Sequential measurement of beta 2-microglobulin levels, p24 antigen levels, and antibody titers following transplantation of a human immunodeficiency virus-infected kidney allograft.

A renal allograft recipient developed symptoms suggestive of AIDS. Serological studies revealed that the donor was positive for human immunodeficiency virus (HIV). Retrospective testing of stored sequential serum samples showed that the recipient was negative for HIV pretransplant; anti-p24 and anti-p41 antibodies appeared 10 and 49 days posttransplant, respectively. The recipient's serum beta 2-microglobulin levels were elevated 14 days posttransplant, with normal renal function, 35 days before the detection of anti-p24 antibody. p24 Antigen was detected for the first time 21 days posttransplant. In addition to p24 antigen, elevated serum beta 2-microglobulins may be a useful marker for HIV infection prior to seroconversion.

The cardiovascular and metabolic effects of mixtures of acetate and succinate: a potential improvement in dialysate solutions.

Various mixtures of acetate (AC) and succinate (SUCC) were studied for their metabolic and cardiovascular (CV) effects in 10 dogs. The CV effects seen with all mixtures were similar to those reported for SUCC alone with the only changes being increased cardiac output and decreased total peripheral resistance. The 50:50 per cent AC/SUCC offered the advantage of a rapid but less marked and more sustained HCO3 production. The pH changes in all mixtures followed HCO3 values. Since the addition of SUCC seems to reduce the untoward CV changes seen with AC alone, the ratio of AC/SUCC should be based on metabolic considerations. The present data suggest that a 50:50 per cent AC/SUCC mixture is optimal for metabolic and CV effects.

Effect of reserpine on relaxant responses of canine femoral arterial strips.

1. We studied relaxant responses to adenosine, glyceryl trinitrate, and hydralazine in control (n=5) and reserpine pretreated (1 mg/kg i.m., 24 h prior; n=5) canine femoral arterial strips contracted with noradrenaline. 2. Reserpine did not alter contractile responses to noradrenaline. 3. Reserpine pretreated tissues were supersensitive to glyceryl trinitrate, but not to adenosine or hydralazine.

Effect of reserpine pretreatment on in vivo femoral arterial responses to vasodilator agents.

This study determined the effects of reserpine pretreatment (1 mg/kg i.m., 24 hr before) on in vivo femoral arterial responses in the dog to the vasodilator agents acetylcholine, isoproterenol, dibutyryl cyclic AMP, adenosine, nitroglycerin and hydralazine. Femoral blood flow was monitored from the right femoral artery into which i.a. injections of the vasodilator agents were given just distal to the flow probe. Femoral vascular resistance was calculated as the ratio of mean systemic blood pressure to femoral blood flow. The response to each dose of vasodilator agent was evaluated by the magnitude of the slope of the regression line relating the resultant decrease in resistance to the resistance before the injection. Reserpine pretreatment increased slopes of these regression lines for adenosine, nitroglycerin, acetylcholine and isoproterenol, suggesting a general enhancement of vasodilator responses by reserpine. Both hydralazine pretreatment (1 mg/kg i.v., 1 hr before testing) and partial aortic occlusion during testing decreased femoral perfusion pressure without increasing vasodilator responses of the femoral arterial bed to adenosine, nitroglycerin, acetylcholine or isoproterenol. Therefore, the enhancement of vasodilator responses by reserpine was apparently not a result of decreased femoral perfusion pressure due to reserpine.

The hypotensive response to compound 48/80 in normotensive and hypertensive rats.

1. The administration of an initial dose of 50 micrograms/kg of 48/80 produced a sharp fall in the blood pressure of normotensive rats but produced little change in blood pressure in spontaneously hypertensive rats. 2. The administration of an additional 50 micrograms/kg and 100 micrograms/kh of 48/80 in normotensive and spontaneously hypertensive rats resulted in equivalent decreases in pressure in both groups. 3. Both groups had equivalent decreases in blood pressure in response to methylhistamine. 4. Spontaneously hypertensive rats appear to have a reduced ability to release histamine in response to 48/80 due to either an increased threshold for 48/80 or a diminished histamine storage pool.

The cardiac and vascular effects of sodium glutamate.

1. The cardiovascular effects of sodium glutamate were investigated in anaesthetized dogs with bolus injections, intravenous infusions and rabbit isolated papillary muscles. 2. The intravenous bolus injections of sodium glutamate resulted in slight, transient decreases in contractile force at doses of 58 and 117 mg/kg, which were followed by brief increases in blood pressure. 3. Sodium glutamate had no effect on contractile responses of isolated papillary muscles at any of the concentrations used. 4. Infusions of glutamate produced no change in blood pressure, an increase in cardiac output, and a decrease in heart rate, total peripheral resistance and femoral vascular resistance. 5. The infusion of sodium glutamate into animals with no renal function resulted in an increased plasma osmolality and a decreased haematocrit. 6. The results from this study show that sodium glutamate had minimal cardiovascular effects. The results from the infusion data suggest that glutamate increases intravascular volume by an osmotic effect.

Tooth pulp pressure: local and systemic influences of epinephrine and acetylcholine.

The local and systemic effects of epinephrine and acetylcholine on tooth pulp pressure were evaluated in dogs by intra-arterial and intravenous injection of these compounds. Control pulp pressure recorded from the dog's canine tooth was 58 +/- 6 mm Hg. Intra-arterial epinephrine produced dose-related decreases in pulp pressure which were antagonized by alpha-adrenergic receptor blockade with phentolamine. These results suggest that the fall in pulp pressure is the result of local vasoconstriction and reduced blood flow into the pulp. Acetylcholine did not affect pulp pressure, suggesting a lack of cholinergic vasodilator receptors in the pulp. The intravenous epinephrine and acetylcholine resulted in alterations in pulp pressure in the same direction as systemic blood pressure changes. This study indicates that pulp pressure is affected by systemic blood pressure changes as well as by local sympathetic nervous system effects.