The Effect of Phenytoin on Embryonic Heart Rate In Vivo

Author(s):  
Helen E. Ritchie ◽  
Dominqiue Abela ◽  
Deena Ababneh ◽  
Emma Farrell ◽  
Elizabeth Hegedus
Keyword(s):  
2017 ◽  
Vol 79 (8) ◽  
pp. 645-653 ◽  
Author(s):  
Jacqueline S. McLaughlin ◽  
Mit A. Patel

The lab presented in this paper utilizes a proven four-step pedagogical framework (McLaughlin & Coyle, 2016) to redesign a classic Association of Biology Laboratory Education (ABLE) undergraduate lab (McLaughlin & McCain, 1999) into an authentic research experience on vertebrate four-chambered heart development and physiology. The model system is the chicken embryo. Through their research, students are also exposed to the embryonic anatomy and physiology of the vertebrate heart, the electrical circuitry of the developing heart, and the effects of pharmacological drugs on heart rate and contractility. Classical embryological micro-techniques, explantation of the embryo, surgical removal of the beating heart, isolation of the heart chambers, and more advanced tissue culture methods are also conducted. In this laboratory paradigm, students work in pairs to ask their own questions concerning the effects of two human cardiovascular drugs, denopamine™ and acebutolol™ on both in vivo and in vitro chicken embryonic heart rate and contractility, develop testable hypotheses based on information gathered from relevant scientific literature, devise and carry out a controlled experiment, and present the data in a professional scientific manner pertaining to a topic of clinical significance.


2016 ◽  
Vol 116 (07) ◽  
pp. 181-190 ◽  
Author(s):  
Luong Le ◽  
Hayley Duckles ◽  
Torsten Schenkel ◽  
Marwa Mahmoud ◽  
Jordi Tremoleda ◽  
...  

SummaryBlood flow generates wall shear stress (WSS) which alters endothelial cell (EC) function. Low WSS promotes vascular inflammation and atherosclerosis whereas high uniform WSS is protective. Ivabradine decreases heart rate leading to altered haemodynamics. Besides its cardio-protective effects, ivabradine protects arteries from inflammation and atherosclerosis via unknown mechanisms. We hypothesised that ivabradine protects arteries by increasing WSS to reduce vascular inflammation. Hypercholesterolaemic mice were treated with ivabradine for seven weeks in drinking water or remained untreated as a control. En face immunostaining demonstrated that treatment with ivabradine reduced the expression of pro-inflammatory VCAM-1 (p<0.01) and enhanced the expression of anti-inflammatory eNOS (p<0.01) at the inner curvature of the aorta. We concluded that ivabradine alters EC physiology indirectly via modulation of flow because treatment with ivabradine had no effect in ligated carotid arteries in vivo, and did not influence the basal or TNFα-induced expression of inflammatory (VCAM-1, MCP-1) or protective (eNOS, HMOX1, KLF2, KLF4) genes in cultured EC. We therefore considered whether ivabradine can alter WSS which is a regulator of EC inflammatory activation. Computational fluid dynamics demonstrated that ivabradine treatment reduced heart rate by 20 % and enhanced WSS in the aorta. In conclusion, ivabradine treatment altered haemodynamics in the murine aorta by increasing the magnitude of shear stress. This was accompanied by induction of eNOS and suppression of VCAM-1, whereas ivabradine did not alter EC that could not respond to flow. Thus ivabradine protects arteries by altering local mechanical conditions to trigger an anti-inflammatory response.


1982 ◽  
Vol 50 (1) ◽  
pp. 219-230 ◽  
Author(s):  
Richard J. Roberts ◽  
Theodore C. Weerts

This study was designed to determine if visualization of anger- and fear-provoking scenes produced differential physiological patterns similar to those produced by in vivo manipulations. Normotensive college students were selected on the basis of their responses to newly developed Anger and Fear/Anxiety questionnaires and for their ability to construct arousing scenes during a screening interview. In a 2 × 2 design (intensity × emotion), four scenes (high and low anger, high and low fear) were constructed individually for each of 16 subjects to imagine. Diastolic blood pressure, systolic blood pressure, and heart rate were monitored during visualization of each scene. Change in diastolic blood pressure was significantly greater for high anger than for high fear as predicted. Analysis of change in heart rate and systolic blood pressure showed significant effects for intensity only. These results provide further support for the concept of physiological differentiation in human emotion and suggest the utility of imagery for systematic study of human emotional responding.


1991 ◽  
Vol 64 (4) ◽  
pp. 1002-1022 ◽  
Author(s):  
H. Tazawa ◽  
T. Hiraguchi ◽  
O. Kuroda ◽  
S. G. Tullett ◽  
D. C. Deeming
Keyword(s):  

2001 ◽  
Vol 204 (1) ◽  
pp. 165-174 ◽  
Author(s):  
H. Tazawa ◽  
J.T. Pearson ◽  
T. Komoro ◽  
A. Ar

Previously, we have measured daily changes (developmental patterns) in embryonic heart rate (fh) in altricial and semi-altricial (ASA) birds (range of mean fresh egg mass approximately 1–20 g), semi-precocial seabirds (egg mass approximately 38–288 g) and precocial birds (egg mass approximately 6–1400 g). An allometric relationship between embryonic fh at 80 % of incubation duration (ID) and fresh egg mass (M) has been derived for six species of precocial bird (fh at 80 % ID=429M(−0.118)). In the present study, additional measurements of embryonic fh in three ASA species, the barn owl Tyto alba, the cattle egret Bubulcus ibis and the lanner falcon Falco biarmicus, were made to extend the egg mass range (20–41 g), and the allometric relationships of embryonic fh for these ASA birds and the precocial and semi-precocial (PSP) groups were investigated from published data. The developmental patterns of embryonic fh in three relatively large ASA species did not show a significant increase prior to the pipping period, unlike those in small ASA birds, but tended to be constant, with a subsequent increase during pipping. The allometric relationship derived for ASA birds was fh at 80 % ID=371M(−0.121) (r=−0.846, P&lt;0.001, N=20) and that for PSP birds was fh at 80 % ID=433M(−0.121) (r=−0.963, P&lt;0.001, N=13). The slopes were parallel, but fh of ASA embryos was low compared with that of PSP embryos with the same egg mass. In ASA birds, embyronic fh was maximal during the pipping (perinatal) period, and the maximum fh (fh(max)) was significantly related to fresh egg mass: fh(max)=440M(−0.127) (r=−0.840, P&lt;0.001, N=20). The allometric relationships for fh at 80 % ID in PSP and fh(max) in ASA embryos were statistically identical. Accordingly, embryonic fh at 80 % ID in PSP birds and fh(max) during pipping in ASA birds can be expressed by a single allometric equation: fh=437M(−0.123) (r=−0.948, P&lt;0.001, N=33).


1990 ◽  
Vol 69 (3) ◽  
pp. 907-913 ◽  
Author(s):  
N. B. Hampson ◽  
E. M. Camporesi ◽  
B. W. Stolp ◽  
R. E. Moon ◽  
J. E. Shook ◽  
...  

The effects of mild hypoxia on brain oxyhemoglobin, cytochrome a,a3 redox status, and cerebral blood volume were studied using near-infrared spectroscopy in eight healthy volunteers. Incremental hypoxia reaching 70% arterial O2 saturation was produced in normocapnia [end-tidal PCO2 (PETCO2) 36.9 +/- 2.6 to 34.9 +/- 3.4 Torr] or hypocapnia (PETCO2 32.8 +/- 0.6 to 23.7 +/- 0.6 Torr) by an 8-min rebreathing technique and regulation of inspired CO2. Normocapnic hypoxia was characterized by progressive reductions in arterial PO2 (PaO2, 89.1 +/- 3.5 to 34.1 +/- 0.1 Torr) with stable PETCO2, arterial PCO2 (PaCO2), and arterial pH and resulted in increases in heart rate (35%) systolic blood pressure (14%), and minute ventilation (5-fold). Hypocapnic hypoxia resulted in progressively decreasing PaO2 (100.2 +/- 3.6 to 28.9 +/- 0.1 Torr), with progressive reduction in PaCO2 (39.0 +/- 1.6 to 27.3 +/- 1.9 Torr), and an increase in arterial pH (7.41 +/- 0.02 to 7.53 +/- 0.03), heart rate (61%), and ventilation (3-fold). In the brain, hypoxia resulted in a steady decline of cerebral oxyhemoglobin content and a decrease in oxidized cytochrome a,a3. Significantly greater loss of oxidized cytochrome a,a3 occurred for a given decrease in oxyhemoglobin during hypocapnic hypoxia relative to normocapnic hypoxia. Total blood volume response during hypoxia also was significantly attenuated by hypocapnia, because the increase in volume was only half that of normocapnic subjects. We conclude that cytochrome a,a3 oxidation level in vivo decreases at mild levels of hypoxia. PaCO is an important determinant of brain oxygenation, because it modulates ventilatory, cardiovascular, and cerebral O2 delivery responses to hypoxia.


2019 ◽  
Vol 64 ◽  
pp. 16-23
Author(s):  
Jennifer Lara Maria Mumm ◽  
Lena Pyrkosch ◽  
Jens Plag ◽  
Patrick Nagel ◽  
Moritz Bruno Petzold ◽  
...  

2003 ◽  
Vol 285 (5) ◽  
pp. H1976-H1979 ◽  
Author(s):  
A. V. Naumova ◽  
R. G. Weiss ◽  
V. P. Chacko

Image-guided, spatially localized 31P magnetic resonance spectroscopy (MRS) was used to study in vivo murine cardiac metabolism under resting and dobutamine-induced stress conditions. Intravenous dobutamine infusion (24 μg · min–1 · kg body wt–1) increased the mean heart rate by ∼39% from 482 ± 46 per min at baseline to 669 ± 77 per min in adult mice. The myocardial phosphocreatine (PCr)-to-ATP (PCr/ATP) ratio remained unchanged at 2.1 ± 0.5 during dobutamine stress, compared with baseline conditions. Therefore, we conclude that a significant increase in heart rate does not result in a decline in the in vivo murine cardiac PCr/ATP ratio. These observations in very small mammals, viz., mice, at extremely high heart rates are consistent with studies in large animals demonstrating that global levels of high-energy phosphate metabolites do not regulate in vivo myocardial metabolism during physiologically relevant increases in cardiac work.


Sign in / Sign up

Export Citation Format

Share Document