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Biomedical subjects

J C Rose

Publications and source records attributed to J C Rose.

At least 181 records · Page 10Linked to original sources
PubMed1977

Circulatory effects of prostaglandin endoperoxide analogues studied in the dog during left ventricular bypass.

1. Intravenous administration of both the 9alpha,11alpha-(epoxymethano) and 11alpha,9alpha-(epoxymethano) analogues of prostaglandin H2 (0.25 microgram/kg) produced a prominent rise in pulmonary arterial pressure and a moderate increase in systemic arterial pressure. 2. Direct administration of the endoperoxide analogues (1.25 microgram/kg) into the bypass reservoir produced a greater rise in systemic arterial pressure and less prominent rise in pulmonary arterial pressure. 3. An intravenous dose of prostaglandin F2alpha that was 20 times larger was needed to produce a comparable rise in pulmonary arterial pressure. 4. The pulmonary and systemic pressor responses produced by the endoperoxide analogues were due to a direct increase in the vascular resistance.

Animals↗
PubMed1977

Effect of electrical stimulation of the canine diencephalon on the secretion of ACTH, growth hormone (GH) and prolactin (P).

Plasma levels of ACTH, growth hormone (GH), prolactin (Prl) and corticoids were simultaneously monitored before, during and after diencephalic stimulation in 18 pentobarbital-anesthetized dogs. Constant-current, monopolar biphasic stimulation of several regions of the canine ventral medial hypothalamus caused rapid increases in ACTH and corticoid concentrations. No increases in plasma GH were seen during stimulation, but plasma GH increased after the stimulus was turned off when the stimulating electrodes were in the arcuate-median eminence region. Plasma Prl concentration was not increased or decreased by stimulation of the ventral medial hypothalamus, but in 2 instances in 1 dog, it was increased by stimulation of the nucleus supraopticus difusus. The data indicate that different areas in the hypothalamus regulate the secretion of these 3 anterior pituitary (AP) hormones.

Adrenocorticotropic Hormone↗
PubMed1977

An intrarenal effect of somatostatin on water excretion.

Intrarenal infusion of somatostatin in anesthetized dogs produced a prompt increase in urine flow in association with a decrease in urinary osmolality and an increase in free water clearance. These changes occurred in the absence of changes in arterial pressure, renal plasma flow, osmolar clearance, electrolyte excretion or cyclic AMP excretion. The diuretic effect occurred primarily in the infused kidney indicating a direct intrarenal action rather than suppression of vasopressin secretion. This diuretic action of somatostatin may result from inhibition of the action of vasopressin on the renal medulla but other possible mechanisms cannot be excluded.

Animals↗
PubMed1977

Vascular responses to the monoenoic prostaglandin precursor dihomo-gamma-linolenic acid in the perfused canine lung.

Dihomo-gamma-linolenic acid (DGLA; 2 mg/kg i.v.), the monoenoic prostaglandin (PG) precursor was reported earlier to produce systemic hypotension in the intact dog. It is shown here to produce pulmonary vasoconstriction when given (50-500 microng/kg) in the pulmonary artery of the isolated perfused canine lung lobe. This effect is similar to that of arachidonic acid (AA), the bisenoic PG precursor. PGF1alpha was vasopressor in both preparations. The DGLA response at 100 microng/kg in the lung was nearly identical with that of AA25 microng/kg; DGLA 200 microng/kg=AA50 microng/kg;DGLA 300microng/kg=AA 100 microng/kg. The DGLA 100 microng/kg response was nearly equal to that with PGF1alpha 1 microng/kg. The equipressor dose ratio, DGLA/AA, varied 2.5 to f1 and DGLA/PGF1alpha was 100:1. DGLA and AA vascular responses were blocked by indomethacin. Linoleic acid, used as a control fatty acid, had no pulmonary pressor action. When a dextran-based artificial perfusate was used, the vasopressor response to DGLA was essentially unchanged from that in the blood-perfused lobe. The effects of DGLA appear to be due to conversion to vasoactive products in the PG biosynthetic pathway. These products are less potent than those formed in the metabolism of AA.

8,11,14-Eicosatrienoic Acid↗
PubMed1976

Antitussive activity of diphenhydramine in chronic cough.

A double-blind crossover study was conducted to evaluate the antitussive effectiveness of diphenhydramine (DPH) in chornic coughs related to bronchitis, at doses of 25 and 50 mg every 4 hr for four doses. Both 25- and 50-mg doses caused a statistically and clinically significant reduction in frequency of coughs, compared to placebo. The most frequently reported side effect was drowsiness, principally at the 50-mg dose level. There was little or no apparent correlation between antitussive effectiveness and incidence of drowsiness, however, suggesting that the two effects were pharmacologically unrelated.

Adult↗
PubMed1976

Effects of drugs on the negative (backflow) component of velocity patterns in the dog aorta.

Using an accurately calibrated flowmeter in the descending thoracic aorta of the dog, a study was made of alterations in aortic flow patterns following intravenous and intra-arterial injections of vasoactive drugs. When injected distal to the flowmeter, vasopressors caused marked backflow while vasodilators raised the level of the lowest portion of the pulsatile flow curve. When injected into the brachiocephalic artery, vasopressors prevented the development of a significant negative component whereas vasodilators caused the appearance of backflow, or augmented that which was already present. All acute elevations or decreases in peripheral resistance due to drugs were accompanied by increases in the negative or "backward" phase of flow in diastole. A significant negative flow component was noted only during these acute adjustments. A temporary differential in resistances of the upper and lower portions of the arterial circulation protected cerebral and coronary blood flow during acute haemodynamic adjustments.

Animals↗
PubMed1976

Effect of electrical stimulation of the canine brain stem on the secretion of ACTH and growth hormone (GH).

The effects of electrical stimulation of the brain stem on ACTH and GH secretion were studied in pentobarbital-anesthetized dogs. Stimulations in or near the subcoeruleus area or ventral ascending noradrenergic pathway inhibited the stress-induced increase in ACTH secretion, while stimulations in other areas of the brain stem did not. No significant changes in GH secretion occurred following stimulation of the subcoeruleus area, ventral ascending noradrenergic pathway or adjacent regions of the canine brain stem. These results are consistent with the hypothesis that there is central noradrenergic input to the hypothalamus which can inhibit ACTH secretion. This input appears to be separate from the postulated noradrenergic input that may increase the secretion of GH.

Adrenocorticotropic Hormone↗
PubMed1976

Vascular responses to arachidonic acid in the perfused canine lung.

We compared the effects of arachidonic acid (AA), the bisenoic prostaglandin precursor, with those of prostaglandin F2a (PGF2a) and norepinephrine (NE) on pulmonary vascular resistance in the isolated (in situ), perfused canine lung lobe. The isolated lobe was perfused with autologous blood or an artificial perfusate under conditions of constant flow. Lobar artery and venous pressures were constantly monitored after bolus injections of AA, PGF2a, and NE into the inflow cannula. AA (100 mug/kg produced a significant increase in the pressure gradient (93.3 +/- 8.4%, SE) in the lobe. Similarly, PGF2a (1 mug/kg) significantly increased the pressure gradient (41.2 +/- 6.5%), as did NE (1 mug/kg, 41.6 +/- 3.2%). Aspirin (25 mg/kg) completely blocked the pulmonary vascular effect of AA, but did not affect the response to PGF2a, Linoleic acid, a control fatty acid, did not produce pulmonary vasoconstriction. The pressor effect of AA was not blocked by pretreatment with phentolamine, propranolol, cyproheptadine, or atropine. The use of an artificial perfusate free of cellular elements did not prevent the vasoconstrictor action of AA. The times to onset of action of the three agents were similar, and short. These results suggest that AA is converted into vasoactive intermediates or a prostaglandin, and the vasoactive intermediates or the prostaglandin act directly on precapillary pulmonary vascular smooth muscle rather than through platelet, plasma, adrenergic, or cholinergic mechanisms.

Animals↗
PubMed1976

Effect of PGA1, PGE2, diazoxide on myocardial contractile force.

Experiments were conducted in anesthetized dogs comparing the effects of PGA1, PGE2, and diazoxide on myocardial contractile force (MC). The three agents were given in successive bolus injections intravenously in equidepressor doses and myocardial contractile force was measured by means of a strain-gauge arch sutured onto the right ventricle. The drugs were administered before and during ganglionic (hexamethonium) and beta-blockade (practolol). Both PGA1, and PGE2 caused a marked rise in MC, 24 and 20 per cent, respectively, before blockade and 10 and 11 per cent during blockade. Diazoxide caused only a minimal rise, 0.9 per cent, before blockade and a marked fall, 27 per cent, during blockade. Diazoxide administration during left ventricular bypass indicates that the decrease in MC is not a direct result of alterations in preload or after load. It is suggested that hypertensive patients treated with autonomic blocking agents may be more susceptible to heart failure in response to diazoxide therapy.

Adrenergic beta-Antagonists↗
PubMed1975

Ultrastructural localization of somatostatin in pancreatic islets of the rat.

In order to determine the precise localization of somatostatin (SRIF) in the pancreas, electron microscopic immunocytochemistry was performed on thin sections of whole pancreas and isolated pancreatic islets of the rat using the peroxidase anti-peroxidase technique. SRIF was localized in secretory granules concentrated in cells sparsely distributed near the periphery of the islet. The granules were closely applied to their limiting membrane, exhibited moderate electron density, and were smaller than those in other islet cells. The location and relative number of SRIF-containing cells as well as the morphology of the granules suggest that SRIF is present in delta cells or a subgroup with small granules. These results provide evidence that SRIF is present in a discrete granule population in a specific type of secretory cell in the pancreatic islets.

Animals↗
PubMed1975

Cardiovascular and platelet responses in the dog to the monoenoic prostaglandin precursor dihomo-gamma-linolenic acid.

The monoenoic prostaglandin precursor, dihomo-gamma-linolenic acid (DGLA), in a single dose intravenously (2.0 mg/kg) in dogs, produced a biphasic alteration in systemic arterial pressure (SAP) with a predominant and marked depressor effect. This SAP response is approximately equidepre-sor to the effect of PGE1 5 mug/kg. DGLA had a positive inotropic effect, causing a greater increase in myocardial contractility than PGE1 in an equidepressor dose. The effect of DGLA on MC was not altered by ganglion blockade or beta-adrenergic blockade. Aspirin blocked the sustained depressor response to DGLA but not an initial drop in SAP and increase of MC of very short duration. Aspirin had no effect on PGE1 or PGF1 alpha responses. DGLA caused no thrombocytopenia, but caused a decrease in sensitivity to platelet aggregation. Control fatty acid injections produced variable effects with no resemblances to DGLA responses. It is concluded that DGLA produces direct depressor and positive inotropic responses as well as responses which may be due to conversion to an endoperoxide formed in the biosynthesis of prostaglandins. In contrast, in equidepressor doses, arachidonic acid (AA), the bisenoic prostaglandin precursor, produces a delayed, single-phase depressor effect which may be due to endoperoxide formation alone. Further, the effect of AA on MC is reflex and is blocked by hexamethonium.

8,11,14-Eicosatrienoic Acid↗
PubMed1975

Effects of ganglionic and beta-adrenergic blockade on cardiovascular responses to the bisenoic prostaglandins and their precursor arachidonic acid.

Arachidonic acid (AA) 300 mug/kg, and PGE2, 5 mug/kg consistently produced a decrease in systemic arterial pressure in anesthetized dogs. PGF2alpha, 5 mug/kg, produced a pressor response. All three compounds increased myocardial contractile force, but the magnitude of the change following AA was less prominent. After ganglionic blockade, the depressor response to AA and PGE2 persisted and the pressor response to PGF2alpha was augmented. Myocardial contractile force did not increase following AA in ganglion-blocked animals indicating that the cardiac responses observed before hexamethonium were mediated by the baroreceptor reflexes. A much larger dose of AA (900 mug/kg) resulted in a small positive inotropic effect on the heart. This possibly represents a direct cardiac effect of AA, or may be indicative of increased biosynthesis of an intermediate endoperoxide, or PGE2 and PGF2alpha. Both PGE2 and PGF2alpha have a direct positive inotropic effect on the heart. The persist cardiac effects of PGE2 and PGF2 after beta-adrenergic blockade suggests that these compounds may not interact with the beta-receptors of the myocardium.

Adrenergic beta-Antagonists↗
PubMed1974

Who will teach the basic medical sciences?

In the United States, circumstances still permit each university to set its own course under relatively broad and generous guidelines. The options for our faculties are relatively unrestricted and they can play important roles in determining university policy. We need never reach a stage which nmany can label "crisis,"if events are predetermined by appropriate planning. The survey described herein points to the need for specific long-range planning of the future of preclinical departments in each university. The overall health care system is clearly involved in the problems described in Britain. The coming of a new order of health care in the United States should cause planners to accelerate their work.

Cross-Cultural Comparison↗