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PubMed1980

Different patterns in essential hypertension and possible choice of antihypertensive drugs.

UNLABELLED: Essential hypertension is not a disease entity, so therefore it is understood that there are several causes of its development. The hemodynamic relation is not the same in all patients. The traditional concept of an increased total peripheral resistance (TPR) and a normal cardiac output (CO) is not valid for all cases. We developed a method to estimate a measure for TPR independently of the CO. The results in six patients are described: three of them show a hemodynamic pattern of increased CO and normal TPR, two of increased TPR and normal CO, while the sixth patient shows a mixed pattern. These results have important implications for therapy: drugs lowering CO are more indicated in the first group, drugs influencing TPR promise a better result in the second one. Furthermore a review is given of other mechanisms governing the bloodpressure and indicating a special kind of treatment, i.e., the reninangiotensin-aldosteron system and the catecholamines. IN CONCLUSION: we know some important determinants of high blood pressure. Most of them can be determined, but in general praxis this is too troublesome. However, for very difficult cases it is now possible to try and find the most promising combination of drugs for that particular case.

Adult↗

PubMed1980

Peripheral vascular response to potassium administration during cardiopulmonary bypass.

Potassium (K+) is often administered to patients during cardiopulmonary bypass (CPB). The effects of rapid K+ administration during CPB were studied in 30 adult patients. Each patient received one bolus dose (2, 4, 8, 12, or 16 mEq) of potassium chloride (KCl) (2 mEq/ml) during CPB. Serum K+ was significantly increased from baseline values at KCl doses of 8 mEq and larger (p less than 0.05). All increases in serum K+ returned to clinically acceptable levels within 5 minutes after the bolus. Mean arterial pressure (MAP) (torr) and total peripheral resistance (TPR) (dynes sec cm-5) changes were biphasic; after an initial transient decrease, maximal with the 16 mEq K+ bolus (MAP -21 +/- 6, TPR - 315 +/- 135), these parameters increased (8 mEq K+ bolus, MAP + 15 +/- 16, TPR + 301 +/- 90; 12 mEq K+ bolus, MAP + 43 +/- 9, TPR + 998 +/- 250; 16 mEq bolus, MAP + 51 +/- 9, TPR + 1,216 +/- 120) with a peak at 3 minutes after the bolus. Hypertension, in nine of 18 patients receiving a KCl bolus of 8 mEq or larger, was of such magnitude (range 132 to 196 torr) as to require rapid therapeutic intervention to lower blood pressure. When KCl supplementation is required on CPB and slow infusion rates seem unreasonable, bolus doses of less than 8 mEq may be administered without vascular effect.

Adult↗

PubMed1994

Centrally mediated reduction in cardiac output elicits the enhanced hypotensive effect of clonidine in conscious aortic barodenervated rats.

In a previous study, we showed that centrally mediated hypotensive responses are enhanced in aortic barodenervated (ABD) rats as compared with sham-operated (SO) rats. In the present study, we tested the hypothesis that the high basal total peripheral resistance (TPR) of ABD rats accounts for enhanced hypotensive responses to clonidine in this rat model. Aortic barodenervation resulted in acute increases in blood pressure (BP) and heart rate (HR) in anesthetized rats, associated with significant increases in plasma norepinephrine (NE) levels and TPR; cardiac index (CI) and stroke volume (SV) were not affected. After recovery from anesthesia, conscious ABD rats had significantly increased BP at 3 h after barodenervation; BP returned to SO levels by 48 h even though plasma NE levels and TPR remained significantly increased. On the other hand, CI and SV showed significant reductions, beginning at 3 h, and remained low throughout the postdenervation period (48 h); the reduction in CI offset the increase in TRP and may therefore account for the restoration of BP of ABD rats to normal levels. Beginning at similar baseline BP values, cumulative intracisternal (i.c.) doses of clonidine (0.02-2.5 micrograms) elicited greater decreases in BP and plasma NE levels in conscious ABD as compared with SO rats. These responses were centrally mediated because systemic administration of 0.12 micrograms clonidine, a dose that elicited near maximal hypotensive response after i.c. administration, affected neither BP nor plasma NE levels. Contrary to the hypothesis, the hypotensive effect of clonidine in ABD rats resulted exclusively from a reduction in CO (owing to reductions in both HR and SV) because TPR was not affected. These findings suggest that (a) in ABD rats, a reduction in CO offsets a sustained sympathetically mediated elevation in TPR and restores BP to normal levels; and (b) an enhanced hypotensive response to clonidine in ABD as compared with SO rats cannot be accounted for by a higher basal TRP but rather by elicitation of greater reductions in CO through a centrally mediated sympathoinhibitory action.

Animals↗

PubMed1994

Different effects of naproxen on the organ blood flows in normo- and hypervolemic anaesthetized rats.

The effects of naproxen, an inhibitor of the enzyme cyclooxigenase (10 mg/kg i.v.) on the distribution of the cardiac output (CO) and on the intrarenal hemodynamics were investigated in normovolemic (free salt and water uptake till the beginning of experiment) and hypervolemic (with i.v. infusion of 50 ml 0.9% NaCl solution/kg/10 min) narcotized rats. The cardiac output was measured on the basis of he Stewart-Hamilton principle, the blood flow of the organs by the Sapirstein method. 86Rb was used as indicator. In hypervolemia, the blood pressure is the same, the cardiac output is higher (CO-normovolemia: 23.1 +/- 7.04, CO-hypervolemia: 29.0 +/- 6.43 ml/min/100 g; p < 0.05) the total peripheral resistance (TPR) is lower (TPR-normovolemia: 40.0 +/- 9.39 R, TPR-hypervolemia: 31.2 +/- 8.34 R, p < 0.05) than in normovolemic animals. In hypervolemia the vascular resistance of the investigated organs (heart, lungs, kidney, skin, muscle, liver, spleen, intestine) is also lower and the intrarenal blood flow shifts toward the medulla. One hour following the naproxen administration a) in normovolemia joining to a slightly decreased cardiac output and increased TPR, the vascular resistance of the skin (R-control: 85.1 +/- 32.7, R-naproxen: 161 +/- 57.4; p < 0.001) and of the skeletal muscle (R-control: 114 +/- 35.1, R-naproxen: 190 +/- 81.9; p < 0.01) increases. The blood flow of the other organs and the intrarenal hemodynamics does not change under the effect of naproxen. b) in hypervolemia the general circulatory parameters (blood pressure, cardiac output, TPR) and the parameters of the organ circulation and intrarenal hemodynamics remain unchanged. The results suggest that in rats the prostanoid compounds (PGE2, PGI2, TXA2) a) can modify the blood flow of the skin and muscle in normovolemic animals, but they do not have any role in determining the blood flow of the other organs or the intrarenal distribution of blood flow. b) in hypervolemia they play no role in determining organ-, or intrarenal blood flow. The consequences of cyclooxygenaze enzyme inhibition--at least in the case of the organ blood flow--depend on the magnitude of sodium and water load in the organism.

Animals↗

PubMed1977

Mechanisms of hypertension during the acute and intermediate phases of the one-clip, two-kidney model in the dog.

The acute and intermediate onset phases of one-clip, two-kidney hypertension were studied in six conscious dogs. Mean arterial pressure (MAP), cardiac output (CO), total peripheral resistance (TPR), serum renin concentration (SRC), plasma aldosterone (PA) and cumulative sodium and water balance were studied prior to unilateral renal artery constriction, at 2, 10, and 24 hours postconstriction, and daily thereafter for 5 days. At 2 hours postconstriction, MAP, CO, TPR, and SRC were elevated, with unchanged fluid balance. At 10 and 24 hours there was a further rise in CO accompanied by positive fluid-sodium balance, with a slight decrease in MAP, TRP, and SRC. During days 2 and 3, MAP, CO, TPR, and SRC remained elevated and stable in the presence of decreasing fluid-sodium balance to preconstriction levels. During days 4 and 5, MAP, SRC, and fluid-sodium balance remained unchanged, TPR demonstrated a secondary increase, whereas CO decreased to preconstriction values. Sequential changes in PA parallel those of SRC, but were significant only at 2 hours postconstriction. These changes suggest that the increased CO is not totally dependent on fluid-sodium balance, and that CO is not the sole determinant of elevated MAP. The temporal relationship between MAP and SRC throughout the study is consistent with renin-mediated hypertension. The secondary rise of TPR may be due to total body autoregulation and/or increased vascular reactivity to high levels of circulating angiotensin. A unitary renin-angiotensin mechanism, therefore, may be responsible for the induction and maintenance of hypertension in this experimental model.

Acute Disease↗

PubMed1996

Hemodynamic responses to brief hyperoxia in healthy and in mild hypertensive human subjects in rest and during dynamic exercise.

Hemodynamic consequences of the withdrawal of arterial chemoreceptor drive (ACD) by brief systemic hyperoxia were studied in 16 mild hypertensive subjects (HT) and in 16 healthy subjects (NT) in horizontal position at resting metabolic rate. In another 9 mild HT and match NT measurements were made in resting sitting position and during steady-state mild physical exercise on cycloergometer, (30% of VO2 max.) Tidal volume, minute ventilation, end tidal CO2 and O2 concentration, K+, Na+, pO2, pCO2 values in blood were recorded. Impedance reography was used for recording stroke volume (SV) and arm blood flow (ABF). Cardiac output (CO), ABF and arterial blood pressure (ABF) values were used for calculation of the total peripheral resistance (TPR) and vascular resistance in the arm (AVR). To assess the neurogenic circulatory response to withdrawal of ACD in HT attenuated by opposite peripheral effects of high oxygen, the values of AVR, ABP, TPR and AVR changes during brief hyperoxia in NT, assumed to be of peripheral origin, were subtracted from respective values in HT, assumed to be of mixed neurogenic and peripheral origin. In HT hyperoxia applied in sitting position produced a brief decrease in systolic and diastolic ABP by 5.4 +/- 0.8% and 3.4 +/- 1.1% respectively, of TPR by 12.4 +/- 3% and of AVR by 4.7 +/- 4.6%. Decrease in AVR during hyperoxia was significantly greater in sitting than in horizontal position. In NT hyperoxia produced opposite effects in ABP, TPR and AVR, as compared to those in HT. In HT subjects during steady-state exercise the TPR decreased by 21 +/- 3.7% reaching a value no different from that in NT. We suggest, that in primary hypertension neurogenic sympathoexcitatory ACD is augmented and interacts with the peripheral mechanisms related to tissue oxygen supply.

Adult↗

PubMed2006

Gab1 is required for cell cycle transition, cell proliferation, and transformation induced by an oncogenic met receptor.

We have shown previously that either Grb2- or Shc-mediated signaling from the oncogenic Met receptor Tpr-Met is sufficient to trigger cell cycle progression in Xenopus oocytes. However, direct binding of these adaptors to Tpr-Met is dispensable, implying that another Met binding partner mediates these responses. In this study, we show that overexpression of Grb2-associated binder 1 (Gab1) promotes cell cycle progression when Tpr-Met is expressed at suboptimal levels. This response requires that Gab1 possess an intact Met-binding motif, the pleckstrin homology domain, and the binding sites for phosphatidylinositol 3-kinase and tyrosine phosphatase SHP-2, but not the Grb2 and CrkII/phospholipase Cgamma binding sites. Importantly, we establish that Gab1-mediated signals are critical for cell cycle transition promoted by the oncogenic Met and fibroblast growth factor receptors, but not by progesterone, the natural inducer of cell cycle transition in Xenopus oocytes. Moreover, Gab1 is essential for Tpr-Met-mediated morphological transformation and proliferation of fibroblasts. This study provides the first evidence that Gab1 is a key binding partner of the Met receptor for induction of cell cycle progression, proliferation, and oncogenic morphological transformation. This study identifies Gab1 and its associated signaling partners as potential therapeutic targets to impair proliferation or transformation of cancer cells in human malignancies harboring a deregulated Met receptor.

Adaptor Proteins, Signal Transducing↗

PubMed1997

Smooth non-parametric receiver operating characteristic (ROC) curves for continuous diagnostic tests.

Receiver operating characteristic (ROC) curves have seen increasing use to assess the accuracy of diagnostic tests that yield continuous test results. We can calculate a fully non-parametric ROC curve from the empirical false positive rate (FPR) and true positive rate (TPR) at each possible decision threshold, but it may be quite jagged. We can obtain a smooth ROC curve by directly fitting a parameteric model, for example, binormal or bilogistic, to the actual test results, but substantial lack-of-fit may result if the distributional assumptions are not valid. A recently proposed alternative algorithm 'LABROC4' is insensitive to such departures, but is not fully flexible in that the form of the resulting ROC curve is restricted to be binormal. We propose a smooth non-parametric ROC curve derived from kernel density estimates of the two test result distributions. We obtain pointwise standard errors for the estimated TPR at each FPR and use them to construct pointwise confidence intervals for the ROC curve, using a logit transformation. We also obtain standard errors for the estimated TPR and FPR at given thresholds and use them to construct confidence rectangles in (FPR, TPR)-space that correspond to a specific threshold. We adapt existing methods for the unsmoothed non-parametric ROC curve to obtain the area under the ROC curve and its standard error; we also give partial areas and corresponding standard errors. We have created a FORTRAN algorithm 'ROC-&-ROL', available upon request. We compare ROC curves and areas obtained by applying our methods and its competitors to two data sets, one of which is fit well by parametric methods and LABROC4, the other of which is not.

Algorithms↗

PubMed1994

Cardiovascular responses to postural changes: differences with age for women and men.

The cardiovascular responses to postural change, and how they are affected by aging, are inadequately described in women. Therefore, the authors examined the influence of age and sex on the responses of blood pressure, cardiac output, heart rate, and other variables to change in posture. Measurements were made after 10 minutes each in the supine, seated, and standing positions in 22 men and 25 women who ranged in age from 21 to 59 years. Several variables differed, both by sex and by age, when subjects were supine. On rising, subjects' diastolic and mean arterial pressures, heart rate, total peripheral resistance (TPR), and thoracic impedance increased; cardiac output, stroke volume, and mean stroke ejection rate decreased; and changes in all variables, except heart rate, were greater from supine to sitting than sitting to standing. The increase in heart rate was greater in the younger subjects, and increases in TPR and thoracic impedance were greater in the older subjects. Stroke volume decreased less, and TPR and thoracic impedance increased more, in the women than in the men. The increase in TPR was particularly pronounced in the older women. These studies show that the cardiovascular responses to standing differ, in some respects, between the sexes and with age. The authors suggest that the sex differences are, in part, related to greater decrease of thoracic blood volume with standing in women than in men, and that the age differences result, in part, from decreased responsiveness of the high-pressure baroreceptor system.

Adult↗

PubMed2006

Characterization of thromboxane A2 receptor signaling in developing rat oligodendrocytes: nuclear receptor localization and stimulation of myelin basic protein expression.

The present work investigates the role of thromboxane A(2) (TXA(2)) receptors in the development of oligodendrocytes (OLGs). The results demonstrate that the proteins of the TXA(2) signaling pathway, i.e., cyclooxygenase (COX-1), TXA(2) synthase (TS), and TXA(2) receptor (TPR) are expressed in the developing rat brain during myelination. Furthermore, culture of OLG progenitor cells (OPCs) revealed that the expression levels of these proteins as well as TXA(2) synthesis increase during OLG maturation. Separate studies established that activation of TPRs by the agonist U46619 increases intracellular calcium in both OPCs and OLGs as visualized by digital fluorescence imaging. Immunocytochemical staining demonstrated that TPRs are localized in the plasma membrane and perinuclear compartments in OPCs. However, during OLG differentiation, TPRs shift their localization pattern and also become associated with the nuclear compartment. This shift to nuclear localization was confirmed by biochemical analysis in cultured cells and by immunocytochemical analysis in developing rat brain. Finally, it was found that U46619 activation of TPRs in maturing OLGs resulted in enhanced myelin basic protein (MBP) expression. Alternatively, inhibition of endogenous TPR signaling led to reduced MBP expression. Furthermore, TPR-mediated MBP expression was found to be associated with increased transcription from the MBP promoter using a MBP-luciferase reporter. Collectively, these findings suggest a novel TPR signaling pathway in OLGs and a potential role for this signaling during OLG maturation and myelin production.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1992

Quantitative 111In antimyosin antibody imaging to predict the age of myocardial infarction.

To establish whether quantitative 111In antimyosin uptake can be used to predict infarct age, we studied the heart-lung ratio in 107 images from 90 patients at various intervals following a Q-wave infarction. Imaging was performed 24 hours following 111In antimyosin injection. The HLR was measured as the ratio of the maximum counts in the infarcted myocardium to the adjacent lung background. The ratio ranged from 1.26 to 3.87, and declined with increasing infarct age. Infarcts were classified on the basis of age as type I (less than 3 days old), type II (less than 14 days), and type III (less than 90 days). True positive and false positive rates (TPR and FPR), and test-likelihood ratio calculations were performed for HLR thresholds ranging from 1 to 4, for the three infarct types. A FPR of 0% and likelihood ratio of infinity was obtained at a HLR threshold of 2.3 for type I infarcts (TPR 40.8%); at a HLR threshold of 2 for type II infarcts (TPR 50.6%), and a threshold of 1.8 for type III infarcts (TPR 52.6%). The likelihood of each infarct type can be estimated directly from the HLR for values below the above thresholds. These results show that quantitative 111In-antimyosin imaging may be used to predict infarct age.

Antibodies, Monoclonal↗

PubMed2000

P58IPK, a novel cochaperone containing tetratricopeptide repeats and a J-domain with oncogenic potential.

Tetratricopeptide repeats (TPRs) are loosely conserved 34-amino acid sequence motifs that have been shown to function as scaffolding structures to mediate protein-protein interactions. TPRs have been identified in a number of proteins with diverse functions and cellular locations. Recent studies suggest that individual TPR motifs can confer specificity in promoting homotypic and/or heterotypic interactions, often in a mutually exclusive manner. These features are best exemplified by the P58IPK protein, an influenza virus-activated cellular inhibitor of the PKR protein kinase, whose different TPR motifs mediate interactions with distinct proteins. P58IPK, which possesses cochaperone and oncogenic properties, represents a unique class of TPR proteins containing a J-domain. Here we review recent progress on the structural and functional characterization of P58IPK, and discuss the possible mechanisms by which P58IPK modulates PKR and induces tumorigenesis in view of present knowledge of TPR proteins and molecular chaperones.

Amino Acid Motifs↗

PubMed1997

Ouabain improves cardiac function in vivo in rats with heart failure after chronic but not acute treatment.

Rats are generally believed to be insensitive for cardiac glycosides. However, like in humans, the hemodynamic effects may be related to the pathophysiological condition. Since the hemodynamic effects of cardiac glycosides have never been investigated in rats with heart failure, the aim of the present experiments was to investigate the role of the pathophysiological condition in the rat. Therefore, hemodynamic and cardiac effects of ouabain were investigated both in normal rats and rats with heart failure due to myocardial infarction (MI). Since the effects of ouabain may also depend on the treatment scheme, rats were treated either for a short-term period or a long-term period. Three weeks after sham surgery or ligation of the left coronary artery (MI), Wistar rats were treated for two weeks with ouabain (14.4 mg/kg.d s.c.), either continuously (osmotic minipumps) or intermittently (once daily). A separate group of rats was treated for 45-60 min (1-100 microg/kg.min ouabain; i.v. infusion 5 weeks after MI). Hemodynamic measurements were performed at rest and after volume loading in conscious rats, chronically instrumented with an electromagnetic flow probe and catheters. Induction of MI resulted in a significant increase in total peripheral resistance (TPR), and a significant decrease in basal and maximal cardiac output following volume loading (basal CO: sham, 92 +/- 5; MI, 74 +/- 5 ml/min; maximal CO: sham, 152 +/- 4; MI, 105 +/- 7 ml/min; n = 7-11). Chronic intermittent ouabain treatment further increased TPR in MI rats. In contrast, continuous ouabain treatment normalized TPR in rats. Only in continuously treated MI rats, basal and maximal CO improved significantly (basal: 83 +/- 4; maximal: 134 +/- 7 ml/min; n = 7). Acute treatment dose-dependently worsened the hemodynamic conditions of MI rats, since TPR and MAP increased and CO and stroke volume decreased significantly. These experiments demonstrate that ouabain can improve cardiac function in rats, although only in MI rats and strongly depending on the delivery regimen. Thus, in contrast to the general belief, the presently used rat model is suitable for investigation of cardiac glycosides in heart failure. The preferential improvement of cardiac function in MI rats continuously treated with ouabain may depend upon changes in Na+,K+-ATPase or altered neurohumoral conditions due to MI and chronic treatment.

Animals↗

PubMed1999

Comparison between angiotensin receptor antagonism and converting enzyme inhibition in heart failure. Differential acute effects according to the renin-angiotensin system activation.

This study was designed to assess the influence of the activation status of the renin angiotensin system (RAS) on the hemodynamic effects of EXP 3174 (an angiotensin AT1 receptor antagonist) and enalaprilat (an angiotensin converting enzyme inhibitor) in tachycardia-induced heart failure. Thirteen dogs were chronically instrumented to measure left ventricular (LV) pressure, its first time derivative (LV dP/dt), atrial and aortic pressures, and cardiac output. EXP 3174 (0.1 mg/kg, i.v.) or enalaprilat (1 mg/kg, i.v.) were administered in conscious dogs with heart failure induced by right ventricular pacing (250 beats/min, 3 weeks). EXP 3174 and enalaprilat produced significant vasodilation but the effects of EXP 3174 on mean aortic pressure (MAP), cardiac output, and total peripheral resistance (TPR) were only 50% of those produced by enalaprilat. When dogs were grouped according to their baseline plasma renin activity (PRA) values, in dogs with normal PRA (0.5 +/- 0.1 ng/ml/h) EXP 3174 did not produce significant change in MAP and TPR, while enalaprilat decreased significantly MAP and TPR. In contrast, in dogs with high PRA (6.7 +/- 3.2 ng/ml/h), EXP 3174 produced significant reductions in MAP and TPR, which were similar to those produced by enalaprilat. Thus, in conscious dogs with heart failure, enalaprilat is effective whether the RAS is activated or not. In contrast, EXP 3174 is effective only when the RAS is activated. These results may help in the choice of inhibitors of the RAS in heart failure.

Angiotensin II↗

PubMed2004

The roles of different regions of the CycH protein in c-type cytochrome biogenesis in Sinorhizobium meliloti.

Cytochrome c heme lyases encoded by the Sinorhizobium meliloti cycHJKL operon are responsible for generating the covalent bond between the heme prosthetic group and apocytochromes c. The CycH protein with its presumably membrane-associated N-terminal and periplasmic C-terminal parts is thought to be responsible for binding apocytochrome and presenting it to the heme ligation machinery. We propose that these two modules of CycH play roles in different functions of the protein. The N-terminal 96 amino acids represent an active subdomain of the protein, which is able to complement the protoporphyrin IX (PPIX) accumulation phenotype of the cycH mutant strain AT342, suggesting that it is involved in the final steps of heme C biosynthesis. Furthermore, three tetratricopeptide (TPR) domains have been identified in the C-terminal periplasmic region of the CycH protein. TPR domains are known to mediate protein-protein interactions. Each of these CycH domains is absolutely required for protein function, since plasmid constructs carrying cycH genes with in-frame TPR deletions were not able to complement cycH mutants for their nitrate reductase (Rnr-) and nitrogen-fixing (Fix-) phenotypes. We also found that the 309-amino acid N-terminal portion of the CycH, which includes all the TPR domains, is able to mediate the assembly of the c-type cytochromes required for the Rnr+ phenotype. In contrast, only the full-length protein confers the ability to fix nitrogen.

Amino Acid Sequence↗

PubMed1993

Fentanyl antagonizes diazepam on carotid sinus baroreflex control of circulation in rabbits.

To investigate the effects of a combination of fentanyl and diazepam on carotid sinus baroreflex in conscious rabbits, we examined the responses of mean systemic arterial pressure (MAP), heart rate (HR) and total peripheral resistance (TPR) to bilateral carotid occlusion (BCO). Seven rabbits were given 0.5 mg.kg(-1) of diazepam i.v. followed by 10 mg.kg(-1) of fentanyl i.v. at 5 min intervals (group 1), and the drugs were given in the reverse order to 5 other rabbits (group 2). BCO was repeated in conscious state (control) and after each drug injection. MAP responses did not differ from control response in either group when both drugs were given. In group 1, however, diazepam decreased HR response to 71.4% of control, and increased TPR response by 36%. Fentanyl administration reversed diazepam-induced changes in BCO responses to the control level. In group 2, fentanyl decreased TPR response to 61.6% of control and increased HR response by 41.5%. Administration of diazepam following fentanyl restored HR and TPR responses to control levels. Carotid sinus baroreflex gain was 3.1 +/- 0.4 (mean +/- SEM) in control and 3.1 +/- 0.4 after administration of both drugs in 12 rabbits. The results suggest that a sedative dose of either fentanyl or diazepam antagonizes the other drug's action on the carotid sinus baroreflex. The combination of fentanyl and diazepam has little influence on carotid sinus baroreflex control of the circulation in rabbits.

Journal Article↗

PubMed1984

Persistence and movement of phorate at high concentrations in soil.

The entrance of a large number of chemicals into the agricultural market has caused concern to both cultivators and scientists because of their effectiveness at the target site, possibility of underground water contamination, and other undesirable effects such as phytotoxicity and effects on nontarget species. The persistence and movement of phorate--a systemic granular insecticide--were studied at high concentrations (4 and 8 kg a.i./ha) in field soil in two seasons, i.e., winter and summer. Periodic sampling for total phorate residues (TPR) at various vertical depths showed that it leached more efficiently at the higher dose (i.e., 8 kg a.i./ha) in both seasons. The horizontal mobility was also higher at this dose. Irrespective of the treatments, TPR leaching was significantly greater in winter with the higher dose, whereas its movement in the horizontal plane was comparatively greater in summer with this dose. The TPR concentration peaks remained stationary at 7.5 cm depth at all the redistribution times until the pesticide was nearly dissipated under both treatments and in both seasons. TPR persistence was higher at the higher dose. Its persistence was comparatively greater in winter than in summer. The present findings show that there seems to be no threat of underground water contamination by this pesticide even at a rate as high as 8 kg a.i./ha.

Insecticides↗

PubMed1982

Role of aortic and carotid sinus baroreceptors on Valsalva-like vasoconstrictor and heart rate reflexes in the conscious rabbit.

Graded 30 s manoeuvers were used to elicit cardiovascular responses in conscious instrumented rabbits by applying pressures from 2.5 to 20 mm Hg (Valsalva Pressure, VP) to the animal's respiratory valve and to a sphygmomanometer cuff wrapped around its thorax and abdomen. In normal rabbits the Valsalva-like manoeuvers elicited VP-related rises in total peripheral resistance (TPR), heart rate and in right atrial pressure (RAP), VP-related fall in cardiac output (CO) and no change in mean arterial pressure (MAP). The rises in TPR and heart rate and the maintenance of MAP were reflexly mediated, whilst the CO and RAP changes were largely a mechanical consequence of the manoeuver as assessed from the responses after autonomic effector blockade. In rabbits with selective section of the carotid sinus nerves the reflex responses were little altered from normal, but after selective section of the aortic nerves there was significant attenuation of the TPR response, indicating that the input from the aortic baroreceptors was more important for this response than that from the carotid receptors. After combined denervation of the aortic and carotid baroreceptor zones (but with the vagi intact) the reflex TPR and heart rate changes were completely abolished, with the responses the same as after autonomic effector block. The results indicate that the arterial baroreceptor zones make a major contribution to the reflex cardiovascular responses to the Valsalva manoeuver in the rabbit and that any reflex effects of cardiopulmonary baroreceptor stimulation are only expressed in the presence of an intact arterial baroreceptor input.

Animals↗