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Biomedical subjects

C M Ferrario

Publications and source records attributed to C M Ferrario.

At least 217 records · Page 12Linked to original sources
PubMed1983

Can the heart initiate some forms of hypertension?

An active role for the heart in the initiation of hypertension can be postulated in two different sets of conditions. 1) Activation of pressor reflexes from the ventricles, coronary arteries, or aorta has been shown to produce substantial rises of arterial pressure; experience with postcoronary bypass hypertension suggests that these reflexes could be responsible for some types of paroxysmal hypertension. 2) Increased cardiac action caused by either neural or humoral factors can initiate a rise in cardiac output and blood pressure; sustained hypertension could be produced experimentally in conscious dogs by electrical stimulation of the stellate ganglion or by continuous infusion of dobutamine in the left coronary artery. Evidence suggesting that this could occur in humans was derived from a study of the relationship of cardiac output to cardiopulmonary volume in essential hypertension.

Animals↗
PubMed1981

Neurogenic suppression of carotid sinus reflexes by vagal afferents in sodium-depleted dogs.

Reduction of sodium intake affects both the renin-angiotensin and sympathetic nervous systems, but the effects on the latter are less well understood. To clarify this relationship, the responsiveness of the baroreceptor reflex was compared in groups of normal and sodium-depleted dogs prepared with a single innervated carotid sinus and left vagus nerve after anesthesia with morphine-chloralose. Three weeks of sodium depletion did not affect the mean arterial blood pressure, but cardiac output (-50%) and stroke volume (-38%) were reduced, whereas there was a large compensatory increase in total peripheral resistance (115%). The pressor response to carotid occlusion in sodium-depleted dogs was significantly less (35 +/- 4 mmHg) than that obtained in normal dogs (61 +/- 5 mmHg). In the dogs treated with cholinergic blockade with atropine, this difference (-51%) persisted. In contrast, the pressor response to carotid occlusion in sodium-depleted dogs was significantly potentiated (112%) and restored in magnitude to that found in normal dogs after severing the only remaining vagus nerve. These data suggest that the cardiopulmonary and/or aortic vagal afferents are responsible for the blunting of baroreceptor reflexes during sodium depletion.

Afferent Pathways↗
PubMed1980

A morphological characterization of the canine area postrema.

The cellular morphology of the dog's area postrema (AP) was demonstrated with the Golgi-Cox technique. Golgi preparations suggested division of the canine AP into three regions: a periventricular mantle zone, a central region, and a junctional zone adjacent to the nucleus tractus solitarii. The distinctive feature of the dog's AP was arrays of periventricular neurons intermixed with glialoid cells. Additional Bodian sections revealed a commissural fiber network connecting the halves of the AP at the obex. The interconnected three-layer structure implies a polysynaptic pathway by which AP stimulation activates central sympathetic outflow.

Animals↗
PubMed1980

Characterization of the sympatho-facilitative area postrema pathway.

1. The mechanism by which the area postrema augments central sympathetic drive during electrical stimulation is presently unknown. This pathway may involve either direct facilitation of brain-stem vasomotor neurons or inhibition of the sympatho-inhibitory baroreceptor relay in the nucleus tractus solitarii. 2. The present study employed selective lesions within the solitary tract nucleus to assess the participation of the primary baroreceptor relay in the pressor response during electrical stimulation of the area postrema. 3. The magnitude of the pressor response was unchanged after destruction of the solitary tract and lateral solitary nucleus which centrally interrupted the baroreceptor reflex. However, microknife cuts through the medial solitary nucleus, which spared the carotid sinus reflex, significantly reduced the magnitude of the area postrema pressor response. 4. Previous anatomical studies support these results and confirm that, although the area postrema pressor pathway traverses the most medial portion of the solitary complex, it does not produce augmented sympathetic outflow by inhibition of the primary baroreflex relay.

Animals↗
PubMed1980

The role of endogenous opiates in the area postrema pressor pathway.

1. Intra-vertebral artery-administered angiotensin II acts at the area postrema to facilitate central sympathetic vasomotor activity. Recent evidence suggests a possible role of the opiate system in the mechanism of action of angiotensin II at the level of the brain stem. 2. In these experiments, we show that the morphine antagonist naloxone reduces significantly the magnitude of the pressor response to vertebral artery-infused angiotensin II. 3. Morphine, in contrast, doubled the peak of the vertebral response to identical doses of the peptide. Neither naloxone nor morphine affected the pressor responses to intravenously administered angiotensin II. 4. The data suggest that the endogenous opiate system in the medulla modulates the cardiovascular effects of angiotensin II at the level of the area postrema.

Angiotensin II↗
PubMed1980

Alterations in cardiac function and cardiopulmonary blood volume in chronic sodium depletion in dogs.

1. Chronic sodium depletion in dogs is associated with a blunting of the pressor response to carotid occlusion. AFter section of the vagus nerves this pressor response reverts to normal although atropine is without effect, suggesting a possible role for increased activity of cardiopulmonary vagal afferents in suppressing sympathetic outflow. Since increases in central blood volume stimulate vagal afferents, cardiopulmonary haemodynamics were studied by radioisotope dilution before and after 3 and 4 weeks of dietary sodium restriction together with frusemide. 2. Sodium depletion was associated with significant decreases in cardiac output, ejection fraction and total blood volume; the cardiopulmonary blood volume increased but the change was not statistically significant (P < 0.2). These changes were accompanied by a significant increase in the ratio cardiopulmonary blood volume/total blood volume and a decrease in the ratio cardiac output/cardiopulmonary blood volume. 3. Results indicate that sodium depletion may be accompanied by a paradoxical translocation of blood to the cardiopulmonary region in part due to depressed ventricular performance.

Animals↗
PubMed1980

Angiotensin and CNS regulation of blood pressure.

It appears that angiotensin II (AII) has access to the CNS by three routes: endogenous formation within the brain, passage into CSF, or transfer across "gaps" in the blood-brain barrier. The mode of access influences both the characteristics and the magnitude of the cardiovascular effects exerted by AII within the CNS. In the dog the effects of blood-borne AII on the area postrema (AP) in the IV ventricle seem to have the most physiological significance. In recent experiments we have characterized both the histological composition of this structure and its physiological effects. While electrical stimulation of the AP, in similarity to the pressor effects of intravertebral AII, produces a hypertensive response dependent on sympathetic vasomotor outflow, ablation of this structure results in mild hypotension associated with decreased hemodynamic variability and altered vascular responsiveness to intravenous AII and norepinephrine. Recent data suggest that the sympatho-facilitative action of AII on the AP may involve endogenous opiates in the brainstem.

Adrenergic Fibers↗
PubMed1980

Lymphoid alterations and impaired T lymphocyte reactivity in experimental renal hypertension.

Alterations in the number and reactivity of thymic and splenic lymphocytes were studied during the development of experimental renal hypertension in Sprague-Dawley rats. The mitotic responses of thymocytes and splenic T and B lymphocytes were tested by the T cell mitogen concanavalin A and the B cell mitogen dextran sulfate 3, 8, 12, and 36 days after the initiation of hypertension. At 3 days, hypertensive rats showed a fourfold increase in plasma corticosteroid levels, marked thymic atrophy, and a 50% reduction in the total number of thymocytes. The mitotic reactivity of the cells remaining in the organ was depressed 60% when compared to sham-operated controls. At 8 days a similar reduction in thymus size was accompanied by similarly decreased lymphocyte populations. Twelve days after initiation of hypertension structural recovery of the gland, lymphoid proliferation, and slightly increased thymocyte populations were observed. Differences with sham-operated controls were, however, still remarkable. Hypertensive rats sacrificed at 36 days showed thymus hypertrophy, and the thymocyte populations were larger than those of sham-operated animals. Despite the fluctuations in the number of thymocytes registered during the development of renal hypertension, the impaired mitotic reactivity of these cells to concanavalin A was sustained throughout the 36 days of the experiment. A similar reduction in the total number of cells and a similar depression in T lymphocyte reactivity was observed in the spleen between 8 and 36 days of hypertension. In contrast, after an initial depressed response, splenic B lymphocytes showed a slight but sustained increase in reactivity throughout the entire experimental period. These results indicate that with evolving renal hypertension there is a reduction in the number of lymphocytes as well as a depression in the ability of the remaining T lymphocytes to react with concanavalin A. Since T lymphocytes are important regulators of immunological homeostasis, this reduction in T cell reactivity may suggest the existence of an immunological imbalance accompanying the development of experimental renal hypertension.

Adrenal Cortex Hormones↗
PubMed1980

Effect of hyaluronidase on acute spinal cord injury.

Three control and five experimental dogs were subjected to 500 gm-cm injury of the midthoracic spinal cord by the weight dropping technique. Five hundred units per kilogram of hyaluronidase injected intravenously 20 minutes after injury in the experimental animals did not alter the loss of dorsal column evoked potentials (nonaveraged) or improve the pathological results up to three hours. These results imply that hyaluronidase will not significantly alter the functional outcome of trauma of the spinal cord in dogs.

Animals↗
PubMed1979

Cardiac pumping ability in rats with experimental renal and genetic hypertension.

In two experimental models of established hypertension in the rat (two kidney, one clip renal and genetic hypertension), the maximum by which stroke volume and cardiac output could be increased during an acute preload stress was significantly reduced despite the concomitant development of left ventricular hypertrophy. Reversal of cardiac hypertrophy by prolonged treatment with methyldopa (range 3 to 6 weeks) during the established phase of spontaneous hypertension normalized arterial blood pressure and improved ventricular pumping ability. The improved performance was in part due to reduced impedance to ventricular ejection because it did not persist when peripheral resistance was increased by an acute administration of phenylephrine hydrochloride. Thus, hemodynamic as well as structural factors contribute to alterations in cardiac function during the chronic established phase of arterial hypertension.

Animals↗
PubMed1979

Hemodynamics of central infusion of angiotensin II in normal and sodium-depleted dogs.

The intraventricular (IVT) administration of angiotensin II (AII) (100 ng.kg-1.min-1) produced significant elevations of arterial blood pressure in pentobarbital-anesthetized dogs on either normal or sodium-deficient diets. In both groups of dogs the intraventricular administration of AII caused comparable and significant elevations in blood pressure averaging 15 +/- 2 and 17 +/- 4 mmHg, respectively, within 10 min after onset of the infusion. The rises in blood pressure were due to increased peripheral resistance (2.87 +/- 1.20 vs. 1.67 +/- 0.43 units). At the peak of the pressor response bradycardia was a constant feature in sodium-depleted animals, but was not present in the normal ones. In both groups of dogs regional cerebral blood flow (rCBF), determined by the xenon-133 washout method, remained unchanged during the development of the pressor response, and peripheral plasma renin activity failed to increase in response to the central infusion of AII. In conclusion, sodium deprivation appears not to influence the sensitivity of the central AII receptor because comparable pressor responses and hemodynamic changes were obtained following the intraventricular administration of AII in both normal and sodium-depleted dogs.

Angiotensin II↗
PubMed1978

Biphasic changes in thymus structure during evolving renal hypertension.

1. Structural changes in the thymus during the evolution experimental renal hypertension were investigated to determine their possible role in the genesis of hypertensive vascular disease. 2. The thymus, adrenal glands and the progression of hypertensive vascular lesions were investigated in rats during the first 30 days after occlusion of the aorta between the two renal arteries. 3. Hypertension was initially accompanied by marked atrophy of the thymus, most pronounced 9 days after operation. During this time, the adrenal glands doubled in size and the heart became enlarged. 4. After 21 days the thymus regenerated and became hypertrophic. Histological features of hyperactivity accompanied by infiltration of plasma cells were evident, while the adrenal glands remained enlarged. 5. The observed structural changes of the regenerated thymus in the presence of sustained adrenal hypertrophy indicate that the thymus may contribute to the production of hypertensive vascular disease.

Animals↗