Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of regression of left ventricular hypertrophy following atenolol and bunazosin therapy on ischemic cardiac function and myocardial metabolism in spontaneously hypertensive rats (SHR) were studied. Atenolol (50 mg/kg/day) and bunazosin (5 mg/kg/day) were administered to SHR from 19 to 26 weeks of age, whereas tap water was given to control SHR and normotensive Wistar-Kyoto rats (WKY). Both atenolol and bunazosin significantly decreased arterial blood pressure and significantly decelerated the increase in left ventricular weight in SHR. At the end of the long-term treatment, hearts were removed and perfused by the working heart technique for 15 min, and then global ischemia was induced for either 10 or 30 min. The ischemic heart was reperfused for 30 min. The pressure-rate product and the extent of recovery of the coronary flow after reperfusion following 30 min of ischemia in the bunazosin-treated SHR were significantly higher than those in the control SHR and the atenolol-treated SHR. The levels of adenosine triphosphate (ATP), creatine phosphate (CrP), and energy charge potential in the SHR heart reperfused after 30 min of ischemia were significantly lower than those in the reperfused WKY. Both atenolol and bunazosin improved the restoration of ATP and CrP in SHR after reperfusion following 30 min of ischemia. In conclusion, antihypertensive therapy with either atenolol or bunazosin was effective in preventing cardiac hypertrophy and ischemic damage caused by different mechanisms. Factors resulting from stimulation of the cardiac alpha 1 adrenoceptor may play an important role in the development of hypertensive cardiac hypertrophy, just as factors resulting from stimulation of the beta 1-adrenoceptor do.
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PMID:Effects of regression of left ventricular hypertrophy following atenolol or bunazosin therapy on ischemic cardiac function and myocardial metabolism in spontaneously hypertensive rats. 183 20

The effects of long-term treatment with diltiazem on the heart in normotensive (WKY) and spontaneously hypertensive rats (SHR) were studied. Diltiazem was added to the drinking fluid (900 mg/liter) and given ad libitum from 19 to 26 weeks of age, whereas tap water was given to the control animals. Although diltiazem did not decrease blood pressure in SHR, it decelerated the increase in their left ventricular weight (p less than 0.01). Hearts were removed and perfused by the working heart technique for 15 min, and then global ischemia was induced for either 10 or 30 min. The ischemic heart was reperfused for 30 min. The extent of recovery of coronary flow after reperfusion, following 30 min of ischemia in the diltiazem-treated SHR, was higher than that in the control SHR (p less than 0.01). The levels of adenosine triphosphate (ATP), creatine phosphate (CrP), and energy charge potential in the SHR heart reperfused after 30 min of ischemia were lower than those in the reperfused WKY heart (p less than 0.01, respectively). Diltiazem improved the restoration of ATP and CrP and prevented the decrease in energy charge potential in SHR after reperfusion following 30 min of ischemia (p less than 0.01, respectively). In conclusion, long-term treatment of SHR with diltiazem may protect the myocardium when myocardial ischemia occurs.
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PMID:Response of isolated perfused heart to ischemia after long-term treatment of spontaneously hypertensive rats with diltiazem. 213 6

This study examines the effects of ischemic hypoxia and cooling of the leg, muscle contraction and vibration on cerebral potentials evoked by Achilles tendon taps and posterior tibial nerve stimulation to obtain indirect evidence leading to the identification of receptors activated by tendon taps. Experiments performed during ischemia of the leg showed that these receptors lie between the ankle and the knee. Cooling of the leg showed that they are located deep in muscles or bone. Experiments performed during vibration and muscle contraction suggest that muscle stretch receptors provide the afferent input responsible for Achilles tendon tap evoked potentials. All of these experiments point to primary muscle spindles in the proximal gastrocnemius-soleus muscle belly as the main source of afferent input for evoking cerebral potentials to Achilles tendon taps in humans.
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PMID:About the origin of cerebral somatosensory potentials evoked by Achilles tendon taps in humans. 257 40

Cerebral intraventricular hemorrhage (IVH), a problem widely recognized in premature infants, was found in six older infants, ages 2 weeks to 3 months. IVH was often initially misdiagnosed as subarachnoid hemorrhage or meningits with a traumatic lumbar tap. IVH occurred primarily in infants with hypoxemia, acidosis, ischemia, and/or hypernatremia, conditions found in association with IVH in premature infants, but also occurred spontaneously. Computerized tomography scans were the most valuable diagnostic procedure for detection of IVH.
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PMID:Cerebral intraventricular hemorrhages in infants: a widening age spectrum. 735 33

The aim of this study was to gain further insight into the greater susceptibility to acute ischemic renal failure (ARF, 30 min of renal arteries clamping) of old rats (O, 18 months) as against young rats (Y, 3 months). All the rats ate a hypoproteic diet (14% of casein) to avoid age-related glomerulosclerosis in O. Basal renal dynamics was similar in O and Y (Groups CON). One day after ARF, the decrease in GFR was more severe in O than in Y (-82% and -57% vs. respective CON, P < 0.05), due to a greater rise of RVR in O (+258%) than in Y (+104%). The histological renal damage after ischemia was comparable in the two groups with ARF. Five days after ARF, the recovery of renal function was characterized by a slower rise of GFR in O than in Y. In two further groups, two different scavengers of oxygen-free radicals, dimethylthiourea (DMTU) and superoxide dismutase (SOD), were administered at the time of arterial occlusion. DMTU had protective effects in Y but not in O (delta GFR was -28% and -72%, respectively); in contrast, SOD was more effective in O (delta GFR = -58%) than in Y rats (delta GFR = -40%). To test the hypothesis that such a difference was related to the capacity of SOD to increase the levels of nitric oxide (NO), four more groups of Y and O rats were pretreated with L-arginine (ARG), precursor of NO, in tap water (1.5%). No difference in renal dynamics was detected in basal conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Functional versus structural changes in the pathophysiology of acute ischemic renal failure in aging rats. 807 48

Two hundred seventy-three Patients with acute SAH were treated within the last 46 months (1.4.1991 to 31.1.1995). Diagnosis was made upon visible SAH on CT-scans or bloody spinal tap regardless of a negative CT-scan. These patients harbored 194 aneurysms, 25 AVM and cavernomas. Within the same time-period we treated 27 Patients without SAH but harboring vascular malformations (17 aneurysms, 10 AVM and cavernomas). In 30 patients (11%) no bleeding source was detectable. Fourteen of these patients (5.1%) had blood concentrated within the perimesencephalic cisterns on the CT-scans. On admission all of these 14 patients (8 men, 6 female, aged 30 to 63 years) were awake and without mentionable neurological deficit, equalling Hunt & Hess grade 1 (11 patients) and 2 (3 patients). Neither the initial nor control angiography revealed a vascular malformation as a bleeding source. MRI-scans performed for 11 patients did not reveal further etiological clues. During a follow-up interval of 3 to 48 months, none of these patients suffered a rebleeding. Vasospasm was not or only slightly present, no ischemia leading to neurological deficit. GOS reached 5 and Karnofsky-scale was 100 for all of these patients. We conclude that the perimesencephalic SAH is a homogeneous entity with a different natural course than the common aneurysmatic SAH. Probably leakage within the capillary or venous circulation causes this form of SAH with a benign clinical course. Further experience is required to determine whether control angiography is mandatory in these patents with a distinct CT appearance.
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PMID:[Perimesencephalic subarachnoid hemorrhage--an independent clinical picture of non-aneurysmatic subarachnoid hemorrhage with a benign course]. 877 69

Somatosensory evoked potentials (SEPs) evoked by stimulation of the tibial nerve (TN) in the popliteal fossa, the sural nerve (Sur) at the lateral malleole, and an Achilles tendon (Achilles) tap were recorded before and during voluntary plantarflexion, dorsiflexion, and cocontraction of the ipsi- and contralateral foot in normal subjects. Suppression (gating) of the TN-SEP began around 60 ms before the onset of electromyographic activity (EMG), and became maximal 50-100 ms after the onset of EMG. Similar gating was observed for the SEP evoked by activation of muscle afferents (Achilles) and cutaneous afferents (Sur). The TN-SEP was similarly depressed at the onset of a plantarflexion as at the onset of dorsiflexion. A depression, although much smaller, was also observed at the onset of movement of the contralateral limb. The depression of the TN-SEP after the onset of EMG decreased when fast-conducting afferents were blocked by ischemia below the knee joint. The TN-SEP was equally depressed during tonic dorsiflexion, plantar-flexion, and cocontraction of dorsi- and plantarflexors. The TN-SEP was depressed for up to 300 ms when preceded by stimulation of Sur or a biceps femoris tendon tap. Gating of lower limb SEPs thus appears to have both central and peripheral components of which neither seems to be specific for the muscle being contracted or the sensory afferents being stimulated. We encourage that caution is taken when drawing functional conclusions regarding movement-specific modulation of afferent inflow to the somatosensory cortex based on observations of gating of lower limb SEP.
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PMID:Gating of somatosensory evoked potentials during voluntary movement of the lower limb in man. 962 56

Hyperhomocysteinemia (HH) is an independent risk factor for atherosclerosis, including peripheral arterial occlusive disease (PAOD). Because angiogenesis and collateral vessel formation are important self-salvage mechanisms for ischemic PAOD, we examined whether HH modulates angiogenesis in vivo in a rat model of hindlimb ischemia. Rats were divided into 3 groups: the control group was given tap water, the HH group was given water containing L-methionine (1 g x kg(-1) x d(-1)), and the HH+L-arg group was given water containing methionine (1 g x kg(-1) x d(-1)) and l-arginine (2.25 vol%). At day 14 of the dietary modifications, the left femoral artery and vein were excised, and the extent of angiogenesis and collateral vessels in the ischemic limb were examined for 4 weeks. Plasma homocysteine levels significantly increased (P:<0.001), and plasma and tissue contents of nitrite+nitrate as well as tissue cGMP levels significantly decreased in the HH group compared with the control group (P:<0.01). Laser Doppler blood flowmetry (LDBF) revealed a significant decrease in the ischemic/normal limb LDBF ratio in the HH group at days 7, 14, 21, and 28 (P:<0.01 versus control). Angiography revealed a significant decrease in the angiographic score in the HH group at day 14 (P:<0.001 versus control). Immunohistochemistry of ischemic tissue sections showed a significant reduction in the capillary density in the HH group (P:<0. 001 versus control). Oral l-arginine supplementation in rats with HH (HH+L-arg) restored the decreased plasma and tissue nitrite+nitrate and cGMP contents (P:<0.05) as well as angiogenesis, as assessed by LDBF (P:<0.05 versus HH), angiographic score (P:<0.01 versus HH), and capillary density (P:<0.001 versus HH). In summary, HH impaired ischemia-induced angiogenesis and collateral vessel formation in a rat model of hindlimb ischemia in vivo. The mechanism of the HH-induced impairment of angiogenesis might be mediated in part by a reduced bioactivity of endogenous NO in the HH state.
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PMID:Hyperhomocysteinemia impairs angiogenesis in response to hindlimb ischemia. 1111 56

The authors report an unusual case of low intracranial pressure (ICP) syndrome that was successfully treated by the placement of an anti-siphon device (ASD). This 36-year-old male had suffered suprasellar germinoma with hydrocephalus and had had a V-P shunt following radiotherapy. Sixteen years later he developed gait disturbance and somnolence and MRI demonstrated a small lateral ventricle as well as a diffuse dural enhancement. A lumbar tap revealed a low ICP of 12 mmH2O. Because of this, an ASD was placed in the patient. Postoperatively, his symptoms of gait and consciousness disturbance improved. Typical clinical findings of low ICP syndrome such as headache were not observed in this case. To our knowledge, no symptom of gait disturbance with low ICP has been reported previously. We present an interesting case of low ICP syndrome with gait disturbance and discuss the mechanism of the symptoms. Symptoms of this patient were due at first to brain ischemia. After convulsion and consciousness disturbance due to low intracranial pressure, the symptoms increased in strength until gait disturbance occurred. The possibility is suggested that gait disturbance in this patient was due both to brain ischemia and low intracranial pressure.
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PMID:[Successful treatment of a patient with low pressure syndrome associated with gait disturbance]. 1159 68

OBJECTIVE: To observe effects of arginine on art erial endothelium injured by ischemia-reperfusion (IR), and explore its possibl e mechanism. METHODS: Fifty-four rats were divided into 3 groups and treate d in respective ways: (1) drinking tap water as the control; (2) drinking tap wa ter containing 2.5% L-arginine; (3) drinking tap water containing 2.5% L-arginine together with intraperitoneal injection of N(G)-nitro-L-arginine methylester 5 mg/kg/d. A segment of the common carotid artery was occluded for 1 h, and then reperfused. Samples taken at different post-IR t ime from the segment were prepared for the ultrastructural and Ce-H(2)O(2) cyto chemical observation. The naked index (NI) of internal elastic lamina (IEL) was measured for comparing the endothelial injure extent and its repair process. RESULTS: Less damage of endothelial cells (EC), more platelets adhering to naked IEL and more regenerating EC were observed in Group 2. The NI values of samples taken at 1, 2, 3 d after the IR were respectively 0.92plus minus0.08, 0.88plus minus0.03 and 0.41plus minus0.02 in Group 1, and reduced to 0.52plus minus0.05, 0.19plus minus0.08 and 0.06plus minus0.01 in Grou p 2 (P<0.05-0.01). In Group 3, the endothelium da mage was not alleviated, and so were the NI. The Ce-H(2)O(2) particles deposite d on the lumen surface of endothelium were much less in Group 2 than in Groups 1 and 3. CONCLUSIONS: L-arginine promotes the repair process of IR-in jured endothelium probably through the removal of oxygen free radicals by NO.
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PMID:L-arginine promotes the repair process of endothelium in ischemia-reperfused arteries of rats. 1187 60


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