Sodium-induced elevation of blood pressure in the anephric state.

Normotensive anephric rats infused with 2 milliliters of a hyperosmolar solution of either sodium chloride or mannitol showed an increase in arterial pressure that was very pronounced with the sodium chloride and that could be partly abolished by administration of an antagonist to the vasopressor action of antidiuretic hormone (ADH). Rats with congenital ADH deficiency subjected to the same treatment showed smaller increments in arterial pressure that remained unchanged after administration of the ADH antagonist. Expansion of intravascular fluid volume was similar in all four groups and bore no correlation to the change in arterial pressure. It is concluded that about half of the increase in blood pressure induced by saline was attributable to the vasopressor effect of stimulated ADH and the remainder to an additional sodium-related factor, since it was more pronounced in the saline-infused than in the mannitol-infused groups. Expansion of the intravascular volume per se could only account for a minimal part of the increment in pressure.

Interaction of the sympathetic nervous system with vasopressin and renin in the maintenance of blood pressure.

To evaluate the partial contributions and interaction of three vasopressor systems in blood pressure maintenance, nephrectomized rats and rats with intact kidneys were submitted sequentially to catecholamine depletion, elimination of vasopressin's vasoconstrictor action, and (for those with kidneys in situ) angiotensin blockade. Catecholamine depletion decreased blood pressure and stimulated vasopressin levels in all rats, but significantly more so in the anephric ones. Subsequent injection of an antagonist to the vasopressor effect of vasopressin produced a lasting fall of blood pressure in anephric rats, but only transient fall in those with intact kidneys. Infusion of teprotide--an angiotensin converting enzyme inhibitor--in the latter animals also produced transient blood pressure fall, but if this were followed by injection of the vasopressin antagonist, the pressure remained low for several hours. Blood pressure levels were closely correlated with those of plasma catecholamines throughout these maneuvers. Catecholamine levels were inversely correlated with those of plasma vasopressin, which were far greater in anephric rats through both stimulation and accumulation. Plasma renin activity was increasingly stimulated by falling blood pressure after each maneuver in rats with intact kidneys. Thus, it appears that in the resting state the sympathetic nervous system is more involved in the maintenance of blood pressure, whereas vasopressin and renin are important backup mechanisms.

Evidence for dopaminergic regulation of vasopressin release in the anephric rat.

Arginine vasopressin (AVP) release elicited by osmotic stimuli induces variable hypertensive responses. In normotensive anephric rats, a significantly greater blood pressure response was elicited by hypertonic saline than by mannitol infusion, and was further enhanced by previous dopaminergic receptor blockade. Plasma levels of AVP were significantly more elevated after saline than after mannitol despite more pronounced elevation of plasma osmolality in the latter animals, and were the highest in dopaminergically blocked animals. These findings indicate that dopamine exerts an inhibitory effect on the release of AVP.

Jejunogastric intussusception presented with hematemesis: a case presentation and review of the literature.

BACKGROUND: Jejunogastric intussusception (JGI) is a rare but potentially very serious complication of gastrectomy or gastrojejunostomy. To avoid mortality early diagnosis and prompt surgical intervention is mandatory. CASE PRESENTATION: A young man presented with epigastric pain and bilous vomiting followed by hematemesis,10 years after vagotomy and gastrojejunostomy for a bleeding duodenal ulcer. Emergency endoscopy showed JGI and the CT scan of the abdomen was compatible with this diagnosis. At laparotomy a retrograde type II, JGI was confirmed and managed by reduction of JGI without intestinal resection. Postoperative recovery was uneventful. CONCLUSIONS: JGI is a rare condition and less than 200 cases have been published since its first description in 1914. The clinical picture is almost diagnostic. Endoscopy performed by someone familiar with this rare entity is certainly diagnostic and CT-Scan of the abdomen could also help. There is no medical treatment for acute JGI and the correct treatment is surgical intervention as soon as possible.

Adamantiadis-Behçet's disease in sisters.

Two sisters with documented Adamantiadis-Behçet's disease of different severity, associated with HLA-B51, are described. Although the overall incidence of this complex disease is not different between sexes, only 4 female siblings, versus 14 male, that fulfill the 1990's International Study Group for Behçet's Disease criteria have been reported in the literature.

Different hemodynamic response after acute diuresis in the normotensive and hypertensive state.

Acute diuresis is considered to alter the hemodynamic responses in the hypertensive state by reducing cardiac preload, mainly due to venodilation. To investigate the magnitude of this event, normotensive and two kidney-one clip hypertensive rats have been subjected to similar plasma volume restrictions by i.v. injection of 0.5 ml of furosemide (1 mg/100 g b.wt.). Two other groups of normotensive and hypertensive rats were subjected to 0.5 ml of 5% dextrose solution injection and served as controls. Mean arterial blood pressure and heart rate did not change after furosemide injection in either the normotensive or the renovascular hypertensive group. Alternatively, cardiac output of the hypertensive rats receiving furosemide injection was significantly lower by 39.9% and total peripheral resistance was significantly higher by 48.4% when compared to hypertensive rats receiving dextrose solution injection, whereas there was no difference concerning these indices in normotensive rats after the same interventions. Due to redistribution of regional blood flow, the coronary, cerebral and renal circulations of the hypertensive rats after furosemide injection have been protected. It is concluded that i.v. injection of furosemide, by decreasing cardiac preload, mainly due to venodilation, reduces cardiac output of renin-dependent hypertensive animals, whereas mean arterial blood pressure and heart rate remain unaltered. Redistribution of blood flow to vital organs prevented a further deterioration of the cardiovascular system.

Regional blood flows and cardiac hemodynamics in renovascular and mineralocorticoid hypertensive rats.

Regional blood flows and cardiac hemodynamics were studied in 3 models of hypertensive rats: one-kidney DOC-saline, one-kidney, one-clip and two-kidney, one-clip hypertension and in normotensive control rats. All hypertensive models were characterized by increased peripheral vascular resistance and normal cardiac output. Coronary and cerebral blood flows varied among the hypertensive models but did not significantly differ from the normotensive rats. However, coronary blood flow of one-kidney, one-clip rats (8.4 +/- 1.3 ml X min-1 X g-1) was significantly higher than that of the two-kidney one-clip rats (6.5 +/- 1.2 ml X min.-1 X g-1, P less than 0.05). Cerebral blood flow of DOC-saline rats was lower than that of two-kidney one-clip or one-kidney one-clip renovascular rats. Renal blood flows of the unclipped kidney of two-kidney renovascular rats (3.77 +/- 0.85 ml X min-1 X g-1) and DOC-saline rats (2.95 +/- 0.83 ml X min-1 X g-1) were significantly lower than those of normotensive rats (5.92 +/- 1.16 ml X min-1 X g-1, P less than 0.05). In conclusion, although vascular resistance becomes elevated in all models of experimental hypertension, regional vascular resistance and blood flow distribution may differ depending on the vasoconstrictor mechanisms that participate in each model.

Systemic and regional hemodynamic effects of propranolol in intact and anephric rats.

We studied the changes in systemic and regional hemodynamics (using the radioactive microsphere technique) and catecholamine levels produced by propranolol in conscious semi-restrained intact or nephrectomized rats. Blood pressure increased by 17 +/- 2 and 32 +/- 2 mmHg in intact and anephric rats respectively, total peripheral vascular resistance by 61.5% and 176.5%, heart rate decreased by 23% and 35% respectively, cardiac index decreased by 35% and 57%, and stroke volume index by 14% and 30%. All changes were significantly more pronounced in anephric rats (p less than 0.05). Baseline norepinephrine, epinephrine, and dopamine were significantly higher in anephric versus intact animals and did not change significantly after B-blockade except for norepinephrine of the anephric rats which decreased. After B-blockade regional blood flows in most organs (including coronary flow) decreased in proportion to the diminished cardiac index except for brain flow which decreased by only 12% in intact and 25% in anephric animals. Local vascular resistances increased concomitantly and these changes were far more pronounced in the absence of kidneys. Thus, anephric state exacerbates all systemic and regional hemodynamic alterations caused by B-blockade in the rat.

Role of vasopressin, catecholamines, and plasma volume in hypertonic saline-induced hypertension.

Elevation of blood pressure induced by an acute sodium and fluid load in the anephric state has been attributed to intravascular fluid volume expansion. The present experiments were designed to study the role of vasopressin and catecholamines in this type of hypertension. Normotensive anephric rats, adrenergically intact or pretreated with alpha- and beta-adrenoceptor blockade, and deoxycorticosterone (DOC)-salt-treated anephric rats, intact or pretreated with alpha- and beta-adrenoceptor blockade, received an infusion of 2 ml containing 3 meq NaCl, followed by intravenous administration of an analogue antagonist of the vasopressor effect of arginine-vasopressin (AVP). Pressure increments induced by hypertonic saline were abolished by an AVP antagonist partly in the adrenergically intact animals (leaving a small residual pressure elevation) and completely in adrenergically blocked animals, which had a larger AVP component. Volumes expansion did not necessarily accompany increase in blood pressure after saline infusion. In fact some DOC-salt-treated animals with the highest blood pressures and norepinephrine levels exhibited contraction of plasma volume. Increments in blood pressure were negatively correlated with plasma volume changes (r = -0.687, P less than 0.05) in these animals and positively with norepinephrine levels in all adrenergically intact animals (r = 0.818, P less than 0.001). It is concluded that the hypertensive response elicited by acute hypertonic saline load is due to vasoconstriction mediated partly by vasopressin and partly by the sympathetic system, which may in some way attenuate the effect of vasopressin.

Systemic and regional hemodynamic effects of endogenous vasopressin stimulation in rats.

We investigated the systemic and regional hemodynamic alterations induced in normotensive anephric rats by stimulation of endogenous vasopressin with an acute sodium and fluid load and following vasopressin inhibition with a specific antagonist of its vasoconstricting action. Blood pressure and total peripheral resistance were significantly higher and cardiac output was lower in rats with stimulated vasopressin, and all were reversed to near control levels in rats receiving the vasopressin inhibitor. Regional blood flows were diminished in most organs and local vascular resistance was elevated compared with control animals, but the magnitude of change varied widely. In fact, heart blood flow did not decrease significantly and brain blood flow actually increased indicating small or no change in vascular resistance of these organs. Moreover, fractional distribution of the diminished cardiac output to these organs was significantly higher, so that blood flow to vital organs was maintained at the expense of blood flow to other tissues. In rats that received the vasopressin antagonist after the saline infusion, regional blood flows were similar to those of control animals. Blood pressures at the base line and after hypertonic NaCl infusion correlated closely with the corresponding plasma levels of control and stimulated vasopressin.

Adamantiadis-Behçet's syndrome: central nervous system involvement.

The prevalence of CNS involvement of Adamantiadis-Behçet's syndrome (A-Bs) vary widely. Long-term follow-up studies of CNS involvement have rarely been reported. Five patients with CNS involvement, who were followed up from 2 to 9 years, are presented. Clinicolaboratory investigations (cerebrospinal fluid examination, electroencephalogram, brain CAT scan and MRI) were carried out. One patient had four and two patients had two attacks of CNS involvement with various clinical manifestations. The other two patients had a rather chronic course with a single slight CNS attack. Raised proteins and IgG were found in the CSF. Abnormal electroencephalographic findings were detected in three patients. Communicating hydrocephalus and various other abnormalities on CT scan and MRI were noted. All patients received corticosteroids and immunosuppressants during the attack period.

Effects of tyrosine infusion in normotensive and hypertensive rats.

To clarify further the action of acute administration of L-tyrosine in lowering blood pressure, L-tyrosine ethylester was infused intravenously into awake [deoxycorticosterone acetate (DOCA)-salt] hypertensive rats, two-kidney Goldblatt hypertensive rats, and normotensive rats. The effects of tyrosine were measured on arterial pressure, heart rate, plasma catecholamine levels, and plasma renin activity. Blood pressure and heart rate were lowered in all groups despite significant elevation of plasma dopamine in all groups and epinephrine in the hypertensive groups, norepinephrine did not rise significantly, and plasma renin activity was always found to be within the ranges expected for each model. It was concluded that tyrosine produced the progressive decline in blood pressure and heart rate by bringing about a sustained state of parasympathetic dominance, as effective sympathetic compensation did not occcur. This could be attributed to increased alpha-adrenergic activity in certain sites in brain secondary to increased catecholaminergic activity in these areas.