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Biomedical subjects

J L Izzo

Publications and source records attributed to J L Izzo.

At least 73 records · Page 4Linked to original sources
PubMed1983

Protective effects of beta blockade on pulmonary function when intracranial pressure is elevated.

Intracranial pressure (ICP) was increased by hyperosmolar intracerebral infusion in dogs and the cardiopulmonary and catecholamine (CA) responses followed for 4 h. Increased ICP evoked persistent increases in endogenous CAs, pulmonary vascular pressures, pulmonary blood volume, and venous admixture. Other dogs similarly monitored were treated with a beta-blocking dose of propranolol 25 min after the onset of increased ICP. Although catecholamines were increased, elevated pulmonary pressures and venous admixture returned to control levels. CO and heart rate (HR) were reduced after beta blockade but systemic vascular resistance increased. It was concluded that increased ICP induces sustained increases in CAs which adversely affect pulmonary pressures and shunting. Selective beta blockade reverses these effects and may be useful in patients with evidence of sympathetic overactivity and progressive hypoxemia after head injury.

Animals↗
PubMed1983

Abnormal norepinephrine release in uremia.

Sympathetic nervous activity, which we defined as the relative rate of appearance of norepinephrine (NE) in plasma, was investigated in normal men (control) and uremic patients with two-step steady-state cold NE infusions. Both basal venous NE and the NE metabolic clearance rate (CNE, calculated from the infusion rate and the steady-state increment in venous NE) were higher in patients than in controls. The calculated appearance rate of NE in venous plasma (CNE X basal NE) was much higher in the patients, suggesting increased NE release and therefore sympathetic nervous hyperactivity in these patients. Of interest was the fall in both CNE and NE appearance rate at the higher infusion rate in controls, but not patients. These data suggest that circulating NE may normally suppress sympathetic nervous activity, but that this negative feedback mechanism is impaired in uremia.

Adult↗
PubMed1981

Physiologic mechanisms opposing the hemodynamic effects of prazosin.

Prazosin was give for 10 to 14 days to eight hypertensive patients on a fixed intake of dietary salt. Except as limited by side effects, the dose was increased from 2 mg/day to a maximum dose of 24 mg/day. During treatment, when subjects were studied in supine and upright positions, mean arterial pressure (MAP) fell 6% and 12% (p less than 0.025 and p less than 0.005), heart rate rose 3% and 9% (p less than 0.05 and p less than 0.005), and plasma norepinephrine increased 95% and 107% (p less than 0.01 and p less than 0.001) over control. Daily excretion of the norepinephrine metabolites methoxyhydroxyphenyl glycol (MHPG) and vanillylmandelic acid (VMA) increased 42% and 17% (p less than 0.05 for each) during treatment. There were no changes in average body weight or plasma renin for the group, but patients whose body weight increased tended to show less reduction in blood pressure (correlation coefficient, r = 0.72, p less than 0.05) and smaller increases in heart rate (r = -.073, p less than 0.05) during treatment with prazosin. These data suggest that expansion of extracellular fluid and activation of the sympathetic nervous system oppose the hemodynamic effects of prazosin.

Adult↗
PubMed1979

Relationship of human urinary and plasma kinins to sodium-retaining steroids and plasma renin activity.

In these studies we have shown that: 1. urinary kallikrein is an index of sodium-retaining steroid activity and may participate in the anti-natriuretic and kaliuretic effects of these hormones; 2. urinary kinin excretion is independent of changes in urinary kallikrein excretion; 3. levels of plasma bradykinin are highly correlated with levels of plasma renin activity probably because both respond to changes in extracellular fluid volume; and, 4. plasma bradykinin may act to antagonize angiotensin II to maintain normal blood pressure in hyper-reninemic states.

Adolescent↗
PubMed1978

The kallikrein-kinin system in Bartter's syndrome and its response to prostaglandin synthetase inhibition.

The kallikrein-kinin system was characterized in seven patients with Bartter's syndrome on constant metabolic regimens before, during, and after treatment with prostaglandin synthetase inhibitors. Patients with Bartter's syndrome had high values for plasma bradykinin, plasma renin activity (PRA), urinary kallikrein, urinary immunoreactive prostaglandin E excretion, and urinary aldosterone; urinary kinins were subnormal and plasma prekallikrein was normal. Treatment with indomethacin or ibuprofen which decreased urinary immunoreactive prostaglandin E excretion by 67%, decreased mean PRA (patients recumbent) from 17.3+/-5.3 (S.E.M.) ng/ml per h to 3.3+/-1.1 ng/ml per h, mean plasma bradykinin (patients recumbent) from 15.4+/-4.4 ng/ml to 3.9+/-0.9 ng/ml, mean urinary kallikrein excretion from 24.8+/-3.2 tosyl-arginine-methyl ester units (TU)/day to 12.4+/-2.0 TU/day, but increased mean urinary kinin excretion from 3.8+/-1.3 mug/day to 8.5+/-2.5 mug/day. Plasma prekallikrein remained unchanged at 1.4 TU/ml. Thus, with prostaglandin synthetase inhibition, values for urinary kallikrein and kinin and plasma bradykinin returned to normal pari passu with changes in PRA, in aldosterone, and in prostaglandin E. The results suggest that, in Bartter's syndrome, prostaglandins mediate the low urinary kinins and the high plasma bradykinin, and that urinary kallikrein, which is aldosterone dependent, does not control kinin excretion. The high plasma bradykinin may be a cause of the pressor hyporesponsiveness to angiotensin II which characterizes the syndrome.

Adolescent↗