta adrenoreceptor blocking agents. Second, the hypothesis is presented that patients with low renin hypertension, at least those who have no volume disturbance, have a blunted sympathetic control of renin release. Therefore a sufficiently precise test of sympathetic activity, and possibly of body fluid volumes, should be associated with renin profiles for a better understanding of the pathophysiology of arterial hypertension and as a better guide to therapeutic management. Indeed, most of the available antihypertensive drugs act on sympathetic activity, body fluid volume or renin, and this multifaceted profile would provide more rational guidelines for treatment.

Adrenergic beta-Antagonists↗