Failure of gated SPECT and echocardiography to detect large apical aneurysm secondary to hyperdynamic left ventricular wall at the aneurysm neck

We present a patient with a history of coronary artery disease and exertional angina after an acute anterior myocardial infarction. Angiography and ventriculography revealed multivessel coronary artery disease and a large apical aneurysm. Echocardiography and gated SPECT studies were performed for further evaluation of ischemia and assessment of left ventricular function. Gated SPECT and echocardiography failed to detect a large apical aneurysm due to a hyperdynamic left ventricular wall at the neck of the aneurysm. This case demonstrates the importance of using multiple imaging modalities in the evaluation of ventricular function in the setting of coronary artery disease.     

Systolic cessation of the flow in the mid stent segment of the previously stented ostial vein graft with normal flow during diastole. A case report and brief review.

We present a case of intermittent cessation of blood flow through stent struts during systole, with normal flow during diastole in the previously stented ostial vein graft. After reviewing the initial procedure, we discovered that the operator had difficulty in positioning the stent. After stent deployment, the ostial stent was malpositioned and was protruding more than 50% into the aorta. During systole, the contrast in the stent struts, which are situated in the aorta, was being washed off by systolic blood flow, while in the diastole, the flow of contrast was normal. This is the first case report of this observation with a brief review.     

Influences of different adenosine receptor subtypes on catalepsy in mice

The effects of adenosine A₁ and A₂ receptors on catalepsy were studied in mice. The adenosine agonists 5-N-ethylcarboxamide-adenosine (NECA), N⁶-phenylisopropyladenosine (PIA) and N⁶-cyclohexyladenosine (CHA) induced dose dependent catalepsy. The A₁ adenosine antagonist 8-phenyltheophylline (8-PT) potentiated catalepsy induced by NECA, R-PIA and CHA. However, theophylline did not potentiate but inhibited the responses induced by NECA, R-PIA and CHA. Neither 8-PT nor theophylline alone has any effect on catalepsy in mice. It is concluded that catalepsy induced by the adenosine agonists may be due to A₂ receptor stimulation and that the A₁ antagonism may potentiate the response.     

Nicotine-induced purposeless chewing in rats: possible dopamine receptor mediation

Intraperitoneal (i.p.) administration of nicotine to rats induced purposeless chewing. The response induced by different doses of the drug (0.0001, 0.001, 0.01 and 0.1 mg/kg) seems to be dose dependent, with a maximum effect at 0.01 mg/kg and then decreasing at a higher dose (0.1 mg/kg). Pre-treatment of animals with the nicotine antagonist mecamylamine (0.01 and 0.1 mg/kg, 30 min) and the D-2 receptor antagonist sulpiride (12.5-100 mg/kg, 90 min), but not the D-1 antagonist SCH 23390 (0.01 and 0.05 mg/kg, 30 min), decreased the chewing induced by nicotine (0.01 mg/kg). When animals were pre-treated with propranolol (5 and 10 mg/kg) 60 min, reserpine (2.5 mg/kg) 18 h or α-methyl-p-tyrosine (α-MPT; 250 mg/kg) 60 min before nicotine, the effect of the drug was reduced. However, reserpine (2.5 mg/kg) at 18 h plus α-MPT (250 mg/kg) 60 min prior to nicotine completely inhibited the drug response. Pre-treatment of animals with phenoxybenzamine (2.5 and 5 mg/kg i.p., 60 min) or atropine (5 and 10 mg/kg) did not change the nicotine response significantly. It is concluded that nicotine- induced purposeless chewing is mediated through dopaminergic and nicotinic mechanisms.     

Nicotine-induced hypothermia through an indirect dopaminergic mechanism

The effect of nicotine on core body temperature was studied in mice. Intraperitoneal (i.p.) injection of nicotine (0.5, 1 and 2 mg/kg) induced a dose-dependent hypothermia. The response was inhibited by reserpine (5 mg/kg), the centrally active nicotinic receptor antagonist mecamylamine (0.1-1 mg/kg) and the D-2 dopamine receptor antagonist sulpiride (25-100 mg/kg). The β-adrenoceptor antagonist propranolol (5 and 10 mg/kg) and the serotonergic blocker methysergide (5 and 10 mg/kg) did not inhibit but increased the nicotine response. The α-adrenoceptor antagonist phenoxybenzamine, the antimuscarinic agent atropine, the D-1 dopamine receptor antagonist SCH 23390, the peripheral dopamine antagonist domperidone and the peripheral nicotinic antagonist hexamethonium did not alter the nicotine-induced hypothermia. It is concluded that nicotine may cause a fall in core body temperature through a central dopaminergic mechanism.     

Effects of GABAergic system on naloxone-induced jumping in morphine-dependent mice.

The effect of GABA (gamma-aminobutyric acid system) receptor agonists and antagonists on naloxone-induced jumping in morphine-dependent mice was examined. Intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) injection of different doses of the GABA(B) receptor agonist, baclofen (2.5, 5 and 10 mg/kg), reduced naloxone-induced jumping in morphine-dependent mice. The i.p. administration of the GABA(B) receptor antagonist, CGP35348 (P-[3-aminopropyl]-p-diethoxymethyl-phosphinic acid), but not the i.c.v. injection of the drug, increased naloxone-induced jumping. The antagonist also decreased the baclofen response. Administration of the GABA(A) receptor agonist, muscimol, but not the GABA(A) receptor antagonists bicuculline and picrotoxin, decreased the naloxone response in morphine-dependent animals. It is concluded that both GABA(A) and GABA(B) receptor subtypes may have an inhibitory influence on naloxone-induced withdrawal jumping in mice.     

Effect of D-1 or D-2 receptor stimulation on memory retrieval in mice

Mice were trained in one-way active avoidance procedure and retention was tested at 4, 8, 16 and 24 h after training of animals and compared with non-shocked or untrained animals. The effect of drugs was tested on retrieval 24 h after training in other groups of mice. High doses of apomorphine or bromocriptine impaired, while low doses of the drugs improved, retrieval of avoidance. High doses of sulpiride reversed the impairment induced by high doses of these dopamine agonists. Low doses of sulpiride antagonized the improvement of retrieval induced by low doses of apomorphine. SKF 38393 treatment of animals also improved the retrieval. The retrieval impairment induced by higher doses of apomorphine or the improvement induced by different doses of SKF 38393 was antagonized by SCH 23390 pre-treatment. Single administration of SCH 23390 or low doses of sulpiride also impaired retrieval. It is concluded that stimulating post-synaptic D-2 dopamine receptors impairs retrieval whilst activation of pre-synaptic D-2 or post-synaptic D-1 receptors improves memory retrieval.     

Does CA1 dopaminergic system play a role in cholestasis induced hypothermia?

ObjectiveThere is some of evidence describing that cholestasis induces hypothermia. Meanwhile, there is paucity of comprehensive data on the mechanism(s) governing this phenomenon. The present study was undertaken to determine the effect of CA1 dopaminergica system on cholestasis induced hypothermia.MethodsMale NMRI mice weighing 25–30 g, were used. Bilateral cannulae were implanted in dorsal hippocampi (CA1) for drug microinjection. Animals were randomly divided into non-operated control, sham-operated and bile duct-ligated (BDL) groups. Cholestasis was induced by means of main bile duct ligation. Body temperatures were measured before, two and four days after BDL.ResultsData indicated that, two and four days post BDL, the body temperature decreases as compared to the sham-operated animals, which indicates hypothermia. Intra-CA1 injection of different doses of sulpiride (SUL; 0.25, 0.5 and 0.75 μg/mouse), SCH23390 (SCH; 0.125, 025 and 0.5 μg/mouse), SKF38393 (SKF; 0.25, 0.5 and 1 μg/mouse) and quinpirole (QUI; 0.25, 05 and 0.75 μg/mouse) exerted no effect on body temperature in non-operated and sham operated mice, by themselves. Moreover, intra-CA1 injection of SUL, QUI or SKF blocked, whereas, SCH tended to increase BDL induced hypothermia.ConclusionsThe present data revealed that the CA1 dopaminergic system is possibly involved in the BDL induced impairment of thermoregulation.     

Intermittent pneumatic compression therapy improves functional and dynamic balance and neuropathy severity in neuropathic patients with type 2 diabetes

Diabetic neuropathy is a common complication of diabetes which increases risk of falling. Reduction in neural blood flow is one proposed theory for this etiology of diabetic neuropathy. Intermittent pneumatic compression (IPC) is a treatment method that increases nutritional supplies for the peripheral nervous system. The current study aims at evaluating the effects of IPC therapy on two aspects of balance dysfunction as one of the most important clinical signs of diabetic neuropathy. This study is a single-blind, randomized, controlled clinical trial that involved 39 patients with diabetic peripheral neuropathy. In this analysis, patients aged 40–75 years (with a mean age of 58.82 years) were randomly divided into intervention (n = 20) and control groups (n = 19). In the first session, all tests of neuropathy severity (using Valk and Michigan diabetic neuropathy questionnaires) and stability (functional and dynamic balance) were performed for both groups. The subjects in intervention group underwent 10 sessions of IPC treatment. At last, balance and neuropathy examinations were carried out in the final session. P < 0.05 was chosen as statistical significance level. Implementation of IPC interventions for 10 sessions significantly decreased APSI and OSI of Biodex balance system in level 6 (P < 0.05). The subjects in intervention group showed significant increases in standing time with their eyes either open or closed by performing functional balance tests. Additionally, Valk and Michigan neuropathy screening scores significantly decreased after 10 sessions of IPC therapy. This study showed that IPC has a positive effect on diabetic neuropathy and balance.