Relationship between intrarenal distribution of blood flow and renin secretion during ureteral occlusion

The present study was undertaken to evaluate the relationship between renin secretion from the denervated kidney and intrarenal distribution of blood flow during reductions in renal perfusion pressure by partial constriction of the aorta with and without ureteral occlusion in the anesthetized dog. In addition, renin contents in different zones of the kidney were measured. A reduction in renal arterial pressure from normal pressure (125-135 mmHg) to 77 mm Hg resulted in significant increase in renin secretion and redistribution of cortical blood flow. A further reduction of renal arterial pressure to 51 mmHg produced a marked increase in renin secretion rate (RSR) without further changes in the intrarenal distribution pattern of blood flow. The pressure reductions during ureteral occlusion increased RSR without any change in the distribution pattern of blood flow, and a decrease in the amounts of extractable renin was found in the outer cortex of the experimental kidney. These findings suggest that renin release occurs mainly in the outer cortex, and this process may be stimulated when the mechanism of autoregulation fails as the perfusion presure approaches to the lower range of autoregulation in the outer cortex.     

Effect of Ouabain on cerebral blood flow (author's transl)

The effect of 0.25 mg ouabain on cerebral blood flow (CBF) was investigated in patients with and without cerebrovascular disease using the xenon clearance method. The 36 patients included in this study did not show any signs of heart failure. Ouabain increased the CBF and this effect was demonstrable 15, as well as 90 min. after administration. This effect was proven statistically using the t-test for a comparison of the values with spontaneous changes in a control group without medication. The perfusion of pathologically-supplied brain regions was altered in the same way as the hemispheric flow; changes in the distribution of blood in the way of a steal effect were not observed. The haemodynamic parameters do not indicate a primary cardiac effect. Hence, an influence of ouabain on cerebral vessels might be responsible. The present results support reported clinical experience with ouabain for the treatment of patients with cerebrosvascular disease.     

Ethacrynic acid induced release of prostaglandin E to increase renal blood flow

Ethacrynic acid administered to anesthetized dogs was found to increase the level of prostaglandin E as determined by radioimmunoassay in renal venous blood at the time when renal blood flow was increased by this agent. No change was found in the renal venous level of prostaglandin F. When ethacrynic acid was administered after treatment with indomethacin, which blocks the increase in renal blood flow induced by the natriuretic agent, no increase in the renal venous level of prostaglandin E was seen. Thus, the dilation of the renal vasculature would appear to be caused by a stimulation of synthesis and release of prostaglandin E by ethacrynic acid.     

Effects of solcoseryl on the cerebral blood flow, intracranial pressure, systemic blood pressure and EEG in acute intracranial hypertensive cats (author's transl)

The experiment was performed on 86 cases under intraperitoneal pentobarbital anesthesia. One balloon was placed in the extradural space of right frontal region, and the other balloon was placed in the left extradural space and the intracranial pressure was measured. A needle was stereotaxically inserted into the subcortical area in order to measure the cerebral blood flow. Systemic blood pressure was recorded by inserting a catheter into the femoral artery, and electrocorticogram was also recorded. An expanding intracranial lesion was made by inflating the extradural balloon with physiological saline. The animals were arbitrarily divided into two groups.: 1) light or moderate groups which intracranial pressure before the injection of drug was below 400 mmH2O. 2) severe groups above 400 mmH2O. After the maintenance of the pressure, Solcoseryl was infused intravenously. The investigation was focused to observe whether Solcoseryl reveales any potent effect on cerebral blood flow, intracranial pressure, systemic blood pressure and on electroencephalogram in acute intracranial hypertension. Results 1) Intravenous injection of Solcoseryl had the effect of lowering intracranial pressure in the light or moderate and severe groups. Particularly, dose of 80 mg/kg showed the marked effect, though with a rebound phenomenon in the light or moderate groups. Furthermore, the effect was more marked and lasting by drip infusion of Solcoseryl and also by intravenous injection of Solcoseryl after pretreatment with hydrocortisone, and at this time no rebound phenomenon was recognized. 2) Solcoseryl had the effect of increasing the cerebral blood flow accompained with the lowering of intracranial pressure. 3) Systemic blood pressure was transiently lowered by the injection of Solcoseryl 20 mg/kg or 80 mg/kg and recovered immediately. 4) Solcoseryl had no effect on electroencephalogram in the severe groups. Conclusion On the basis of these results, it is rational to conclude that Solcoseryl could be superior agent render to lower intracranial pressure and to improve cerebral blood flow in acute intracranial hypertension.     

Hydroxyproline fractions in blood (author's transl)

Modified methods for the determination of bound hydroxyproline in blood are presented. The fractionated and hydrolyzed samples are separated from interfering material by ion exchange chromatography. Internal standards are used to correct for recovery. After a several fold concentration of samples it is possible to work with reduced blood volumes. Up to 6.12 mumol/l of free and peptide-bound and 11.5 mumol/l of protein-bound hydroxyproline are detectable. Using the described methods hydroxyproline was determined in a pooled human plasma and in the sera of rats.     

Renal and intrarenal blood flow distribution in swine during severe exercise

It is known that a compensatory reduction and diversion of renal flow occurs in severe exercise in humans but not in dogs. We investigated this in miniature swine by measuring changes in total renal blood flow (TRF) and intra-renal blood flow (IRBF) distribution with tracer microspheres (15 +/- 5 mum) at rest and during steady-state exercise at 4.8-7.2 kph and 0% grade, and during severe exercise at 4.8-7.2 kph and 10% grade. We measured heart rate and cardiac output (Q) via implanted probes. TRF was determined as a percent of Q and as ml/100 g per min. IRBF was determined for the outer cortex, inner cortex, outer medulla, and inner medulla. Our results show that renal blood flow is significantly (P less than 0.05) reduced in pigs with exercise. Steady-state exercise reduced flow to about 66% of control and severe exercise reduced renal flow to 30% of control. IRBF was unchanged throughout. These results show that the exercising pig augments blood flow to skeletal muscle by reducing blood flow to kidneys, a response known to occur in man.     

Mechanism of LH release with synthetic LH-RH (author's transl)

The purpose of this study is to examine the effect of LH-RH on LH release in the baboon. Fifteen female baboons having the normal menstrual cycle were used for this study. On hundred mug of synthetic LH-RH was injected subcutaneously in both the early follicular phase and the early luteal phase. For control purposes, 1 ml of saline was injected subcutaneously in the luteal phase. Blood samples were collected by femoral vein puncture with light anesthesia under prearranged schedule and were assayed for LH-RH, LH, estrogen and progestin. The plasma level of LH-RH reached a maximum within 4 minutes after s.c. injection of 100 mug LH-RH, decreased sharply at first, and then slowly later. Fast and slow disappearance components (t1/2 = 4.7 min., 37.1 min. respectively) were observed. In the baboon given LH-RH during the luteal phase, peaks in plasma levels of LH were observed within 30 minutes and within 90 to 150 minutes after injection. A lesser pituitary response to LH-RH for LH release occurred during the follicular phase. The first peak of LH was well-correlated with the peak of plasma LH-RH but the later elevations of LH (observed within 90 to 150 minutes after LH-RH injection) were not necessarily related to the plasma level of immunoassayable LH-RH. Elevation of plasma levels of estrogen and progestin was observed wtihin 45 minutes after LH-RH injection. In saline control, the plasma level of LH was not elevated; however, plasma levels of estrogen and progestin were increased within 45 minutes after saline injection. Later elevation of plasma LH observed between 90 and 150 minutes after LH-RH injection may be due to administered LH-RH in cooperation with elevated levels of plasma estrogen and progestin. To pursue this problem, injections of estrogen and/or progesterone were performed during the early follicular phase. Injection of 600 mug of estrodiol benzoate (EB) for 3 days caused an elevation of plasma level of LH and enhanced pituitary LH responsiveness to LH-RH for LH release; however, injection of 100 mug EB for 3 days showed less effect on LH release. Injection of 10 mg of progesterone for 3 days also caused an elevation of plasma level of LH and enhanced the pituitary responsiveness to LH-RH release. Injection of both 600 mug EB and 10 mg progesterone for 3 days did not elevate plasma level of LH and showed no significant effect of LH-RH on LH release as compared to control. These results suggest that elevated levels of circulating estrogen and progestin may determine LH release and exposure of the pituitary to LH-RH is necessary for LH release. In dose and time schedule used in this study, it is inferred that estrogen and progesterone may exert their direct effect to hypothalamus on endogenous LH-RH secretion and also may exert their effect on pituitary gonadotrophs to change the sensitivity to LH-RH, i.e. these steroid hormones may be major factors in the control of gonadotropin release in the baboon.     

A new contrast-medium (author's transl)

Infusion urograms were carried out on 2 groups of 100 in-patients each. The first group had injections of Conray FL 36, the second of Conray FL. Contrast in the early phase after 7 minutes was better with Conray FL 36 than with Conray FL. At later stages there was no clear difference.     

A panel on vascular surgery (author's transl)

For this second panel by correspondence, we have asked 3 distinguished experts to answer 7 questions and to comment on 3 case histories concerning vascular surgery. Although a direct discussion between the participants was not possible an impressive degree of agreement is here being demonstrated.     

Effect of prostaglandin endoperoxide analogue on canine renal function, hemodynamics and renin release

We studied the effect of a stable, cyclic ether analogue of prostaglandin endoperoxide (EPA) on canine renal function, hemodynamics, and renin release. Infusion of EPA into one renal artery decreased renal blood flow in a dose dependent manner. At a dose of 10(-7) g/kg/min the renal blood flow decreased from a baseline of 384 to 267 ml/min/100 g. This flow decrease was unaltered by phentolamine and saralasin, but was potentiated by prior treatment with indomethacin. Urine flow, glomerular filtration rate, sodium, and potassium excretion all decreased in a dose dependent manner; however, neigher fractional excretion of sodium nor free water clearance showed any significant change, making direct tubular effects of EPA unlikely. EPA caused a significant increase in renin release that was completely blocked by prior treatment with indomethacin. We conclude that EPA is a potent renal vasoconstrictor and that this vasoconstriction is responsible for the renal functional changes observed. Renin release is not a direct effect of EPA but probably is secondary to an endogenously generated prostaglandin. Since EPA mimics the effects of natural prostaglandin endoperoxides on smooth muscle in vitro, it is possible that prostaglandin endoperoxide-induced vasoconstriction in vivo modulates the effects of their vasodilatory products, prostaglandin E2 and I2.     

Studies of sustained release cephalexin (S-6437) in pediatrics (author's transl)

S-6437 is granule of sustained-release cephalexin which is prepared as longer acting cephalexin. Each gram of the granule contains 200 mg of cephalexin. Absorption and excretion study of this preparation was performed in 8 patients (3 school children, 3 infants and 2 babies). Mean blood levels of cephalexin following a single oral administration of 25 mg/kg in the school children, for instance, were 1.73, 2.47, 3.11, 2.28, 3.84 and 2.86 mcg/ml at 0.5, 1.0, 2.0, 4.0, 6.0 and 8.0 hours, respectively. Fifty-two patients with acute respiratory tract infections were treated with this preparation and out of the 52, 33 were evaluable cases. The daily dose used was 50 mg/kg divided in two doses. Of the 33 patients 29 responded to this preparation showing 87.8% of effectiveness. Four patients who did not respond were 1 with acute pharyngitis, 2 with acute tonsillitis, and 1 with acute bronchitis. No severe side effects due to this preparation were observed.