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Biomedical subjects

A Iaina

Publications and source records attributed to A Iaina.

At least 145 records · Page 8Linked to original sources
PubMed1977

Alleviation of anoxic experimental acute renal failure in rats by beta-adrenergic blockade.

Acute renal failure induced in Charles River rats by right nephrectomy and left renal artery clamping for 70 min, constantly produced high blood urea and serum creatinine levels 24 h following the experimental procedure. The intravascular administration of propranolol in different doses persistently alleviated the severity of uremia seen on the following day. The optimum dose in this experimental set-up was 1 mg/kg/h. The mean blood urea level was 237 +/- 15.5 (SEM) mg% in the saline-treated controls and 116 +/- 16 mg% in the group treated with propranolol 1 mg/kg/h. P113 alone and prostaglandin A1 alone were not effective in alleviating the ARF. The combination of P113 and propranolol produced the same amount of alleviation in uremia as propranolol alone. The PRA was low in the propranolol-treated rats and high in the group which received both P113 and propranolol, even though alleivation of ARF was produced in both of these groups. The mechanism by which the beta-adrenergic blockade produced by propranolol alleviates the anoxic type of acute renal failure is unknown. However, it does not seem to act through the suppression of renin release from the kidney.

Acute Kidney Injury↗
PubMed1977

Postnatal changes in plasma and renal renin of the rat.

Plasma renin activity (PRA) of infant rats is high until some time between the 3rd and 4th week after birth. Mothers, however, return PRA to normal by 2 weeks post partum. The rate of disappearance endogenous PRA of nephrectomized rats is slower in those animals having gigh PRA than in mature rats. Disappearance curves of endogenous PRA of mothers post partum is also the same as that of normal mature females. Part of the high PRA of the neonate can thereby be the related to the lower rate of destruction. Total kidney renin content increases with age. Renal renin activity (RRA) is low only during the 1st postnatal week when expressed in terms of whole kidney weight and compared to later postnatal times. Although there are some slight differences in the means in older animals, none are statistically significant.

Age Factors↗
PubMed1977

Probability of survival in hypertensive and nonhypertensive patients on maintenance hemodialysis.

The actuarial survival rate for 58 unselected patients who entered a program of maintenance hemodialysis and transplantation was found to be 43.0 +/- 8.3 (SE)% for the six-year period of observation. The survival rate was considerably lower in hypertensive patients as well as in patients with familial Mediterranean fever with amyloidosis, all of whom were nonhypertensive. When the patients with familial Mediterranean fever were excluded from the non-hypertensive group, the expected survival rate of this group became greater than that of the hypertensive group, the difference being about 25% in five years and about 50% in six years. This difference in the survival rate approaches that between normotensive subjects and untreated severely hypertensive patients in the general population. It is concluded that hypertension is a serious limiting factor in the survival of patients on chronic hemodialysis, and that the difference in survival between the hypertensive and the non-hypertensive patients is attributable to hypertension.

Adolescent↗
PubMed1977

Reduction in severity of acute renal failure (ARF) in rats by dopamine.

Dopamine was administered to rats at the time of initiation of anoxic acute renal failure. Dopamine partially reduced the severity of ARF as evidenced by a reduction in blood urea, serum creatinine as well as an increase in glomerular filtration rate (GFR). (UNaV) in dopamine treated ARF was similar to sham operated animals and both were significantly lower than control ARF.

Acute Kidney Injury↗
PubMed1976

Chronic saline loading in anoxic renal failure in rats.

The effect of saline loading was compared in two types of experimental acute renal failure--due to i.m. administration of glycerol or to anoxia. In the glycerol model, chronic saline loading for about three weeks prior to the experiment achieved almost complete prevention of the uremia. The blood urea and serum creatinine levels 24 h after the experiment were 44 +/- 2 and 1.3 +/- 0.3 se) mg/dl, respectively. The values for the water-drinking rats were 292 +/- 23 and 3.7 +/- 0.4 mg/dl, respectively. In the anoxic model of acute renal failure, produced by uninephrectomy and contralateral renal artery clamping, chronic saline loading reduced the severity of the resultant uremia, although less impressively than in the glycerol model. The blood urea and serum creatinine 24 h after the experiment were 148 +/- 15 and 1.8 +/- 0.2 mg/dl, respectively. The values for the water-drinking rats were 237 +/- 15 and 2.3 +/- 0.2 mg/dl, respectively. Plasma renin activity was similar in the saline-loaded rats in both the toxic and anoxic models. It seems, therefore, that all known models of acute renal failure have at least a common pathogenic mechanism, which can be influenced by chronic saline loading prior to onset of the disease, and which is most probably not renin dependent. In the anoxic model additional factors, which cannot be counteracted by chronic saline loading, are active in the development of uremia.

Acute Kidney Injury↗
PubMed1976

High renin activity accompanying angiotensin II inhibition in rats with ischemic renal failure.

Acute renal failure was produced in rats by right nephrectomy and total occlusion of the left renal artery for 70 min. Angiotensin II competitive inhibitor, P113 (1-sar-8-ala-angiotensin II), was administered intravascularly for 100 min, starting 15 min before the clamping of the renal artery. A marked rise in plasma renin activity was observed 15 min after declamping and was significantly higher in the P113-treated rats than in saline-treated animals. The rise in plasma renin activity was observed 15 min after declamping and was similar in the two groups, indicating that P113 does not prevent the development of acute renal failure in this experimental model. It is suggested that the marked rise in plasma renin activity may be due to interruption of the normal feedback mechanisms which suppress renin release, as a result of occupation of the angiotensin II receptor sites by P113.

Acute Kidney Injury↗
PubMed1976

beta-Adrenergic blockade reduces the severity of acute renal failure in rats.

Propranolol administration in the hypoxic model of acute renal failure (ARF) in rats has reduced plasma renin activity (PRA) and uraemia as compared to untreated controls. P113 has no effect on uraemia but increased PRA in ARF. A combination of both drugs is no more effective in reducing uraemia than propranolol alone. These results support the view that beta-adrenergic blockade by propranolol reduces the severity of ARF by preventing the post-hypoxic release of renin.

Acute Kidney Injury↗
PubMed1975

Reduction in severity of acute renal failure in rats by beta-adrenergic blockade.

The effectiveness of beta-adrenergic blockade in preventing acute renal failure (A.R.F.) in rats was studied in the hypoxia model produced by unilateral nephrectomy and clamping of the contralateral renal artery for 70 minutes. Beta-adrenergic blockade effectively reduced the severity of A.R.F. in this experimental model. Treatment with a combination of propranolol and a synthetic angiotensin-II competitive inhibitor (P113) produced no further improvement. These results are consistent with the view that intrarenal release of renin is to some extent involved in the pathogenesis of A.R.F.

Acute Kidney Injury↗
PubMed1975

Acute renal failure in combat injuries.

The mortality in 25 patients suffering from post-combat injury acute renal failure (ARF) was 64%. Abdominal injuries were present in 17 patients with a mortality rate of 64.7%. Respiratory insufficiency occurred in 14 patients, jaundice occurred in 13, and septicemia in 10. The mean period of oliguria was high, 24.1 days per survivor, and the number of hemodialyses averaged 21.6 per survivor. It is concluded that the high mortality is primary due to the severity of the underlying injury itself and not due to the renal failure, that the ARF is more severe than in civilian injuries, as evidenced by a prolonged oliguric phase, and that frequent and intensive hemodialysis regimen is necessary for the elimination of deaths from uremia per se.

Acute Kidney Injury↗