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V S Westerberg

Publications and source records attributed to V S Westerberg.

8 recordsLinked to original sources
PubMed1992

Alcohol measuring scales may influence conclusions about the role of alcohol in human immunodeficiency virus (HIV) risk and progression to acquired immunodeficiency syndrome (AIDS).

In an effort to clarify the role of alcohol in human immunodeficiency virus (HIV) risk and progression to acquired immunodeficiency syndrome (AIDS), the author reviewed the method of measuring alcohol consumption across 10 studies published from 1986 through 1990. When the reports in which the association between alcohol and HIV has been evaluated in at-risk groups are compared, the role of alcohol remains unclear. Although there are fewer reports available for analysis, the role of alcohol in the progression of the disease to AIDS has been consistent in indicating that there is no effect of alcohol use. However, the research in both of these areas has utilized different methods to measure alcohol use. There are data relevant to the association between alcohol and HIV that indicate that the estimate of alcohol use is at least partially dependent on the type of measuring instrument used. The application of different measures of alcohol use may have led to different conclusions regarding the role of alcohol in HIV. With regard to the role of alcohol in the progression of the disease to AIDS, even in the consistent findings that alcohol does not lead to progression of the disease to AIDS, a more sensitive measure of alcohol use might yield different results.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Norepinephrine and brain damage: alpha noradrenergic pharmacology alters functional recovery after cortical trauma.

The goal of these experiments was to evaluate the effects of some drugs affecting noradrenergic (NE) synaptic transmission, commonly prescribed following stroke or traumatic brain injury, on functional recovery. Measurement of recovery from a transient hemiplegia produced by a traumatic unilateral focal contusion in sensorimotor cortex (SMCX) of rats was used to assess the effects of chronic haloperidol (HAL) treatment begun early (1 day) or late (18 days to recovered animals) after injury. Additionally, using the same model, the effects of a single administration of drugs with selective action at NE receptors were also evaluated early or late (30 days) after injury. These drugs were: phenoxybenzamine (PBZ), an alpha 1-NE antagonist; prazosin (PRAZ), an alpha 1-NE antagonist; yohimbine (YOH), an alpha 2-NE antagonist; propranolol (PROP), a beta 1- and 2-NE receptor antagonist; methoxymine (METHOX), an alpha 1-NE agonist; and clonidine (CLON), an alpha 2-NE agonist. The data indicate that drugs with antagonistic effects at alpha 1 NE receptors, including HAL and PRAZ but not PROP, administered early after SMCX contusion retard locomotor recovery. Beneficial effects of enhancing NE transmission by METHOX or YOH were not observed. In animals recovered from beam walk (BW) deficits, a single administration of PBZ or PRAZ (alpha 1 NE antagonists) or CLON (alpha 2 NE agonist) transiently reinstated hemiplegic symptoms. The nonspecific beta NE receptor antagonist PROP had no effect in recovered animals. A single dose of HAL had no effect in recovered animals, but a BW deficit transiently developed in some animals following chronic treatment. The data are discussed with reference to drug contraindications noted in clinical studies of recovery from poststroke aphasia and cognition in demented patients with degenerative brain disease.

Animals↗
PubMed1989

Adenosine analogs inhibit gastric acid secretion.

The potencies with which four adenosine deaminase-resistant analogs of adenosine affected the volume, pH and acid output of basal gastric acid secretions were examined in unanesthetized rats with chronic indwelling gastric cannulas. All four adenosine receptor agonists, R-phenylisopropyladenosine (R-PIA), S-phenylisopropyladenosine (S-PIA), N-ethylcarboxamide adenosine (NECA), and 2-chloroadenosine (CADO) significantly decreased gastric acid output in a dose-dependent manner. The rank order of potency was NECA, R-PIA greater than CADO greater than S-PIA. NECA and R-PIA were approximately equipotent in reducing gastric acid output. The levels of gastric acid output tended to increase at the lowest doses of the agonists. NECA decreased the volume of gastric secretion, whereas R-PIA had no effect on volume, but significantly increased the pH of the secretions. Valid measurements of pH in NECA-treated rats were not always obtainable because of near total inhibition of gastric secretions. S-PIA did not significantly affect volume, but increased pH at the higher doses tested. CADO decreased volume, but did not affect pH. These results indicate that adenosine analogs regulate not only the hydrogen ion concentration, but also the volume of gastric secretions.

2-Chloroadenosine↗
PubMed1989

Mechanisms of general anesthesia: brain regional responses to baclofen.

The GABAB agonist baclofen is reported to produce general anesthesia when administered either centrally into the lateral ventricles of rats or peripherally to mice. Previously we demonstrated that beta-endorphin given intracerebrally produces anesthesia in rats, a response localized to sites in or adjacent to the inferior third and fourth ventricles. In order to compare the anatomical localization of these two anesthetic responses, we administered baclofen into the inferior or superior lateral or third ventricles, the aqueduct, or fourth ventricle in rats. Although 10 micrograms baclofen infusions into several regions caused loss of the righting reflex, in no case did animals exhibit an unconscious state which satisfied strict criteria of anesthesia. Infusions of 20 micrograms into the inferior third and fourth ventricles elicited seizures followed by a postictal depression. Although unresponsive to some stimuli, these animals showed no impairment in the corneal reflex. Since this dose was often lethal, higher doses not tested. Baclofen, given to mice intraperitoneally at doses of 25, 50, or 75 mg/kg, failed to elicit strictly defined anesthesia, although, to varying degrees, animals exhibited analgesia, loss of the righting reflex, and loss of behavioral responses to loud sounds. Animals continued to show motor responses when handled and retained corneal reflexes. Baclofen does not evoke an unconscious anesthetic state when administered centrally or systemically, emphasizing the need for strict criteria to define general anesthesia and to categorize drugs that promote this state.

Anesthesia, General↗
PubMed1987

Central effects of adenosine analogs on stress-induced gastric ulcer formation.

Rats subjected to restraint stress developed gastric lesions that could be reduced by R-phenylisopropyladenosine (R-PIA) administered intracerebroventricularly. This protective effect was reversed by 8-sulfophenyltheophylline given centrally, and by peripherally administered 8-phenyltheophylline. These results suggest that central adenosine receptors mediate the effect. In subsequent studies it was found that if the absolute level of ulcer formation in control rats was low, R-PIA had no ulcer protective effect. Thus, although it appears that adenosine receptors are important in attenuating pathological gastric responses to stress, this attenuation seems to be dependent on the level of ulcer formation in control animals.

Adenosine↗
PubMed1987

Inhibitors of histidine decarboxylase decrease basal gastric acid secretion in the rat.

We examined the ability of two specific inhibitors of histidine decarboxylase, (s)-alpha-fluoromethylhistidine (FMHd) and (s)-alpha-fluoromethylhistamine (FMHm), to inhibit basal gastric acid secretion. The two highest doses of FMHd administered, 50 and 100 mg/kg, decreased basal gastric acid secretion and total secretion volume but did not affect intraluminal pH. FMHm decreased gastric acid secretion, raised intraluminal pH, and to a lesser degree decreased total secretion volume. Neither compound changed the severity of gastric ulcers produced by cold restraint stress.

Animals↗
PubMed1987

Modulation of gastric acid secretion by adenosine in conscious rats.

Basal (nonstimulated) gastric acid output was determined in conscious rats fitted with indwelling gastric cannulae. The adenosine deaminase resistant analog of adenosine, R-phenylisopropyladenosine, elevated intraluminal pH beyond 7.0 and decreased gastric acid secretion when given at doses of 0.10 or 1.0 mg/kg, while S-phenylisopropyladenosine at similar doses did not affect either gastric acid output or pH. The potent adenosine receptor antagonist, 8-phenyltheophylline, given at doses of 0.1, 1.0, and 2.5 mg/kg augmented gastric acid output and, at doses of 0.01, 0.1, 1.0, and 2.5 mg/kg, blocked the acid-reducing effect of R-phenylisopropyladenosine (0.1 mg/kg). These data suggest that adenosine systems may be important regulators of gastric function.

Adenosine↗