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Biomedical subjects

K R Olson

Publications and source records attributed to K R Olson.

At least 19 recordsLinked to original sources
PubMed1992

Atrial natriuretic peptide clearance receptors in trout: effects of receptor inhibition in vivo.

Inactivation of circulating atrial natriuretic peptides (ANP) by specialized clearance (C) receptors has been characterized in mammals but has not been examined in fish. In the present study arterial blood pressure, urine flow, and urine electrolytes were measured in chronically cannulated rainbow trout, Oncorhynchus mykiss, during infusion of the specific C receptor inhibitor, SC-46542. C receptor inhibition decreased blood pressure and pulse pressure, increased heart rate and urine flow, but did not affect urinary electrolyte concentrations. These responses are consistent with those produced by exogenous ANP administration and indicate that: (1) trout possess C-type receptors capable of ANP inactivation, and (2) ANP-like molecules are continuously released and metabolized by trout in vivo. Phosphoramidon, an inhibitor of neutral endopeptidase, did not enhance the SC-46542 response, indicating that C receptors predominate in ANP inactivation in these fish.

Animals↗
PubMed1992

Cardiovascular and renal effects of eel and rat atrial natriuretic peptide in rainbow trout, Salmo gairdneri.

The renal and in vitro vascular effects of atrial natriuretic peptides have been examined in several species of fish. However, comparatively few investigations have described the effects of these peptides on the cardiovascular system in vivo. In the present experiments the dorsal aorta and urinary bladder were cannulated and the effects of atrial natriuretic peptides from rat and eel were monitored in conscious trout during bolus injection or continuous atrial natriuretic peptide infusion. The results show that the initial pressor effect of atrial natriuretic peptides is independent of environmental salinity adaptation (fresh or seawater) and the chemical form of atrial natriuretic peptide injected, but it is affected by the rate of atrial natriuretic peptide administration. This pressor response, and the accompanying diuresis, are mediated through alpha-adrenergic activation. Continuous infusion of either rat or eel atrial natriuretic peptide produces a steady fall in mean arterial blood pressure, which is temporally preceded by an increase in heart rate and a decrease in pulse pressure. Diuresis induced by atrial natriuretic peptides is only partially sustained during continuous infusion. Propranolol partially blocks the increase induced in heart rate by atrial natriuretic peptides, but does not affect either pulse pressure or mean arterial pressure. Propranolol significantly increases urine flow in saline-infused animals but has no apparent effect on animals subjected to infusions of atrial natriuretic peptides. These results indicate that there are multiple foci for the action of atrial natriuretic peptides in trout and that in many instances the effects of atrial natriuretic peptides are mediated through secondary effector systems.

Adrenergic alpha-Antagonists↗
PubMed1992

Effects of a major earthquake on calls to regional poison control centers.

We retrospectively evaluated the effect of the Loma Prieta earthquake on calls to 2 designated regional poison control centers (San Francisco and Santa Clara) in the area. In the immediate 12 hours after the earthquake, there was an initial drop (31%) in call volume, related to telephone system overload and other technical problems. Calls from Bay Area counties outside of San Francisco and Santa Clara decreased more dramatically than those from within the host counties where the poison control centers are located. In the next 2 days, each poison control center then handled a 27% increase in call volume. Requests for information regarding safety of water supplies and other environmental concerns were significantly increased. The number of cases of actual poisoning exposure decreased, particularly poison and drug ingestions in children. Most calls directly related to the earthquake included spills and leaks of hazardous materials and questions about water and food safety. Regional poison control centers play an essential role in the emergency medical response to major disasters and are critically dependent on an operational telephone system.

Disasters↗
PubMed1991

Morbidity following acute irritant inhalation in a population-based study.

STUDY OBJECTIVE: To estimate the incidence of and risk factors for morbidity due to inhalation of respiratory irritants. DESIGN: Six-month case series of inhalational exposures reported to a poison control center with follow-up, structured interviews of subjects. SETTING: A regional poison control center providing 24-hour telephone consultation to health professionals and the public. PATIENTS: Consecutive sample of 683 inhalation cases, with interviews of 323 subjects. MEASUREMENTS AND MAIN RESULTS: Moderate to severe irritants accounted for 160 (50%) of the inhalational exposures in interviewed subjects. Persistent symptoms lasting 14 days or longer were reported by only 20 (6%) of the subjects. Irritant exposure was a statistically significant risk factor for acute respiratory symptoms (relative risk [RR] = 1.7; 95% confidence interval [Cl], 1.4 to 2.1) but was unrelated to persistent symptoms. Preexisting lung conditions (RR = 2.4; 95% Cl, 1.4 to 4.2) and cigarette smoking (RR = 1.7; 95% Cl, 1.3 to 2.2) were both statistically significant risk factors for persistent symptoms. CONCLUSIONS: Symptomatic inhalational exposures due to irritants are frequent in reports from poison control centers. Residual morbidity was uncommon and did not appear to be statistically related to the degree of irritant exposure. Host-related factors may be better predictors of ongoing morbidity after inhalational exposure.

Age Factors↗
PubMed1991

Vasculature of the fish gill: anatomical correlates of physiological functions.

The fish gill is a multifunctional organ responsible for respiration, osmoregulation, acid base balance, nitrogen excretion, and metabolism of circulating hormones. Two or more microcirculatory systems subserve these activities and form one of the most complex vascular networks found in any vertebrate. In this article the vascular anatomy of the teleost gill and the role of gill vessels in mediating physiological function are examined. Vascular corrosion replication techniques have been instrumental in resolving the spatial organization of gill microcirculation. Variations in the replication procedures provide information on the interrelationships between the vascular pathways, factors that govern flow distribution, and the physical characteristics of the vessels themselves. Anatomically, gill vessels are as diverse as their physiological functions. Pillar cells, unique to the fish gill, form the lining of the respiratory vasculature and may have substantial metabolic effects on circulating hormones. The non-respiratory pathways appear to be lined with both typical and unusual endothelial cells, although the fine structure and function(s) of these vessels are largely unknown. To date most of the information on gill vessels has been derived from descriptive morphological studies. Further evaluation of the anatomical and physiological correlations of these tissues is predicated upon the application of histocytochemical, morphometric, and other quantitative methodologies as well as an examination of gills from fish with various evolutionary and environmental backgrounds.

Acid-Base Equilibrium↗
PubMed1991

Cardiovascular effects of endothelin in trout.

The cardiovascular effects of endothelin-1 (ET-1) in trout were examined in unanesthetized fish, perfused tissues, and isolated vascular rings. In vivo, a bolus of 500 ng/kg body wt ET-1 transiently lowered arterial (postgill) blood pressure (BP) by nearly 30%; 1,500 ng/kg body wt produced a triphasic, pressor-depressor-pressor, response. Continuous infusion of 0.1, 1, 10, and 30 ng.kg-1.min-1 progressively lowered BP but did not affect heart rate (HR), urine flow, or electrolyte excretion. In the in situ perfused heart ET-1 (10(-11) to 10(-8) M) had no effect on HR or power output. ET-1 produced dose-dependent increases in vascular resistance in the perfused gill, renal-skeletal muscle, and splanchnic circulations, and increased tension, independent of endothelium, in vascular rings from celiacomesenteric (CA) and coronary arteries and anterior cardinal veins (CV). Ventral aortas were refractory to ET-1. In vitro, ET-1 effects were slow in onset and long lasting. External calcium was required for maximal ET-1 responses in gill and CA. ET-1 effects on CA but not CV were partially inhibited by calcium channel blockers, diltiazem, and D 600, and by the guanylate cyclase activators, atrial natriuretic factor, and sodium nitroprusside. [3H]water flux across the perfused gill was stimulated by ET-1 through what appeared to be a vascular-independent mechanism. These experiments show that the trout vasculature is exquisitely sensitive to ET-1, and they suggest that the physiological expression of this peptide has been highly conserved during the course of vertebrate evolution.

Animals↗
PubMed1991

Evidence against nonprostanoid endothelium-derived relaxing factor(s) in trout vessels.

Bradykinin (BK)- or acetylcholine (ACh)-mediated vasodilation has only rarely been observed in fish. This suggests that many fish vessels lack the endothelium-dependent relaxing mechanisms recently identified in mammals. To examine this hypothesis, isolated vascular rings were prepared from trout ventral aortas (VA), efferent branchial and celiacomesenteric (CM) arteries, and anterior cardinal veins (CV) and examined for endothelium-mediated responses. A doubly perfused trunk preparation was also used to evaluate the response of the microcirculation. ACh produced dose-dependent contractions in all vascular rings and increased vascular resistance when perfused into the CM but had no affect when perfused into the dorsal aorta. Neither ACh nor BK relaxed precontracted vessels or lowered resting tone. Removal of the endothelium did not affect ACh or BK responses. The calcium ionophore A23187 produced an endothelium-dependent relaxation of precontracted VA, CM, and CV. The A23187 response was abolished by indomethacin, indicating that a prostanoid was involved in the relaxation. ATP contracted and/or relaxed precontracted CM and CV. ATP effects were independent of an intact endothelium. Sodium nitroprusside and atrial natriuretic factor partially or completely relaxed all vessels, indicating the presence of soluble and particulate guanylate cyclases, respectively. These results suggest that nonprostanoid endothelium-derived relaxing factors (EDRFs) or EDRF-like vasodilator mechanisms are not present in trout vessels or, if they are, they are not released by classical agonists.

Acetylcholine↗
PubMed1990

Microvasculature of the nasal salt gland of the duckling, Anas platyrhynchos: quantitative responses to osmotic adaptation and deadaptation studied with vascular corrosion casting.

The three-dimensional microvasculature of the nasal salt gland of the duckling was studied by vascular corrosion casting and scanning electron microscopy. Changes in the vascular volume of the gland in response to osmotic stress were also determined using cast weights and densities. The richly vascularized gland is supplied on its medial surface by large branches of the supraorbital and ethmoidal arteries. Numerous arterial branches enter the gland and distribute to lobes via the interlobar connective tissue. Lobar arterioles penetrate to the periductal areas of the lobes before dividing into capillaries supplying the ductal epithelium and secretory tubules. Capillaries envelope the secretory tubules and run radially from the ducts toward the lobe periphery, so that blood flows counter to the tubular secretion. Blood is collected via venous plexuses seen as distinct drainage units on the periphery of each lobe. Veins exhibit large numbers of bicuspid valves. Following 1 day and 4 days of osmotic loading (feeding 1% NaCl), vascular volume of the gland increased fivefold and ninefold, respectively, a response that precedes and exceeds that of the gland weight or Na,K-ATPase activity. When salt water-adapted ducklings were fed fresh water for only 24 hr (deadaptation), vascular volume fell to 2.8 times the control level. Changes in blood flow to the gland during osmotic adaptation and deadaptation are rapid and dramatic and may represent the initial steps in the control of gland secretion.

Adaptation, Physiological↗
PubMed1990

Enzymes of the kallikrein-kinin system in rainbow trout.

Evidence for a kallikrein-kinin system (KKS) in fish is incomplete. In the present study, components of the KKS were identified in rainbow trout. Tissues were assayed for kallikrein-like esterolytic activity using three synthetic kallikrein substrates (TAME, VGAN, and PPAN), and the presence of kallikrein substrate (kininogen) in trout plasma was estimated by bradykinin (BK) radioimmunoassay of plasma activated with trypsin (T). Formation of pressor-depressor substances in vivo by porcine glandular kallikrein (GK) and T was measured after intra-arterial injection into unanesthetized trout. Gill and kidney contained kallikrein activity (TAME and VGAN assays); little activity was observed with PPAN. Aprotinin inhibited gill activity (TAME assay). T liberated 42 +/- 3 (SE) ng (n = 10) of immunoreactive BK per milliliter of plasma. Injection of GK in vivo reduced plasma kininogen levels for over 24 h. GK produced pressor responses only in fish pretreated with the angiotensin-converting enzyme (ACE) inhibitor captopril. This effect was mediated partly through stimulation of alpha-adrenergic receptors. T produced slight pressor responses that were captopril insensitive. These results show that trout possess elements of the KKS system including kallikrein-like enzymatic activity, kininogen, receptor-mediated vascular sensitivity to kallikrein products, and kininolytic activity consistent with ACE (kininase II).

Animals↗
PubMed1990

Generation of vasoactive substances in trout and rat plasma by trypsin and kallikrein.

In the preceding study we demonstrated kallikrein-like enzymatic activity in trout tissues and showed that kallikrein incubated with trout plasma (T60K) produces a vasopressor substance(s). The present study further examines the effects of T60K in fish and mammals in vitro and in vivo. T60K produced a dose-dependent pressor response in both trout and rats, whereas kallikrein-activated rat plasma (R60K) was pressor in trout and depressor in rats. Captopril did not affect the response of rats to T60K or R60K. Phenoxybenzamine attenuated the T60K response in trout but not in rats, thus T60K effects in trout are partially mediated through catecholamines. Blockade of angiotensin II (ANG II) receptors in rats with [Sar1,Ala8]-ANG II abolished the pressor effects of T60K. T60K produced dose-dependent contractions in isolated trout and rabbit arteries; ANG II was ineffective in trout arteries. T60K-contracted trout arteries were relaxed by atrial natriuretic peptide and forskolin, whereas diltiazem and sodium nitroprusside were without effect. [Sar1,Ala8]ANG II inhibited T60K-induced contractions of rabbit arteries and relaxed rings previously contracted with T60K. The active component of T60K has a molecular weight less than 10,000, is heat stable, and is inactivated by peptidases. It is immunologically different than mammalian angiotensins but binds to and displaces radiolabeled ANG II from ANG II receptors. These results suggest that kallikrein forms a vasoactive substance(s) in trout plasma that is neither bradykinin nor ANG II but is similar to the latter in its pharmacological effects.

Animals↗
PubMed1990

Vascular effects of kinins in trout and bradykinin metabolism by perfused gill.

In the preceding studies we have shown that elements of a kallikrein-kinin system (KKS) are present in trout. The present study examines the cardiovascular effects of intra-arterial kinin injection and the ability of perfused gills or gill homogenates to metabolize bradykinin or the pressor substance generated in trout plasma by glandular kallikrein (T60K). Bradykinin (BK), t-kinin, kallidin, and Met-kallidin produced pressor responses in vivo. BK responses were unaffected by alpha-adrenergic blockade or cyclooxygenase inhibition. Perfused gills extracted approximately 40% of a [3H]BK bolus, however, metabolites were not recovered from the effluent perfusate. Gill homogenates completely metabolized [3H]BK and inactivated the pressor substance T60K. Captopril reduced BK and T60K metabolism by gill homogenates. The present study demonstrates that kinins have pressor effects in trout that are not mediated through adrenergic or prostanoid-derived mechanisms. The results also suggest that trout do not release endothelium-derived relaxing factors in response to kinin injection. The gill is able to metabolize BK and T60K, although, with respect to BK, this process appears to involve intracellular hydrolysis and may be only partially dependent on angiotensin-converting enzyme. Inactivation of BK by gill tissue may be fundamentally different from kinin metabolism by the mammalian lung.

Animals↗
PubMed1990

Quantitative assessment and reduction of long-term autoradiographic background.

Quantitative autoradiography can measure distribution patterns in an animal exposed to radiolabeled compounds. A comparison of autoradiographs of rat brain containing low levels of 14C showed that a highly variable background signal had been produced. This resulted in several overexposed autoradiographs which could not be quantitatively compared. The background, believed to be produced by light emanating from the phosphor coating in the X-ray cassette, was a major impediment because it hindered correct analysis of the specimen. This article details our experiments demonstrating the sources of variance contributing to background and offers methods for its reduction. We found that placement of black polyethylene plastic between the slides and phosphor in the X-ray film cassette minimized autoradiographic background and effectively eliminated the effects caused by inherently different levels of radioactivity in the glass slides.

Animals↗
PubMed1990

Cocaine.

There has been a dramatic rise in the number of adverse medical effects related to cocaine abuse since the widespread introduction of crystallized freebase cocaine or "crack" in the mid-1980s. In particular, cardiovascular and central nervous system toxicity is becoming more widely recognized and requires aggressive medical management to prevent potentially high morbidity and mortality.

Cocaine↗