Proper Choice of Vessels for Supermicrosurgery Training: An Experimental Animal study

2018 ◽  
Vol 34 (09) ◽  
pp. 742-748
Author(s):  
Yooseok Ha ◽  
Seung Song ◽  
Nak Kang ◽  
Sang-Ha Oh

Background Reconstruction using supermicrosurgery, a technique of microneurovascular anastomosis for smaller vessels (< 0.8 mm), has become popular. Experimental animal studies for supermicrosurgery training have been reported; however, there have been few studies performed according to vessel diameter and pedicle length. In this study, the external diameters of four vessels (femoral, superficial epigastric, axillary, and common thoracic) and pedicle length of two flaps (superficial epigastric and common thoracic–long thoracic) were measured. Methods The inguinal and pectoral regions of Sprague-Dawley rats (n = 19) were dissected anatomically, and the external diameters of the four vessels were measured (right and left, artery and vein measured separately). After elevating the superficial epigastric and common thoracic–long thoracic flaps, the pedicle length of the flaps was also measured. Results Among the 16 vessels examined, the external diameters of 11 and 5 vessels were above and below 0.8 mm, respectively. The external diameters of the superficial epigastric vessel and common thoracic vessel (both arteries and veins) were below 0.8 mm. The external diameters of the femoral and axillary vessels (veins) were above 0.8 mm. The length of the common thoracic–long thoracic pedicle was approximately10 mm longer than that of the superficial epigastric pedicle. Conclusions The external diameters of the superficial epigastric vessel and common thoracic vessel are small enough for supermicrosurgery training. The pedicle lengths of both the superficial epigastric and common thoracic–long thoracic flaps are sufficient to perform free flap experiments. Supermicrosurgical free flaps using these two vessels and a study of the physiology and pharmacology of the flaps will likely be possible in the future.

1987 ◽  
Vol 253 (5) ◽  
pp. H1253-H1260 ◽  
Author(s):  
R. G. Dacey ◽  
J. E. Bassett

Much morphological and physiological evidence indicates that cholinergic mechanisms play a significant role in the control of cerebral blood flow. Despite in situ data suggesting that an intrinsic cholinergic mechanism produces vasodilation in the intracerebral microcirculation, there is no direct information on the effect of acetylcholine (ACh) on intracerebral arterioles. We investigated cholinergic mechanisms in isolated perfused intracerebral arterioles from pentobarbital sodium-anesthetized Sprague-Dawley rats. In arterioles with resting diameters of 46.8 +/- 6.6 microns (mean +/- SE) ACh produced no significant dilation at pH 7.30. At pH 7.60, however, a significant dose-dependent dilation to a maximum of 119.0 +/- 1.0% of control diameter was observed. Carbachol, a long-acting cholinergic agonist, similarly failed to dilate vessels at pH 7.30 but significantly dilated vessels at pH 7.60. Prostaglandin F2 alpha produced a maximum contraction to 68.3 +/- 2.7% of control diameter (n = 8). ACh at concentrations of 10(-4) and 2 X 10(-4) M induced a significant dilation of this prostaglandin-induced contraction. In vessels similarly preconstricted with serotonin, 10(-4) M ACh produced significant dilation. Atropine, having no effect on vessel diameter when administered alone, blocked cholinergic vasodilation of intracerebral arterioles at pH 7.60. Attempts at endothelial removal, although successful in eliminating endothelial cells from the preparation, significantly impaired smooth muscle contractility. ACh has no significant effect on the spontaneous cerebrovascular tone in this preparation, but in vessels preconstricted by a variety of means it produced vasodilation mediated by atropine sensitive receptors.


1994 ◽  
Vol 267 (2) ◽  
pp. H837-H843 ◽  
Author(s):  
K. Irikura ◽  
K. I. Maynard ◽  
W. S. Lee ◽  
M. A. Moskowitz

The role of nitric oxide (NO) in the response to 5% CO2 inhalation was investigated by measuring 1) regional cerebral blood flow (rCBF) by laser-Doppler flowmetry and pial vessel diameter through a closed cranial window after topical NG-nitro-L-arginine (L-NNA, 1 mM), and 2) the time-dependent changes in brain guanosine 3',5'-cyclic monophosphate (cGMP) levels after L-NNA (10 mg/kg ip). When L-NNA (but not NG-nitro-D-arginine) was applied topically for 30 or 60 min, the response to hypercapnia was significantly attenuated. A correlation was found between inhibition of brain NO synthase (NOS) activity and the rCBF response (r = 0.77; P < 0.01). However, L-NNA applied 15 min before hypercapnia did not attenuate the increase in rCBF but did attenuate the dilation to topical acetylcholine. Inhalation of CO2 (5%) elevated brain cGMP levels by 20–25%, and L-NNA reduced this response. These data from the rat suggest that 1) a product of NOS activity is associated with hypercapnic hyperemia and the attendant increase in brain cGMP levels, and 2) hypercapnic blood flow changes may not be dependent on endothelial NOS activity within pial vessels.


1995 ◽  
Vol 3 (3) ◽  
pp. 1-7 ◽  
Author(s):  
Patrick G Harris ◽  
Sharon Chase ◽  
Bang Kao Hong ◽  
Jon B Loftus ◽  
John F Mosher

Knowledge of the initial time required to repair the endothelial surface of small vessels after microsurgical vascular anastomosis of veins and arteries is required to determine the preferable duration of antiplatelet prophylaxis and anticoagulation after emergency or elective microsurgery. To determine this, the femoral arteries and veins of 16 Sprague-Dawley rats were isolated, sectioned and repaired with microsurgical technique. The animals were then killed at one day intervals from the first to the 16th postoperative day. Femoral veins and arteries were harvested, sectioned and prepared for scanning electron microscopy. The results show that endothelialization of the repair line is begun by day 3 and completed by day 7 in the veins and arteries. Endothelialization of the intraluminal protruding sutures takes nine days in the veins while it is only starting at day 15 in the arteries. If this model can be extended to the human clinical situation, antiplatelet prophylaxis or anticoagulation should be administered for at least seven days. Further study is required to evaluate the thrombogenic potential of intraluminal protruding sutures.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Samantha L. Baglot ◽  
Catherine Hume ◽  
Gavin N. Petrie ◽  
Robert J. Aukema ◽  
Savannah H. M. Lightfoot ◽  
...  

AbstractUp to a third of North Americans report using cannabis in the prior month, most commonly through inhalation. Animal models that reflect human consumption are critical to study the impact of cannabis on brain and behaviour. Most animal studies to date utilize injection of delta-9-tetrahydrocannabinol (THC; primary psychoactive component of cannabis). THC injections produce markedly different physiological and behavioural effects than inhalation, likely due to distinctive pharmacokinetics. The current study directly examined if administration route (injection versus inhalation) alters metabolism and central accumulation of THC and metabolites over time. Adult male and female Sprague–Dawley rats received either an intraperitoneal injection or a 15-min session of inhaled exposure to THC. Blood and brains were collected at 15, 30, 60, 90 and 240-min post-exposure for analysis of THC and metabolites. Despite achieving comparable peak blood THC concentrations in both groups, our results indicate higher initial brain THC concentration following inhalation, whereas injection resulted in dramatically higher 11-OH-THC concentration, a potent THC metabolite, in blood and brain that increased over time. Our results provide evidence of different pharmacokinetic profiles following inhalation versus injection. Accordingly, administration route should be considered during data interpretation, and translational animal work should strongly consider using inhalation models.


2021 ◽  
Author(s):  
Samantha L Baglot ◽  
Catherine Hume ◽  
Gavin N. Petrie ◽  
Robert J Aukema ◽  
Savannah HM Lightfoot ◽  
...  

Up to a third of North Americans over 16 years old report using cannabis in the prior month, most commonly through inhalation. Animal models that reflect human cannabis consumption are critical to study its impacts on brain and behaviour. Nevertheless, most animal studies to date examine effects of cannabis through injection of delta-9-tetrahydrocannabinol (THC; primary psychoactive component of cannabis). THC injections produce markedly different physiological and behavioural effects than inhalation, likely due to distinctive pharmacokinetics of each administration route. The current study directly examined if administration route (injection versus inhalation), with dosing being matched on peak THC blood levels, alters the metabolism of THC, and the central accumulation of THC and its metabolites over time. Adult male and female Sprague-Dawley rats received either a single intraperitoneal injection of THC (2.5 mg/kg) or a single (15 min) session of inhaled exposure to THC distillate (100 mg/mL) vapour. Blood and brains were collected at 15, 30, 60, 90 and 240 minutes post-exposure for analysis of THC and metabolites through mass spectrometry-liquid chromatography. Inhalation results in immediate hypothermia, whereas injection results in delayed hypothermia. Despite achieving comparable peak concentrations of blood THC in both groups, our results indicate higher initial brain THC concentration following inhalation, whereas injection resulted in dramatically higher 11-OH-THC concentrations, a potent THC metabolite, in blood and brain that increased over time. Our results provide evidence that THC and its metabolites exhibit different pharmacokinetic profiles following inhalation versus injection, which could have significant impacts for data interpretation and generalizability. Accordingly, we suggest that translational work in the realm of THC and cannabis strongly consider using inhalation models over those that employ injection.


1993 ◽  
Vol 13 (2) ◽  
pp. 214-220 ◽  
Author(s):  
Joseph R. Meno ◽  
Al C. Ngai ◽  
H. Richard Winn

We measured the changes in pial arteriolar diameter and CSF concentrations of adenosine, inosine, and hypoxanthine during hypoxia in the absence and presence of topically applied dipyridamole (10−6 M) and erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA; 10−5 M). Closed cranial windows were implanted in halothane-anesthetized adult male Sprague–Dawley rats for the observation of the pial circulation and collection of CSF. The mean resting arteriolar diameter in mock CSF was 31.2 ± 5.9 μm. Topically applied dipyridamole and EHNA, in combination, caused a slight but significant ( p < 0.05) increase in resting arteriolar diameter (33.8 ± 4.3 μm). With mock CSF, moderate hypoxia caused a 22.1 ± 9.7% increase in pial vessel diameter. Topically applied dipyridamole and EHNA significantly ( p < 0.01) potentiated pial arteriolar vasodilation in response to hypoxia. Moreover, the potentiating effects of dipyridamole and EHNA during hypoxia were completely abolished by theophylline (0.20 μmol/g, i.p.; p < 0.05), an adenosine receptor antagonist. Resting concentrations of adenosine, inosine, and hypoxanthine in the subwindow CSF were 0.18 ± 0.09, 0.35 ± 0.21, and 0.62 ± 0.12 μ M, respectively. In the absence of dipyridamole and EHNA, these levels were not affected by sustained moderate hypoxia (Pao2 = 36 ± 6 mm Hg). However, in the presence of dipyridamole and EHNA, the concentration of adenosine in the CSF during hypoxia was significantly ( p < 0.05) increased. Our data indicate that dipyridamole and EHNA potentiate hypoxic vasodilation of pial arterioles while simultaneously increasing extracellular adenosine levels, thus supporting the hypothesis that adenosine is involved in the regulation of cerebral blood flow.


1979 ◽  
Author(s):  
A.A. Smokovitis ◽  
B.R. Binder

Subcutaneous injection of alloxan (10mg/100g)induced severe diabetes in Sprague-Dawley rats (hyperglycemia, glucosuria, weight loss, polydypsia, polyphagia and polyuria). The effect on tissue plasminogen activator activity (PAA) was studied histocheraically in key organs (heart, kidney, lung, aorta, and caudal vena cava) 4 days, 2, 3, 4, 6, and 8 weeks after induction of diabetes. After an initially increased vascular PAA (release reaction) seen in lung, kidney, aorta, and myocardium, but not in caudal vena cava, a decreased PAA was found in arteries of the renal medulla and particularly of the renal cortex and in arteries of the myocardium two bo eight weeks after the induction of diabetes. Compared to the normal PAA level, the intima of the aorta showed after the initial rise, a fall in two to three weeks, a second rise by four to six weeks, followed by a fall to the normal value at the eighth week. In the lung the initially increased PAA continued to be slightly elevated until the sixth week; by the eighth week it was normal. In the caudal vena cava no changes in the PAA were seen. Of interest are the observed differences in PAA patterns; (1) between arteries and veins, (2) large and small arteries, and (3) arteries in different tissues up to at least eight weeks post induction of diabetes.Supp-. by the Austrian Acad, of Sciences, Arteriosclerosis research group.


2020 ◽  
Vol 318 (1) ◽  
pp. F86-F95
Author(s):  
D. Angoli ◽  
A. Geramipour ◽  
Z. C. Danziger

The postvoid residual (PVR) is an important measure of bladder function, but obtaining PVR is burdensome because bladder volume must be measured at the time of voiding. The PVR measurement problem has led to experimental tricks in animal studies (infusing the bladder at supraphysiological rates and limiting animal observation windows) to keep the number of observed voids statistically robust while reducing the time an experimenter must be present. Our solution to the PVR measurement problem is a system called Automatic Monitoring for Efficient, Awake, Sensitive, Urine Residual Estimation (AMEASURE). AMEASURE combines metabolic cages and optimization algorithms to estimate continuously PVR for every voiding event 24 h/day for multiple weeks, without artificial bladder infusion, continuous experimenter supervision, anesthesia, or restraints. Using AMEASURE, we obtained voided volumes, PVRs, and other urodynamic parameters continuously for 21 days in 10 healthy female Sprague-Dawley rats. Importantly, this required only one manual measurement of animals’ bladder volume every 12 h. We validated the accuracy of the system experimentally and in simulation. We detected marked differences in voiding frequency and efficiency between light and dark cycles and found that voiding frequency increased over time during the dark cycle (but not the light cycle), due to surgical recovery, cage acclimation, and socialization. This tool enhances the relevance of rodent models to the study of human lower urinary tract by expanding observation periods and obviating the need to infuse the bladder and facilitates the study of conditions for which behavioral, social, or circadian factors play essential roles.


2021 ◽  
Vol 9 ◽  
Author(s):  
Stéphane Personne ◽  
Céline Brochot ◽  
Paulo Marcelo ◽  
Aurélie Corona ◽  
Sophie Desmots ◽  
...  

Biomonitoring studies have highlighted the exposure of pregnant women to pyrethroids based on the measurement of their metabolites in urine. Pyrethroids can cross the placental barrier and be distributed in the fetus as some pyrethroids were also measured in the meconium of newborns. Prenatal exposure to pyrethroids is suspected to alter the neurodevelopment of children, and animal studies have shown that early life exposure to permethrin, one of the most commonly used pyrethroid in household applications, can alter the brain development. This study aimed to characterize the fetal permethrin exposure throughout gestation in rats. We developed a pregnancy physiologically based pharmacokinetic (pPBPK) model that describes the maternal and fetal kinetics of the cis- and trans- isomers of permethrin during the whole gestation period. Pregnant Sprague–Dawley rats were exposed daily to permethrin (50 mg/kg) by oral route from the start of gestation to day 20. Permethrin isomers were quantified in the feces, kidney, mammary gland, fat, and placenta in dams and in both maternal and fetal blood, brain, and liver. Cis- and trans-permethrin were quantified in fetal blood and tissues, with higher concentrations for the cis-isomer. The pPBPK model was fitted to the toxicokinetic maternal and fetal data in a Bayesian framework. Several parameters were adjusted, such as hepatic clearances, partition coefficients, and intestinal absorption. Our work allowed to estimate the prenatal exposure to permethrin in rats, especially in the fetal brain, and to quantitatively estimate the placental transfer. These transfers could be extrapolated to humans and be incorporated in a human pPBPK model to estimate the fetal exposure to permethrin from biomonitoring data.


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