Biomedical subjects

U S Vasthare

Publications and source records attributed to U S Vasthare.

13 recordsLinked to original sources

PubMed1998

Effect of hypertonic saline on leukocyte activity after spinal cord injury.

STUDY DESIGN: The effect of intravenous administration of hypertonic saline on leukocyte adhesion after compression injury of the spinal cord was evaluated. OBJECTIVES: To investigate changes in leukocyte adhesion after spinal cord injury and to evaluate the effect of hypertonic saline on this process. SUMMARY OF BACKGROUND DATA: Leukocytes have been thought to exacerbate tissue injury after ischemia-reperfusion. Downregulating and reducing the number of circulating leukocytes has attenuated tissue damage in various models of cerebral ischemia. Recently, investigators have reported that leukocytes exacerbate injury in the spinal cord after trauma. Other recent findings have indicated that hypertonic saline may play a role in decreasing leukocyte adhesion and activation. METHODS: Sprague-Dawley rats were anesthetized, and a C3-C5 laminectomy was performed. Injury was caused by 35 g of compression applied to the cord for 10 minutes. Animals were divided into three groups: sham treated, untreated, and treated. The treated animals received 7.5% hypertonic saline (5 mL/kg, intravenously) 5 minutes after the injury. Sticking leukocytes and shear rate were measured using fluorescence microscopy. RESULTS: Administration of 7.5% hypertonic saline after injury significantly decreased the number of sticking leukocytes in the venules and arterioles. Shear rate was unchanged between the groups. CONCLUSIONS: The results show that an increase in leukocyte adhesion after a compressive injury is attenuated by the administration of 7.5% hypertonic saline. The decrease in adhesion cannot be attributed to changes in the shearing forces, because no significant change was observed in the shear rate. Hypertonic saline may interfere with leukocytes directly by interfering with their ability to swell and thus may prevent activation.

Animals↗

PubMed1998

Complement depletion improves neurological function in cerebral ischemia.

The contribution of the complement system to the exacerbation of cerebral ischemia/reperfusion injury was studied by comparing a group of rats with normal complement levels to another group that was complement depleted by cobra venom factor (CVF). The magnitude of reactive hyperemia was significantly greater in the complement depleted animals. There was also better preservation of somatosensory evoked potentials (SSEPs) in the complement depleted animals. These differences were not associated with changes in leukocyte infiltration as evidenced by myeloperoxidase and Leukotriene B4 activity. These data demonstrate that depleting the complement system can improve flow and outcome following cerebral ischemia with reperfusion.

Animals↗

PubMed1997

Hypertonic saline administration attenuates spinal cord injury.

BACKGROUND: This manuscript describes the results of three studies designed to test the hypothesis that the intravenous administration of hypertonic saline could help to preserve spinal cord function after injury. METHODS: A static compression model was used to injure rat spinal cords. Somatosensory evoked potentials and spinal cord blood flow changes were monitored in the acute studies. The first study compared the effects of administration of hypertonic saline with isotonic saline solutions. The second study evaluated the effect of hypertonic saline administration at 5, 15, and 60 minutes after injury. A chronic injury model was evaluated in the third study. Spontaneous voiding, neurologic function, and evidence of histologic changes were evaluated. RESULTS AND CONCLUSIONS: The administration of hypertonic saline after spinal cord injury increased blood flow and helped preserve spinal cord function in the acute models. The rate of recovery with the chronic model was significantly faster in hypertonic saline treated animals.

Acute Disease↗

PubMed1994

Vascular permeability and microcirculation of gliomas and mammary carcinomas transplanted in rat and mouse cranial windows.

Many brain tumors are highly resistant to chemotherapy, presumably due to the presence of a tight blood-tumor barrier. For a better understanding of the regulation of this barrier by the brain environment, a new intravital microscopy model was established by transplanting tumor tissue into cranial windows in both rats and mice. The model was characterized by RBC velocities, vessel diameters, and vascular permeabilities of various tumors: R3230AC (a rat mammary adenocarcinoma), MCaIV (a mouse mammary adenocarcinoma), and U87 and HGL21 (human malignant astrocytomas). Our results showed that tumor blood flow in cranial windows was one to three orders of magnitude lower than the blood flow in pial vessels and similar to that in dorsal skin-fold chambers observed in previous studies. The mean vessel diameter ranged from 6.8 +/- 1.3 microns for HGL21 to 30.4 +/- 8.5 microns for MCaIV. At least one order of magnitude difference in vascular permeability to albumin was observed between tumor lines: 0.11 +/- 0.05 x 10(-7) cm/s for HGL21 versus 3.8 +/- 1.2 x 10(-7) cm/s for U87. The low vascular permeability of HGL21, which was also confirmed by both sodium fluorescein and Lissamine green injections, suggests that not all tumors are leaky to tracer molecules and that the blood-tumor barrier of this tumor still possesses some characteristics of blood-brain barrier as observed in other intracranial tumors. The model presented here will allow us to manipulate the vascular permeability in brain tumors and thus may provide new information on the regulation of the blood-tumor barrier and new strategies for improving drug delivery in brain tumors.

Animals↗

PubMed1994

Leukocyte involvement in cerebral infarct generation after ischemia and reperfusion.

White blood cell involvement in the generation of cerebral infarcts was evaluated following ischemia and reperfusion injury in the rat. Control and leukopenic rats (induced by vinblastine, WBC counts < 1500/mm3) were compared in a global forebrain ischemic model after 1 h of ischemia and 1 h 15 min of reperfusion. Cerebral infarcts were defined on coronal brain sections using Triphenyl tetrazolium chloride (TTC) staining. Electroencephalographic activity (EEG) and somatosensory evoked potentials (SSEP) were also compared. Results indicate that the area infarcted in leukopenic rats was significantly less than infarcts generated in corresponding controls (21 +/- 16% vs. 70 +/- 16%). In addition, EEG was preserved in all leukopenic animals when compared to controls, both during ischemia and after reperfusion. The cortical peak component of the SSEP was also better preserved in the leukopenic animals both during ischemia and at 60 min of reperfusion. These results indicate white blood cell participation in the generation of cerebral damage in a model of global forebrain ischemia and reperfusion as indicated by TTC staining of cerebral infarcts.

Animals↗

PubMed1994

Preservation of post-compression spinal cord function by infusion of hypertonic saline.

We tested the hypothesis that the administration of hypertonic saline, following traumatic injury to the spinal cord, could enhance blood flow to the cord and preserve function. Rats were used as the experimental model. Direct compression of the spinal cord for a period of 10 min was done to produce the injury. Somatosensory evoked potentials (SSEPs) and spinal cord blood flow were measured using a laser Doppler flow meter throughout the experiment. Comparisons of the blood flow values and SSEPs were made among four different groups of animals. The control group received no fluid resuscitation after injury. A second group received a bolus injection of isotonic saline (0.5 ml/100 g) as an i.v. infusion over a period of 1 min. A third group received a bolus infusion of 7.5% NaCl (0.5 ml/100 g) over a period of 1 min. The final group received 4 ml/100 g of 0.9% NaCl over a period of 10 min. The administration of hypertonic saline significantly reduced spinal cord vascular resistance during the first 10 min after infusion. During the first 30 min after the removal of compression, spinal cord blood flow was greater in the hypertonic saline group than in the other three groups. The hypertonic saline group had a reactive hyperemia whereas the flow in the other groups remained at or below control values. Beginning 10 min after injury and for the remainder of the 1-h observation period, the latency of the cortical peak of the SSEP in the group receiving hypertonic saline was significantly shorter than in any of the other three groups. These results indicate that the administration of hypertonic saline enhances blood flow and preserves spinal cord conduction following traumatic injury to the spinal cord.

Animals↗

PubMed1992

Age-related alterations in the arterial microvasculature of skeletal muscle.

This study investigated the possibility that the aging process results in alterations in the structure and/or functional reactivity of the microvessels that could contribute to increased resistance to blood flow in working skeletal muscle. Initially, latex casts were made of the cremaster muscle microvasculature in adult (12 mo) and senescent (24 mo) male Fischer 344 rats. Although the average diameter was not different between age groups, segmental length (distance between adjacent branches) increased significantly (3rd order) during aging. Additionally, in vivo experiments were performed to determine the response of the vessels to the topical application of norepinephrine and adenosine. There was no increase in vasoconstriction produced by norepinephrine; however, the vasodilation in response to adenosine declined dramatically (1st and 2nd order) with advancing age. It can be concluded that the increase in skeletal muscle vascular resistance during contraction in aged male rats could be explained by morphological changes and/or the diminished vasodilation elicited by adenosine.

Adenosine↗

PubMed1991

Influence of nitrous oxide administration and discontinuation thereof on blood flow in cerebral cortex, cerebellum and brain stem in the rat.

The effect of nitrous oxide on blood flow in the cerebral cortex, the cerebellum and the brain stem was evaluated in a rat model. Catheters were surgically implanted in advance to avoid influence from other anaesthetics. The animals were housed in a plastic tube where they were allowed to breathe spontaneously. Blood flow was determined with a microsphere technique. Animals were exposed to nitrous oxide, 75-80%, for 45 min and blood flow was measured after 15 and 45 min exposure and was compared to values obtained during room air breathing. In one animal group, nitrous oxide was administered for 45 min and blood flows were measured after 5 and 30 min withdrawal of the gas. Results showed that all animals had significant hyperventilation. In three groups CO2 had to be added to inspiratory gases to normalize arterial blood gases. This was interpreted as caused by stressful experimental conditions, not blunted by the nitrous oxide. Cortical blood flow values in the control situation were also higher than obtained in other animal studies. Despite this, nitrous oxide showed a significant vasodilation in the cerebral cortex and the brain stem at 15 min exposure. At discontinuation of nitrous oxide administration, blood flow values had decreased at 5 min.

Animals↗

PubMed1990

Leukocyte involvement in cerebral ischemia and reperfusion injury.

Leukocytes have been postulated to contribute to cerebral ischemia and reperfusion injury. The present study implies that leukocytes have a deleterious effect in the brain following ischemia. We compared the alteration of cortical electrical activity following transient, incomplete cerebral ischemia in control and leukopenic rats by monitoring somatosensory evoked potentials and electroencephalographic activity. There was complete cessation of electroencephalographic activity, and the cortical peak of the evoked potential was abolished during ischemia in the control animals. However, when the animals were rendered leukopenic, there was maintenance of electroencephalographic activity with reduced amplitude and preservation of the cortical peak of the evoked response during the ischemic period. This indicates that when the animals are made leukopenic, even under ischemic conditions, the neurophysiologic functioning is still maintained to a certain extent.

Animals↗

PubMed1988

Preservation of skeletal muscle hyperemic response to contraction with aging in female rats.

In a previous investigation (Irion et al., 1987), a significant age-related decline in skeletal muscle blood flow during intermittent tetanic contractions was observed in male Fischer 344 rats. This decline in the hyperemic response to muscle contraction was accompanied by an increased fatigability of skeletal muscle of senescent male rats. In the present investigation, anesthetized female adult and senescent Fischer 344 rats were instrumented for stimulation of the plantar flexor muscles in situ, and blood flow measurement by the tracer microsphere technique. After determination of optimum length and maximum tetanic force, muscles were stimulated to contract at the rate of 120 tetani/min. No significant differences could be observed between adult and senescent females in skeletal muscle fatigability or blood flow. The only significant differences observed between senescent and younger females were a decrease in splenic blood flow and an increase in body weight. In contrast to male rats of the same age, no impairment of skeletal muscle blood flow or change in fatigability could be detected in senescent female rats.

Aging↗

PubMed1987

Age-related change in skeletal muscle blood flow in the rat.

Anesthetized adult and senescent male Fischer 344 rats were instrumented for stimulation of in situ plantar flexor muscles and blood flow measurement by the tracer microsphere technique. After determination of optimum length and maximum tetanic force, muscles were stimulated to contract at the rate of 120 tetani/min. Senescent rats displayed significantly lower muscle blood flow and greater muscle fatigue than younger rats. Infusion of a nonspecific vasodilator in resting anesthetized rats also revealed a significantly lower potential to increase muscle blood flow in the senescent rats. Lower muscle blood flow of senescent rats during muscle contractions might be responsible, at least in part, for decreased performance of muscles of senescent male rats.

Aging↗

PubMed1986

Considerations in use of microspheres for flow measurements in anesthetized rat.

The results of single injections of different doses of microspheres (60,000, 100,000, and 375,000) demonstrated a significant reduction in measured heart and kidney blood flows as a function of the number of microspheres injected. Measured flow to other organs was unaffected by a single injection of these doses of microspheres. The injection of microspheres at a faster rate (0.8 ml/min microsphere injection; 1.0 ml/min flush) resulted in higher calculated heart flow when compared with the slow rate (0.2 ml/min microsphere injection; 0.25 ml/min flush). A significant decrease (approximately 21%) in measured blood flow to the right side of the brain that was observed in all the groups is due to the occlusion of the right carotid artery by the cannulation procedure. Intra-aortic injection of microspheres resulted in reduced measured brain blood flow when compared with intraventricular injections. Accurate and reliable heart and brain blood flows were not obtained with intra-aortic injection of microspheres. However, intra-aortic injection of microspheres does provide accurate and reliable flow measurements for more distal organs.

Anesthesia↗

PubMed1985

Age-related changes in regional blood flow in the rat.

The purpose of this investigation was to characterize the changes in regional blood flow and central hemodynamic measures that occur in the rat as a result of the aging process. The isotope-labeled microsphere technique was used to measure cardiac output and regional blood flows in conscious and anesthetized adult (12 mo) and senescent (24 mo) Fischer 344 virgin female rats. No significant changes were observed in central hemodynamic measurements or regional blood flows in conscious rats with the exception of a 25% reduction in splenic blood flow. Pentobarbital anesthesia significantly reduced cardiac index and heart rate but elevated total peripheral resistance and mean arterial blood pressure. There was a decrease in blood flow to skeletal muscle, spleen, duodenum, stomach, and brain tissue samples and increased hepatic arterial blood flow in both age groups. The use of anesthesia caused a greater reduction in the cardiac index and brain blood flow in the senescent anesthetized rats than in the adult rats. Heart and kidney blood flows were decreased by anesthesia in the senescent rats but not in the adult rats. Skeletal muscle blood flow, however, was significantly greater in the senescent anesthetized rats than in the younger anesthetized animals. Although body weight and organ weights of the liver, spleen, kidneys, stomach, heart, and brain were significantly greater for the senescent rats, no differences could be demonstrated in tibial length or lean body mass.

Aging↗