Biomedical subjects

C M Ferrario

Publications and source records attributed to C M Ferrario.

At least 235 records · Page 13Linked to original sources

PubMed1978

Cutaneous tubeless ureterostomy as a procedure to study renal function in conscious dogs.

We describe the results obtained with a modified technique for single-side cutaneous ureterostomy in awake mongrel dogs. The success of this surgical procedure was evaluated by intravenous pyelography and urinary cultures that ruled out infection. In addition, we investigated the effects of this procedure on the excretory capacity of the kidney with a diverted ureter. Average values for effective renal plasma flow and glomerular filtration rate were comparable to those obtained in the literature and in the constralateral untouched kidney of the same dogs. The results indicate that cutaneous ureterostomy can be used successfully to monitor renal function in awake dogs over periods of weeks or months.

Animals↗

PubMed1977

The course of arterial pressure and the effect of Sar1-Thr8-angiotensin II in a new model of two-kidney hypertension in conscious dogs.

1. We describe a new method of producing two-kidney hypertension in dogs by a two-step procedure with complete occlusion of a renal artery 2 weeks after it was partially constricted. 2. Control mean arterial pressure (96 +/- 3 mmHg) of nine conscious, trained dogs rose to 107 +/- 3 mmHg 2 weeks after partial constriction of a renal artery, and it stabilized at a sustained hypertensive plateau (124 +/- 7 mmHg) 3 weeks after complete occlusion. 3. Intravenous infusion of an angiotensin II antagonist (Sar1-Thr8-angiotensin II) caused arterial pressure to fall during the acute but not the chronic phase of renal hypertension. In this latter phase plasma renin activity had returned to control values. 4. We conclude that the renin-angiotensin system appears not to be directly involved in the chronic phase of two-kidney hypertension in the dog.

Angiotensin II↗

PubMed1977

Animal models, hypertension, and central nervous system mechanisms.

Accumulating evidence suggests that the central nervous system plays a fundamental role in chronic hypertension. On the other hand, the means by which nervous factors influence the long-term control of blood pressure remain obscure. Animal models that replicate some of the functional aspects of essential hypertension in man have been of value and continue to provide insight into the complexity of the problem. Although none of the experimental models gives definitive answers, separate and combined analyses suggest the multiplicity of sites at which the stimulus must be applied for blood pressure to remain elevated.

Animals↗

PubMed1976

Ventricular performance after onset of renal hypertension.

1. In renal hypertensive dogs, the slope of the relation between either stroke volume or cardiac output and end-diastolic pressure is shifted to the right of the normal curves. 2. The maximum to which stroke volume or cardiac output can be raised during loading is significantly less. These changes in cardiac performance appear to be unrelated to the severity of hypertension.

Animals↗

PubMed1976

Method for chronic recording of electroencephalographic activity in conscious dogs.

The difficulties involved in recording high-quality electroencephalograms chronically from conscious dogs have been resolved by devising an implantable pure silver electrode assembly that can be screwed permanently into the skull. The assembly eliminates electromyographic artifacts and provides high-fidelity tracings. Construction is simple and commercially available, inexpensive parts are used. Highly satisfactory records can be obtained over periods of months.

Animals↗

PubMed1976

Cardiac performance in rats with renal hypertension.

To evaluate cardiac performance in renal hypertension more precisely we determined cardiac function curves for 12 normotensive rats and 11 other rats with two-kidney Goldblatt hypertension. The hypertensive group (BP = 134 +/- 8 mm Hg) showed significant cardiac hypertrophy (44 +/- 1% increased ratio of heart weight to body weight, P less than 0.01) and markedly increased left ventricular stroke work with a moderate but not significant increase in left ventricular end-diastolic pressure (LVEDP) (5.9 +/- 0.8 vs. 4.7 +/- 0.4 mm Hg). We evaluated cardiac function by recording left ventricular end-diastolic pressure, stroke volume (SV), and cardiac output (CO) (by electromagnetic flowmeter) during rapid alteration in venous return. Analysis of variations of stroke volume vs. left ventricular end-diastolic pressure showed that renal hypertension is accompanied by a significant decrease in ventricular performance [SV = 0.0190 + 0.0509 LVEDP - 0.0025 (LVEDP)2 + 0.0001 (LVEDP)3] compared to the normotensive group [SV = 0.0430 + 0.0644 LVEDP - 0.0040 (LVEDP)2 + 0.001 (LVEDP)3]. The alterations in stroke volume and cardiac output were associated with a lack of significant changes in the work performed at matched end-diastolic pressures. The data indicate that chronic renal hypertension is accompanied by a depression of cardiac reserve which is not revealed by measurements of cardiac output and left ventricular end-diastolic pressure at rest. This impairment in cardiac function might be related to either diminished cardiac contractility or reduced left ventricular compliance; the latter possibility is in accord with our finding of a 2-fold increase in the hydroxyproline content (P less than 0.001) and a significant decrease in the DNA concentration of ventricular tissue.

Animals↗

PubMed1976

Effects of angiotensin antagonists in various forms of experimental arterial hypertension.

The dependence of renal hypertension on increased levels of angiotensin II was investigated in conscious dogs at various stages of hypertension of four different types. Two of the most potent angiotensin inhibitors, Sar1-Ile8- and Sar1-Thr8-angiotensin II, were infused separately in various doses and at different times throughout the evolution of renal hypertension. The results of these experiments are consistent with the view that the renin-angiotensin system may participate in the acute and malignant phases of renal hypertension; they do not provide evidence for its participation when hypertension enters the chronic phase.

Angiotensin II↗

PubMed1975

Hemodynamic and humoral characteristics of hypertension induced by prolonged stellate ganglion stimulation in conscious dogs.

Recent evidence has suggested that cardiac factors may play a role in the evolution of arterial hypertension. To test the possibility that an increase in cardiac-performance can lead to a sustained increase in systemic blood pressure, we electrically stimulated the left stellate ganglion of six conscious dogs continuously for a 7-day period and monitored cardiac output and arterial blood pressure. In all six dogs, stimulation elicited an abrupt rise in systemic blood pre-sure that was entirely due to rise in cardiac output that lasted at least 6 hours. After 1 day of continuous stimulation, cardiac output retured to control values, but blood pressure remained elevated. After 7 days of stimulation, blood pressure was increased by an average of 25 mm Hg and peripheral resistance by 35 plus and minus 4%. Measurements of blood volume, plasma renin activity, circulating catecholamines (three of the six dogs), and sodium balance showed that none of these factors could explain the development pf this sustained hypertension. Pharmacologic blockade with phenoxybenzamine prevented in large part the rise in blood pressure in short-term stellate ganglion stimulations, whereas propranolol had very little effect on the pressor response, although it nearly abolished the increase in cardiac output. The data indicate that continuous stimulation of the stellate ganglion in conscious dogs leads to substained rises in both blood pressure and peripheral resistance; these changes are apparently mediated by increased activity of the sympathetic nervous system.

Animals↗

PubMed1974