Age-Dependent Difference of Kidney Response to Temporary Ischaemia in the Rat

1978 ◽  
Vol 55 (4) ◽  
pp. 365-368
Author(s):  
J. Kuneš ◽  
K. Čapek ◽  
J. Stejskal ◽  
J. JelíNek
Keyword(s):  
Blood Pressure ◽  
Cytochrome Oxidase ◽  
Arterial Blood Pressure ◽  
Oxidase Activity ◽  
Renal Damage ◽  
Plasma Urea ◽  
Systemic Arterial Blood Pressure ◽  
Renal Ischaemia ◽  
Arterial Blood ◽  
Plasma Urea Concentration

1. The response to 60 min ischaemia was studied in male uninephrectomized 30-, 60-and 90-day-old rats in regard to changes of renal cytochrome oxidase activity and the effect on systemic arterial blood pressure. Mortality due to renal failure, changes in plasma urea concentration and in kidney morphology were used as indicators of the renal response. 2. Mortality was lowest in 30-day-old animals (13%) and highest in 60-day-old animals (77%). Renal cytochrome oxidase activity increased by 44% during the same period. The mortality decreased to 34% between the ages of 60 and 90 days without change in renal content of cytochrome oxidase; survival time after renal ischaemia was prolonged from 2 to 4 days. 3. Fifty days after renal ischaemia plasma urea concentration correlated positively with kidney weight. Both variables were increased in rats exposed to ischaemia at the ages of 60 and 90 days. The kidneys of these rats exhibited lesions. No relation was found between the degree of renal damage and blood pressure. 4. It is concluded that (a) the kidney of immature rats is more resistant to temporary ischaemia due to immaturity of renal oxidative metabolism, (b) the ability to survive ischaemic renal damage in less-resistant mature rats increases with age and (c) the postischaemic impairment of renal function does not influence systemic arterial blood pressure.

Seizure-related modulation of systemic arterial blood pressure in focal epilepsy

Epilepsia ◽  
2016 ◽  
Vol 57 (10) ◽  
pp. 1709-1718 ◽  
Author(s):  
Kevin G. Hampel ◽  
Amirhossein Jahanbekam ◽  
Christian E. Elger ◽  
Rainer Surges
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Focal Epilepsy ◽  
Systemic Arterial Blood Pressure ◽  
Arterial Blood

Age-dependent blood pressure response to increased salt intake in rats influenced by a transient renal ischaemia

1986 ◽  
Vol 70 (2) ◽  
pp. 185-189 ◽  
Author(s):  
J. Kuneš ◽  
J. Jelínek ◽  
J. Zicha
Keyword(s):  
Blood Pressure ◽  
Renal Dysfunction ◽  
Renal Mass ◽  
Urea Concentration ◽  
Ischaemic Injury ◽  
Pronounced Increase ◽  
Plasma Urea ◽  
Renal Ischaemia ◽  
Salt Hypertension ◽  
Plasma Urea Concentration

1. The influence of renal dysfunction (induced by ischaemic injury) on the development of salt hypertension was studied in rats which were exposed to 60 min of renal ischaemia when either immature or adult. Saline-drinking age-matched animals served as controls. The blood pressure, plasma urea concentration, extracellular fluid volume (ECFV) and renal mass were measured 21 and 50 days after renal ischaemia. 2. Increments of plasma urea concentration and ECFV were considered to be indicators of renal dysfunction. Increased renal mass was used as an estimate of the degree of renal injury. 3. In adult rats, both plasma urea concentration and ECFV were increased 3 weeks after renal ischaemia. This correlated with a pronounced increase of renal mass. A similar relation of renal mass to ECFV was still present 50 days after renal ischaemia. 4. In rats treated when immature the increment of plasma urea concentration was much smaller and ECFV did not differ significantly from the control volumes. 5. A mild salt hypertension developed only in those rats which were treated when immature. On the other hand, the blood pressure tended to decrease in animals treated when adult. 6. It is concluded that mild renal dysfunction facilitates the development of salt hypertension in immature rats. This is in contrast with the reversed effects of extensive renal dysfunction in adult animals. 7. It is suggested that the age of animals is more important for the induction of salt hypertension than the degree of renal dysfunction.

Noninvasive Measurement of Systemic Arterial Blood Pressure in the Conscious Beagle Dog

1988 ◽  
Vol 10 (1) ◽  
pp. 89-97
Author(s):  
JOHN C. PETTERSEN ◽  
RONALD R. LINARTZ ◽  
ROBERT L. HAMLIN ◽  
RAYMOND E. STOLL
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Noninvasive Measurement ◽  
Beagle Dog ◽  
Systemic Arterial Blood Pressure ◽  
Arterial Blood

Regulation of Cardiac Output during 2,4-Dinitrophenol-Induced Tissue Hypermetabolism in the Dog

1977 ◽  
Vol 53 (1) ◽  
pp. 17-25
Author(s):  
C. Liang ◽  
W. B. Hood
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Venous Blood ◽  
The Other ◽  
Pulmonary Artery Wedge Pressure ◽  
Systemic Arterial Blood Pressure ◽  
Arterial Blood ◽  
Wedge Pressure

1. Cardiac output increased in proportion to oxygen consumption in intact chloralose-anaesthetized dogs after four successive intravenous infusions of 2,4-dinitrophenol (11 μmol/kg; 2 mg/kg). 2. Splenectomy abolished the increase in cardiac output after the first three doses of 2,4-dinitrophenol. β-Adrenoreceptor blockade by practolol, on the other hand, did not prevent the cardiac output rise after the first 2,4-dinitrophenol infusion, but further increases by 2,4-dinitrophenol infusion were abolished. When splenectomy and β-adrenoreceptor blockade were combined, cardiac output did not increase significantly after all four doses of 2,4-dinitrophenol. 3. Cardiac output and mean systemic arterial blood pressure increased when the splenic venous blood collected after 2,4-dinitrophenol infusion was infused intraportally. 4. In a vascularly isolated, but normally innervated, lower half-body cross-perfusion preparation, cardiac output and mean systemic arterial blood pressure increased in the upper half-body when tissue hypermetabolism was produced in the cross-perfused area by 2,4-dinitrophenol. Neither pulmonary artery wedge pressure nor heart rate changed significantly. 5. This circulatory stimulation, after regional 2,4-dinitrophenol infusion, was abolished or was prevented from occurring by splenectomy. 6. It appears that the normal cardiac output response to tissue hypermetabolism requires both an intact spleen and normally functioning β-adrenoreceptors.

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