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Biomedical subjects

J D Irvin

Publications and source records attributed to J D Irvin.

69 records · Page 4Linked to original sources
PubMed1979

Influence of arterial blood pressure upon central hemorrhagic necrosis after severe spinal cord injury.

To determine the influence of systemic arterial blood pressure upon the pathogenesis of spinal cord injury, we eliminated the increase in systemic blood pressure normally observed after trauma to the spinal cord with the ganglionic blocker chlorisondamine. Blockade of the pressure response did not influence the development of hemorrhagic necrosis in the spinal cord. We conclude that the transient pressure response accompanying spinal cord injury is probably not a major factor in the pathogenesis of hemorrhagic necrosis at the site of the spinal cord injury.

Animals↗
PubMed1976

The nature of the differential inhibition of polyphenylalanine synthesis in extracts from Artemia salina and rabbit reticulocytes by the Phytolacca americana protein.

The difference in sensitivity of polyphenylalanine synthesis in extracts from Artemia salina and rabbit reticulocytes to inhibition by the Phytolacca americana protein (PAP) has been found to be linked to the source of the supernatant enzyme fraction and not the ribosomes. In the presence of reticulocyte supernatant enzyme fraction polyphenylalanine synthesis in less sensitive to inhibition by PAP than that observed in the presence of A. salina supernatant enzyme fraction. The results suggest that reticulocyte elongation factor 2 is responsible for this effect.

Animals↗
PubMedDate not supplied

Evidence for route dependent biotransformation of cyclobenzaprine hydrochloride.

Cyclobenzaprine hydrochloride was administered to healthy volunteers as a 10 mg oral tablet, 10 mg and 20 mg intramuscular injections, and a 10 mg intravenous injection. Urinary excretion and plasma level data for cyclobenzaprine together provide evidence for route dependent biotransformation. Urinary excretion of total cyclobenzaprine (unchanged plus the glucuronide conjugate) was greater for the oral treatment than for the parenteral treatments (i.m. and i.v.). Area under the plasma concentration-time curve for unchanged cyclobenzaprine, however, was less for the oral treatment than for the parenteral treatments. Based on area calculations, the bioavailability of the 10 mg oral tablet, 10 mg i.m. and 20 mg i.m. injection was 0.33, 0.76, and 0.56, respectively, when compared to the 10 mg i.v. injection of cyclobenzaprine hydrochloride. The four treatments were well tolerated and no clinically adverse effects were observed.

Adult↗
PubMedDate not supplied

Comparative antihypertensive effects of enalapril maleate and hydrochlorothiazide, alone and in combination.

Enalapril maleate is an investigational oral prodrug whose hydrolyzed diacid metabolite is a potent angiotensin-converting enzyme inhibitor. Fourteen patients with mild to moderate hypertension were evaluated after receiving placebo, and two weeks of treatment with each of the following: enalapril maleate (20 mg b.i.d.), hydrochlorothiazide (25 mg b.i.d.), and the two in combination. In comparison to placebo, the magnitudes of the blood pressure reduction after enalapril and hydrochlorothiazide alone were comparable. The reduction in blood pressure following enalapril was evident throughout the 12-hour dosing interval. The combination of enalapril and hydrochlorothiazide resulted in a marked further reduction in blood pressure that was greater than that predicted from the responses to the individual drugs (P less than 0.05). Biochemical parameters confirmed inhibition of angiotensin-converting enzyme during enalapril treatment; serum angiotensin-converting enzyme activity proved an excellent monitor of compliance. Enalapril was generally well tolerated. Adverse effects included symptomatic hypotension in three patients when enalapril was first added to hydrochlorothiazide and hyperesthesia of the oral mucosa without a loss of taste in one patient on enalapril. Enalapril maleate alone and especially in combination with hydrochlorothiazide appears to be an effective, well-tolerated converting enzyme inhibitor with at least a 12-hour duration of action.

Adult↗
PubMedDate not supplied

Indacrinone: natriuretic and uricosuric effects of various ratios of its enantiomers in healthy men.

Indacrinone is an investigational loop-acting diuretic. To evaluate the natriuretic and uricosuric effects of varying ratios of its enantiomers, 10 healthy men, on a controlled Na+ (100 mEq) and K+ (80 mEq) diet, participated in a double-blind, randomized, balanced incomplete block, multiple-dose (one week) study of a fixed daily dose (10 mg) of (-) enantiomer combined with increasing doses (40, 90 and 140 mg) of (+) enantiomer versus 50 mg hydrochlorothiazide and placebo. On day 1, mean 24-h urinary Na+ increased (p less than 0.01) comparably (approximately 285 mEq) after each enantiomer combination and hydrochlorothiazide; however, the enantiomer combinations had marked uricosuric and hypouricemic effects that were enhanced with increased (+) enantiomer doses. By day 7, while enantiomer combinations and hydrochlorothiazide demonstrated comparable natriuretic activity, mean serum uric acid levels (mg/dl), in comparison to placebo, were increased (p less than 0.05) with hydrochlorothiazide but progressively decreased with increases in (+) enantiomer. Thus varying the ratio [(+, uricosuric): (-, natriuretic)] of the enantiomers of indacrinone caused natriuresis similar to hydrochlorothiazide, but had an opposite effect on serum uric acid.

Adult↗
PubMedDate not supplied

Tolerability of long term therapy with enalapril maleate in patients resistant to other therapies and intolerant to captopril.

Patients with severe hypertension and/or congestive heart failure (n = 281) who were unresponsive to other therapies and intolerant to captopril received enalapril treatment (mean dose 19.5 mg/day) under study conditions as part of a Compassionate Use Program. Many of these patients had serious concurrent disorders known to predispose them to a greater risk of adverse experiences and death. The mean duration of enalapril treatment was 29 weeks, with a range of 1 day to approximately 3.5 years. Enalapril was generally well tolerated, and the estimated long term probability of patients terminating enalapril therapy because of adverse effects was low. 20 patients had discontinued captopril treatment because of low white blood cell counts; during subsequent enalapril treatment these reactions resolved in 14 patients, persisted in 2 patients, and could not be evaluated in 4 patients. Captopril-related proteinuria improved or resolved in 9 and persisted in 2 of 15 patients, taste disturbances resolved in 35 and persisted in 2 of 38 patients; and rash resolved in all but 7 of 178 patients during enalapril treatment. 18 patients (6%) discontinued enalapril treatment because of lack of efficacy; 6 of these 18 patients died due to a progression of heart failure, and another 11 patients died for other reasons. The deaths were considered unrelated to therapy with enalapril. Adverse reactions were the reason for discontinuation of enalapril treatment in 53 patients (19%). The most common adverse experiences that resulted in discontinuation of enalapril were: impairment of renal function (5%), hypotension (2%) and rash (2%). No neutropenia, proteinuria, or new taste disturbances were recorded as reasons for discontinuation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

Role of adrenergic nerves in blood-induced cerebral vasospasm.

Cerebral arteries have an abundant supply of adrenergic nerve fibers which are believed to release vasoactive substances responsible for the induction of cerebral vasospasm. To assess the importance of adrenergic nerves in this phenomenon, high doses (600 microgram/ml) of 6-hydroxydopamine (6-OHDA) were used to produce in vitro chemical sympathectomy in bovine middle cerebral artery. 6-OHDA reduced catecholamine fluorescence to undectable limits. H3-norepinephrine re-uptake was reduced to 1.5% of intact controls. Arterial norepinephrine content was reduced by 92%. Contractile responses to norepinephrine, serotonin, and fresh human whole blood were modestly reduced after denervation. This reduction was probably due to alpha receptor inactivation by 6-OHDA, because after protection of the alpha receptors with phentolamine the vessel response was the same as in untreated controls. Contractions in response to aged human whole blood were not affected by denervation. The results suggest that the endogenous release of catecholamines does not play a major role in the initiation or spread of blood-induced vasospasm in large cerebral arteries.

Adrenergic Fibers↗