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Biomedical subjects

R Albertini

Publications and source records attributed to R Albertini.

At least 91 records · Page 5Linked to original sources
PubMed1979

Cardiovascular changes during spontaneous micturition in conscious cats.

The hemodynamic changes occurring during spontaneous micturition were recorded in conscious cats. Arterial blood pressure was continuously measured by chronically implanted arterial catheter, heart rate (HR) by a cardiotachometer, and cardiac output (CO), superior mesenteric (MF), renal (RF), and external iliac blood flows (IF) by chronically implanted electromagnetic flow probes. Spontaneous micturition was accompanied by little change in mean arterial pressure (-9.7 +/- 0.7%), but by a marked decrease in HR (-49.0 +/- 1.2%) and CO (-28.6 +/- 2.5%), and therefore by a marked decrease in total peripheral conductance (-21.0 +/- 3.5%). Visceral and hindlimb blood flows were markedly reduced during micturition (MF, -34.7 +/- 2.1%; RF, -22.6 +/- 1.5%; and IF, -48.7 +/- 1.5%, respectively) due to a marked reduction in regional conductances in both these areas. The vasomotor changes in the regional circulations were prevented by local sympathectomy. Thus spontaneous micturition is associated with marked changes in cardiac function and systemic circulation. Cardiac output is decreased, but diffuse nervous systemic vasoconstriction compensates for this and provides maintenance of arterial blood pressure level.

Animals↗
PubMed1978

Control of regional circulations by the sino-aortic reflexes during desynchronised sleep in the cat.

In the intact cat desynchronised sleep induces arterial hypotension and mesenteric vasodilatation, whereas in limb muscles vasoconstriction occurs because of the concurrent action of a spinal vasoconstriction reflex. After sino-aortic denervation arterial hypotension is exaggerated and mesenteric vasodilatation is greater, while the muscular bed of the limbs also becomes vasodilated rather than constricted. It is concluded that during desynchronised sleep the sino-aortic afferents act to check a central influence inhibiting vasoconstrictor tone both in the viscera and muscles: thus an excessive fall in blood pressure is prevented by avoiding a too large visceral vasodilatation and by unmasking the vasoconstrictor action of the spinal reflex in the limbs.

Animals↗
PubMed1977

Renal kallikrein system, volemia, and renal hypertension.

Plasma, blood, and urine volumes, renal kallikrein, and arterial pressure were measured in control and renal hypertensive rats in order to study the role of the renal kallikrein system in regulating arterial pressure and its relation with the alterations in water handling observed in hypertension. A decrease in kallikrein content of the kidney (157 +/- 17 versus 236 +/- 16 ng bradykinin equivalents per gram of tissue in control rats) was associated with an increase in plasma volume (38.0 "/- 1.6 versus 32.0 +/- 0.9 ml/kg body weight in control rats) and an increase in urine volume (45.5 +/- 4.9 versus 20.3 +/- 1.6 ml/kg body weight per 24 hours in control rats). No linear correlation was found between these factors and the arterial pressure of hypertensive animals. These findings support the hypothesis that changes in renal kallikrein are more directly related to water and electrolyte metabolism than to the arterial pressure regulation. Our results also suggest an interaction between the kallikrein-kinin and the renin-angiotensin-aldosterone systems. The possible relations of both enzymatic systems to the regulation of arterial pressure and of water-electrolyte handling are summarized schematically.

Animals↗
PubMed1976

The effect of water, sodium overloading and diuretics upon urinary kallikrein.

The effects of acute administration of either water or 2% NaCl solution via a stomach tube and injections of diurecits, furosemide (5, 10 mg) and acetazoleamide (5, 20 mg per rat), in adult rats upon urinary kallikrein (Kal), Na and K, were studied. Hyperhydration with water (5% b.w.) produced in 121% increase and 2% NaCl overloading (5% b.w.) 275% increase in urinary Kal within 120 min after gavage, when compared with the excretion of non hyperhydrated rats. Furosemide 5 mg in hyperhydrated animals produced in the same period an excretion of 645 +/- 52 ng BR of Kal, which is 147% higher to that excreted by the hyperhydrated controls. The same dose of furosemide in 2% NaCl loaded rats, produced an excretion of Kal equivalent to 1333 +/- 72 ng BR which is 180% greater than in controls similarly loaded. Acetazoleamide 20 mg and furosemide 5 mg produced similar excretions of Kal even though natriuresis is greater tna kalliuresis is lesser in furosemide injected rats. Evaluation of total kidney Kal has shown that a single (10 mg) or a series of furosemide injections (8 days 5 mg + 1 day 10 mg), brings about a significant (p is less than 0.001) decrease in renal Kal, but the increase of Kal excreted in the urine (120 min) is 3.5 times more (under a single injection) and 42 times more (under 9 injections) than the amount which disappears from the kidneys. Apparently furosemide not only stimulates Kal excretion, but also Kal synthesis in the kidney. The results support the concept that the Kal system would be involved in excretory functions dealing both with sodium and water excretion.

Acetazolamide↗
PubMed1976

Renal urinary kallikrein in normotensive and hypertensive rats during enhanced excretion of water and electrolytes.

1. Urinary kallikrein excreted by normal rats is significantly increased (P less than 0-001) 2 h after: (a) water loading, (b) water loading plus frusemide, 0-27 mmol (10 mg) per rat, (c) salt loading. In water-loaded rats, 5 i.u. of renin strikingly reduced kallikrein excretion (P less than 0-01) but considerably increased sodium excretion (P less than 0-001). 2. Renal kallikrein, measured by its kininogenase activity within 2 h of water loading, was significantly increased (P less than 0-05); after water loading and frusemide it was 40% decreased (P less than 0-001) and after salt loading it was reduced by approximately 50% (P less than 0-02). Renin did not change renal kallikrein. 3. Severely hypertensive (one-kidney) rats (blood pressure greater than 150 mmHg) showed no increase of urinary kallikrein after water loading, although there was a marked natriuresis, in moderately hypertensive rats (blood pressure less than 150 mmHg) urinary kallikrein was only one-third of that observed in control normotensive rats, after an equal degree of water loading.

Animals↗
PubMed1976

Interplay of sino-aortic reflexes and haemodynamic changes during natural sleep in the cat.

1. When the sino-aortic afferents are intact, desynchronized sleep causes a small decrease in the blood pressure, a vasodilation in the mesenteric and renal beds, and a vasoconstriction in the external iliac bed. 2. After sino-aortic deafferentation desynchronized sleep causes a larger fall in the blood pressure, a greater vasodilatation in the mesenteric and renal beds, and a vasodilatation replaces the vasoconstriction in the external iliac bed. 3. The sino-aortic reflexes play an active role in controlling circulation during desynchronized sleep by opposing the centrally induced reduction in adrenergic sympathetic tone. This effect of sino-aortic reflexes is similar on both visceral and muscular vessels. In addition, the muscular bed, but not the visceral one, is regulated by a spinal reflex vasoconstriction mechanism which is apparent only when the sino-aortic reflexes are intact.

Animals↗
PubMed1976

Interactions between sino-aortic reflexes and cardiovascular effects of sleep and emotional behavior in the cat.

The role of sino-aortic reflexes in the control of circulation during normal behavior was investigated by comparing cardiovascular reactions during various but reproducible types of behavior before and after bilateral sino-aortic deafferentation. Chronic deafferentation caused little change in baseline blood pressure, but a subtler, important role of sino-aortic reflexes was revealed by examining the integrated cardiovascular responses to behavioral stimuli. During desynchronized sleep, the buffering action of sino-aortic reflexes prevented a marked and diffuse vasodilation, with an action that was particularly evident on muscle blood vessels. During emotional behavior, especially when emotion was accompanied by movement, sino-aortic reflexes opposed the consequences of muscle vasodilation by inducing tachycardia and vasoconstriction in the viscera and in noncontracting muscles. A reciprocal type of interaction between behavior and sino-aortic reflexes was shown by testing the amplitude of the carotid occlusion response before and during desynchronized sleep; the latter condition was consistently associated with decreased effectiveness of the reflex response. The possibility is considered that this might indicate central suppression of the carotid sinus reflex during desynchronized sleep and that a similar inhibitory interference might occur during emotional behavior. Alternatively, reduction of the reflex response might result from a shift of the stimulus-response curve on either side of its steep portion.

Animals↗
PubMedDate not supplied

The use of bromodeoxyuridine labeling in the human lymphocyte HGPRT somatic mutation assay.

The autoradiographic assay developed by Strauss and Albertini (1979) to quantitate human in vivo somatic mutation at the hypoxanthine guanine phosphoribosyl-transferase locus uses tritiated thymidine to identify mutant cells by their ability to pass through 'S' phase in the presence of 6-thioguanine. An alternative method, based on the incorporation of bromodeoxyuridine (BrdUrd) into the DNA of proliferative cells, followed by differential staining with the fluorescence-plus-Giemsa method, was used to identify 3 classes of lymphocyte nuclei: (a) small darkly stained nuclei, (b) large, reddish-colored nuclei with an apparent nucleolus, and (c) large, bluish-colored nuclei. By double labeling with BrdUrd and tritiated thymidine, it was determined that only the nuclei of the third class had incorporated BrdUrd. These results demonstrate that the technique used for sister-chromatid differentiation can be used to detect putative HGPRT mutants and to determine variant frequencies at the HGPRT locus.

Autoradiography↗