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Biomedical subjects

J G Gerber

Publications and source records attributed to J G Gerber.

At least 109 records · Page 6Linked to original sources
PubMed1980

Moderation of hypoxic vasoconstriction by infused arachidonic acid: role of PGI2.

To determine the role of prostaglandins in modulating pulmonary circulatory responses, we examined the effect of the prostaglandin precursor, sodium arachidonate, on the pulmonary vascular resistance of mongrel dogs during alveolar hypoxia. When infused intravenously for 5 min during hypoxia, sodium arachidonate (1 mg/min) decreased pulmonary vascular resistance from 6.9 +/- 1.1 to 4.9 +/- 0.6 U (P less than 0.05). The vasodilation produced by sodium arachidonate was blocked by sodium meclofenamate, a cyclooxygenase inhibitor. By infusing radiolabeled sodium arachidonate and collecting aortic blood samples, we found from chromatographic and mass spectrometric analysis that a major prostaglandin produced was 6-keto-PGF1 alpha, the stable hydrolysis product of PGI2. Infusion of PGI2, but not PGE2, during hypoxia decreased pulmonary vascular resistance. We concluded that the prostaglandin precursor, sodium arachidonate, is a vasodilator of the pulmonary vasculature that has been constricted by alveolar hypoxia, probably because PGI2 is formed from the arachidonate. The pulmonary circulation may be similar to the systemic circulation where vasoconstriction results in the generation of vasodilatory prostaglandins that attenuate the constrictor effect.

Animals↗
PubMed1980

Antihypertensive pharmacology.

Although drug treatment of hypertension is associated with improved survival and decreased vascular complications, drug compliance is a major problem in the control of hypertension. All antihypertensive medications are associated with side effects; thus, it is a physician's responsibility to explain to each patient the side effects of the drugs he prescribes to treat hypertension, and to instill in the patient a sense of necessity for the treatment of hypertension. The choice of antihypertensive drug should be made based on each patient's lifestyle, overall health and ability to tolerate the drug. Ideally, the antihypertensive regimen should be simple, effective, convenient to take and have very few side effects.

Adolescent↗
PubMed1980

Furosemide-induced renal vasodilation: the role of the release of arachidonic acid.

Furosemide administration results in an increase in blood flow through the prostaglandin system by causing the release of arachidonic acid from a small pool of lipid stores from the kidney without affecting the total arachidonic acid concentration in the blood. The stimulus for arachidonic acid release from the kidney depends on an intrarenal mechanism whereby the diuresis is coupled to the increase in renal blood flow.

Animals↗
PubMed1979

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.

Animals↗
PubMed1979

Uterine vein prostaglandin levels in late pregnant dogs.

We studied the uterine venous plasma concentrations of prostaglandins E2, F2 alpha, 15 keto 13,14 dihydro E2 and 15 keto 13,14 dihydro F2 alpha in late pregnant dogs in order to evaluate the rates of production and metabolism of prostaglandin E2 and F2 alpha in pregnancy in vivo. We used a very specific and sensitive gas chromatography-mass spectrometry assay to measure these prostaglandins. The uterine venous concentrations of prostaglandin E2 and 15 keto 13,14 dihydro E2 were 1.35 +/- .27 ng/ml and 1.89 +/- .37 ng/ml, respectively; however, we could not find any prostaglandin F2 alpha and very little of its plasma metabolite in uterine venous plasma. Since uterine microsomes can generate prostaglandin F2 alpha and E2 from endoperoxides, prostaglandin F2 alpha production in vivo must be regulated through an enzymatic step after endoperoxide formation. Prostaglandin E2 is produced by pregnant canine uterus in quantities high enough to have a biological effect in late pregnancy; however, prostaglandin F2 alpha does not appear to play a role at this stage of pregnancy.

Animals↗
PubMed1979

Tartrazine and the prostaglandin system.

The effect of tartrazine on prostaglandin production was evaluated in several in vitro systems in order to elucidate the interrelationship between aspirin-sensitive asthma and tartrazine. Unlike the nonsteroidal anti-inflammatory drugs, tartrazine did not inhibit cyclooxygenase activity in sheep seminal vesicles, guinea pig lung microsomes, and human platelets. Tartrazine had no effect on the activation of acyl hydrolase, which is the rate-limiting step in prostaglandin production. The major metabolite of tartrazine, sulfanilic acid, also had no inhibitory effect on the sheep seminal vesicle cyclooxygenase. In view of these findings, if there is a cross-sensitivity between tartrazine and aspirin in aspirin-sensitive asthmatics, it is unlikely to be on the basis of prostaglandin inhibition.

Animals↗
PubMed1979

The role of renal metabolism of PGE2 in determining its activity as a renal vasodilator in the dog.

Since the mammalian renal cortex avidly metabolizes prostaglandin E2 (PGE2), we examined the importance of renal metabolism of PGE2 in determining its renal vascular activity in the dog. We used 13, 14 dihydro PGE2 (DHPGE2) as a model compound to study this because DHPGE2 retains similar activity to the parent prostaglandin, PGE2, but is a poorer substrate than PGE2 for both the metabolism and the cellular uptake of the prostaglandins. Using dog renal cortical slices, we found that under similar experimental conditions, PGE2 was metabolized several-fold faster than DHPGE2. Both prostaglandins were metabolized to the 15 keto 13, 14 dihydro PGE2, which was positively identified using GC-MS. In vivo, we infused increasing concentrations of DHPGE2 into the renal artery of dogs and measured renal hemodynamic changes using radioactive microspheres. DHPGE2 was a potent renal vasodilator beginning at an infusion rate of 10(-9)g/kg/min. When compared to PGE2, DHPGE2 was about 10 times more potent in affecting renal vasodilation. The intrarenal redistribution of blood flow towards the inner cortex seen with DHPGE2 was identical to that seen with PGE2. We conclude that renal catabolism of PGE2 is very important in limiting the in vivo biological activity of PGE2, but regional differences in metabolism of PGE2 within the cortex are an unlikely determinant of the pattern of redistribution of renal blood flow.

Animals↗
PubMed1979

Severe leukopenia secondary to carbamazepine administration.

We have reported the first case of severe leukopenia, complicated by infection, associated with the use of carbamazepine. In the literature, most cases of leukopenia secondary to carbamazepine are transient and benign, but any increase in dosage of the drug warrants a close follow-up of blood counts even if previous blood counts were normal.

Adult↗
PubMed1979

The failure of indomethacin to alter ACTH-induced adrenal hyperaemia or steroidogenesis in the anaesthetized dog.

1 The response of adrenal blood flow to adrenocorticotropic hormone (ACTH) was measured with radioactive microspheres in anaesthetized, dexamethasone-treated, mongrel dog. 2 Adrenocorticotropic hormone (2 u/h i.v.) increased adrenal blood flow within 15 min and this persisted for the duration of the infusion. 3 Cortisol concentrations also rose with ACTH infusion. 4 Indomethacin (6 mg/kg i.v. followed by 1 mg/min) did not effect the adrenal response to ACTH although plasma concentrations of indomethacin (21.9 +/- 2.5 micrograms/ml) adequate to suppress prostaglandin synthesis were achieved. 5 We conclude that prostaglandins are not required for steroidogenesis or the adrenal haemodynamic response to ACTH.

Adrenal Glands↗
PubMed1979

The hemodynamic effects of prostaglandins in the rat. Evidence for important species variation in renovascular responses.

The hemodynamic effects of prostaglandins E2, F2alpha, D2, and I2, and of indomethacin and arachidonic acid were studied in Sprague-Dawley rats, by means of the radioactive microsphere technique. In contrast to effects in other species, PGE2, PGD2, and arachidonic acid were renal vasoconstrictors in the rat, although PGE2 and arachidonic acid reduced total vascular resistance. PGF2alpha and indomethacin had no effect on the renal vasculature, but PGI2 produced renal and systemic vasodilation. These data indicate that if prostaglandin-mediated renal vasodilation occurs in the rat, PGI2 may be the substance responsible. In view of the species differences in renal vascular responses to the prostaglandins, the rat may not be an appropriate model for study of the prostaglandin system as it relates to other species.

Animals↗