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PubMedDate not supplied

Inhibition by intraventricular microinfusion of ketanserin of the cardiovascular responses to peripheral administration of methoxamine in rats.

The cardiovascular responses induced by intracerebroventricular or intravenous administration of ketanserin in normotensive rats were evaluated. Ketanserin, which is an antagonist at 5-HT2 receptors, when microinfused into the third cerebral ventricle, did not induce significant cardiovascular effects, except for a slight and transitory hypotensive response after the microinfusion of the highest dose (200 micrograms). However, at doses which were unable to affect directly blood pressure or heart rate, ketanserin, microinfused into the same site, antagonized the pressor response induced by peripheral administration of methoxamine, an alpha 1-adrenoceptor agonist. Furthermore, peripheral administration of ketanserin produced dose-dependent hypotension and bradycardia and antagonized the pressor effect of an intravenous bolus injection of methoxamine. In conclusion, the present experiments confirmed the ability of ketanserin to produce cardiovascular effects when administered peripherally and provides evidence for an involvement of ketanserin-sensitive receptors in the brain in the regulation of phasic responses during experimentally induced hypertension.

Animals↗

PubMed1996

Autonomic dysfunction and peripheral vasodilatory response in diabetes.

Twenty three diabetes mellitus patients were investigated for peripheral vasodilatory response in relation to degree of autonomic dysfunction. The non-insulin dependent diabetes mellitus (NIDDM) patients had significant degree of autonomic dysfunction. Based on standard scoring system for evaluating autonomic dysfunction, diabetics were divided into 'borderline' (n = 12) and 'severe' (n = 11) diabetic autonomic neuropathy (DAN) groups. The severe DAN patients showed significantly lower pressor response when compared to borderline DAN patients. Severe DAN was also associated with significant peripheral vascular dysfunction. The severe DAN patients largely had no clinical manifestation of peripheral vascular dysfunction. Thus, at subclinical level patients with significant autonomic dysfunction do exhibit peripheral vascular dysfunction.

Adult↗

PubMed2005

[Effects of protein tyrosine kinase within the brainstem nucleus tractus solitarius on the ventilatory responses of peripheral chemoreflex].

The aim of the present study was to observe whether protein tyrosine kinase (PTK) within the nucleus tractus solitarius (NTS) was involved in the regulation of ventilatory responses of peripheral chemoreflex. The experiments were performed on anesthetized, immobilized and artificially ventilated rabbits. Peripheral chemoreflex was elicited by ventilating the animal with 10% O2-balance 90% N2. Changes in the peak amplitude and frequency of integrated phrenic nerve activity were observed. The ventilatory responses of peripheral chemoreflex following 0.1 microl microinjection within the NTS of either PTK inhibitor genistein (10 mol/L), AMPA glutamate receptor inhibitor CNQX (10 mol/L),or inactive PTK inhibitor daidzein (10 mol/L) were recorded. The results are as follows: Both genistein and CNQX attenuated the ventilatory responses of peripheral chemoreflex, while no changes occurred following daidzein. The amplitude of integrated phrenic nerve discharge and the phrenic burst frequency were decreased by (-21.77+/-6.93)% and (-24.70+/-7.61)% respectively after administration of genistein. CNQX resulted in similar decreases in the amplitude of phrenic nerve discharge (-27.13+/-7.63)% and the burst frequency (-21.34+/-4.88)%. In addition, the inhibitory effects of CNQX and genistein were the same whether they were applied alone or one after another, indicating that they had no cooperative effects. The results obtained suggest that PTK within the NTS regulates the peripheral chemoreflex control of respiration and that this regulation of PTK may be mediated through the phosphorylation of AMPA receptors in NTS neurons.

Animals↗

PubMed1995

Cortico-cortical mediation of short-latency (lemniscal) sensory input to the motor cortex in deeply pentobarbitone anaesthetized cats.

In pentobarbitone-anaesthetized cats, responses were recorded as surface positive potentials in the motor cortex on forelimb and brachium conjunctivum stimulation. In such a preparation, the forelimb nerve responses are mediated via the spino-cervical tract and the dorsal column-lemniscal pathway. Lesions of the sensory cortex (sparing only the depth of the coronary sulcus) abolished or reduced short-latency peripheral responses, in the motor cortex, on both skin and muscle nerve stimulation to less than 10% of control, while brachium conjunctivum responses were unchanged. Lesions of the second somatosensory area alone reduced the motor cortex responses on peripheral nerve stimulation by 10-20%. When the sensory cortex was inactivated by spreading depression, peripheral responses in the motor cortex were abolished before the spreading depression reached the recording point, as judged from the brachium conjunctivum response. The depth distribution of positive and negative field potentials, constituting the early components of a peripheral response in the motor cortex, closely resembled that of a cortico-cortical response evoked on stimulation in area 3. It differed from that of thalamo-cortical response evoked on brachium conjunctivum stimulation. These data suggest that most, if not all, sensory input through the dorsal column and spino-cervical tract to the motor cortex is mediated via the sensory cortex.

Anesthesia↗

PubMed1988

Canine peripheral vascular response to endotoxin shock at a constant cardiac output.

The peripheral vascular response to Escherichia coli endotoxin (1 mg/kg/i.v.) was measured for 2 hr in the pentobarbital anesthetized dog. Total venous return was collected and returned by a pump to the right atrium to maintain a constant cardiac output. Occlusion of the venous lines permitted estimation of venous compliance in the systems drained by the superior (SVC) and inferior vena cavae (IVC). After endotoxin administration, arterial pressure and total peripheral resistance rapidly dropped and remained low for 2 hr. IVC compliance was decreased at 10-30 min and SVC compliance at 10 min after endotoxin. The decrease in compliance is interpreted as venous dilation and probably venous pooling. The latter may account for a substantial portion of the total venous pooling reported in early endotoxin shock. After 30 min, compliance increased and by 60 min was equal to control. Left ventricular relaxation ability decreased as indicated by maximal negative dp/dt. Ibuprofen, 10 mg/kg, was administered at 120 min or earlier, depending on the state of the animal; rapid recovery of arterial pressure and ventricular function occurred without a significant change in venous compliance.

Animals↗

PubMed1979

Genetic differences in the mitogenic response of peripheral blood lymphocytes in the chicken.

The mitogenic responses of chicken peripheral blood lymphocytes were compared in two partially inbred chicken lines and in their hybrids. The lymphocytes of line P chickens showed a higher phytohaemagglutinin (PHA) response than those of line V chickens and (P X V)F1 hybrids. The Con A responses were of the same magnitude in all chicken lines. The higher PHA response in line P chickens was not sex-linked, apparently was not associated with the major histocompatibility complex and it did not correlate with immunoglobulin G allotypes.

Animals↗

PubMed2005

Plasma hyperosmolality augments peripheral vascular response to baroreceptor unloading during heat stress.

The aim of this study was to elucidate the interactive effect of central hypovolemia and plasma hyperosmolality on regulation of peripheral vascular response and AVP secretion during heat stress. Seven male subjects were infused with either isotonic (0.9%; NOSM) or hypertonic (3.0%; HOSM) NaCl solution and then heated by perfusing 42 degrees C (heat stress; HT) or 34.5 degrees C water (normothermia; NT) through water perfusion suits. Sixty minutes later, subjects were exposed to progressive lower body negative pressure (LBNP) to -40 mmHg. Plasma osmolality (P(osmol)) increased by approximately 11 mosmol/kgH(2)O in HOSM conditions. The increase in esophageal temperature before LBNP was much larger in HT-HOSM (0.90 +/- 0.09 degrees C) than in HT-NOSM (0.30 +/- 0.07 degrees C) (P < 0.01) because of osmotic inhibition of thermoregulation. During LBNP, mean arterial pressure was well maintained, and changes in thoracic impedance and stroke volume were similar in all conditions. Forearm vascular conductance (FVC) before application of LBNP was higher in HT than in NT conditions (P < 0.001) and was not influenced by P(osmol) within the thermal conditions. The reduction in FVC at -40 mmHg in HT-HOSM (-9.99 +/- 0.96 units; 58.8 +/- 4.1%) was significantly larger than in HT-NOSM (-6.02 +/- 1.23 units; 44.7 +/- 8.1%) (P < 0.05), whereas the FVC response was not different between NT-NOSM and NT-HOSM. Plasma AVP response to LBNP did not interact with P(osmol) in either NT or HT conditions. These data indicate that there apparently exists an interactive effect of P(osmol) and central hypovolemia on the peripheral vascular response during heat stress, or peripheral vasodilated conditions, but not in normothermia.

Adult↗

PubMed1989

Phytohaemagglutinin responsiveness of peripheral lymphocytes and survival in patients with primary breast cancer.

The response of peripheral blood lymphocytes from 153 breast cancer patients to the T-cell mitogen phytohaemagglutinin (PHA) was measured prior to surgery and patients assigned to either high (Hi/PHA) or low (Lo/PHA) PHA response groups. Patients were followed up for between 8 and 12 years, or until death. Clinical characteristics were similar in Hi/PHA and Lo/PHA groups. In the 96 patients who received no postoperative adjuvant therapy, overall and relapse-free survival was significantly longer in Hi/PHA than in Lo/PHA patients (p less than 0.005, and p less than 0.025 respectively); relative risk of death within 12 years was 0.52 and of relapse was 0.64. In 47 patients who were treated with radiotherapy postoperatively, there was no correlation between the PHA response and overall or relapse-free survival. The implications of these findings for the selection of breast cancer patients for adjuvant treatment following surgery are discussed.

Adult↗

PubMed1993

Effect of a specific platelet-activating factor antagonist on cardiovascular and peripheral cellular responses to colonic ischemia and reperfusion in anesthetized ponies.

The role of platelet-activating factor in mediating the cardiovascular and peripheral cellular responses to large-colon ischemia and reperfusion, was explored in anesthetized ponies. A specific platelet-activating factor (PAF) antagonist (WEB 2086) was administered to a group of 6 ponies, and another 6 ponies (controls) were given an equivalent volume of saline solution, prior to 1 hour of large-colon torsion. After correction of the torsion, ponies were monitored during the reperfusion period. Significant (P < 0.05) hypotension and metabolic acidosis developed in all ponies after correction of colonic torsion, cardiac index increased initially, but then decreased significantly (P < 0.05) over the study period. Mean times between correction of torsion and onset of cardiac failure and death were not different between groups. Significant (P < 0.05) thrombocytopenia developed during the reperfusion period in control ponies, but not in WEB-treated ponies. Blood leukocyte concentration in control ponies was more variable and significantly (P < 0.05) decreased immediately upon reperfusion, compared with that in WEB-treated ponies. We conclude that although the cardiovascular responses to colonic ischemia and reperfusion are not prevented by use of a specific PAF-antagonist, specific peripheral cellular responses are mediated by PAF.

Analysis of Variance↗

PubMed1989

Cerebral and peripheral circulatory responses to intracranial hypertension in fetal sheep.

Fetal head compression during normal labor can increase intracranial pressure (ICP). We studied the cerebral and peripheral blood flow responses to ICP elevation in utero in chronically catheterized fetal sheep using the radiolabeled microsphere technique. ICP was elevated, stepwise, in increments of 6 +/- 1 mm Hg by infusion of artificial cerebrospinal fluid into a lateral ventricle. When ICP was raised to within 28 mm Hg of baseline mean arterial blood pressure (i.e., ICP above 22 mm Hg), arterial pressure began to increase. Above this ICP level, up to 41 mm Hg, mean cerebral perfusion pressure was maintained by equivalent increases in arterial pressure. Cerebral blood flow and O2 uptake at the highest ICP levels were not different from baseline values. Changes in peripheral organ blood flow were graded according to the level of ICP. At the highest level (ICP = 41 mm Hg), renal, gastrointestinal, and skin blood flow decreased by 68%, 69%, and 65%, respectively. Myocardial and adrenal blood flow doubled, whereas heart rate and cardiac output were unchanged. Placental blood flow increased in proportion to arterial pressure. Arterial plasma epinephrine, norepinephrine and arginine vasopressin increased by nearly two orders of magnitude. Therefore, as ICP approaches baseline mean arterial pressure, fetal lambs are capable of sustaining cerebral perfusion by initiating profound visceral vasoconstriction without curtailing placental blood flow. Since cerebral O2 uptake was maintained, there is no evidence that stimulation of the peripheral response requires pronounced cerebral ischemia. This highly developed Cushing response may be important for ensuring cerebral viability when the fetal head is compressed during parturition.

Animals↗

PubMed1997

Local cytokine induction by LPS in the rat air pouch and its relationship to the febrile response.

Peripheral induction of cytokines is a critical event in the induction of febrile responses. The sequence of induction and site of action of these cytokines, however, remain unclear. The objective of the present study was to investigate the kinetics of local and systemic production of interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF), with the aim of identifying the relationship between these cytokines and the febrile response induced by injection of lipopolysaccharide (LPS) into a subcutaneous air pouch in the rat. Intrapouch injection of LPS induced dose-dependent fevers and increases in the concentration of bioactive IL-6 in the plasma. Further studies using 100 microg/kg LPS demonstrated significant increases in local (air pouch) concentrations of bioactive IL-1, TNF and IL-6, and circulating IL-6. No significant increases in TNF or IL-1 were detected in the plasma of the same animals. Local TNF was induced rapidly and peaked 1 h after LPS injection. The kinetics of local IL-1 and IL-6 induction were similar and both peaked after 3 h. The rise in local IL-6 preceded that of plasma IL-6 and reached a peak concentration that was 25-fold higher than that observed in the plasma. The data indicate that IL-1 and TNF act locally at the site of inflammation and that locally induced IL-6 is the important systemic mediator of the response.

Animals↗

PubMed1988

Identification of an intestinal immune response using peripheral blood lymphocytes.

The intestinal immune response of volunteers given the oral vaccine Salmonella typhi Ty21a was assessed with a new immunoassay which measures specific antibody secretion by peripheral blood lymphocytes (PBL). Peak IgA, IgG, and IgM production by PBL occurred on day 7 after the start of vaccination. Peak antibody secretion by PBL occurred several days earlier than the serum antibody peak. All volunteers showed a specific PBL antibody response, but serum or intestinal immune responses, when demonstrable, were highly variable. Peak PBL IgA antibody response correlated with degree of rise in IgA antibody in serum (p = 0.00098) and the intestinal fluid (p = 0.0024). The assay is a useful means of measuring humoral immune response at a mucosal surface after local administration of antigen.

Adult↗

PubMed2001

Analysis of the peripheral immune response in patients with neurocysticercosis: evidence for T cell reactivity to parasite glycoprotein and vesicular fluid antigens.

In neurocysticercosis (NCC), it is thought that the long-term survival of the parasite within the human brain is due in part to the ability of the cestode to suppress the local immune response. When the parasite dies, the immunosuppression is apparently lost and a strong local inflammatory response then develops. In contrast, little is known about the immunologic response that may occur in the peripheral immune system of these patients. In this study, the status of the peripheral (extracerebral) cellular and humoral response was evaluated in patients with a history of NCC. The in vitro proliferation of peripheral blood mononuclear cells to mitogens and foreign antigens was similar in patients and controls. Importantly, a substantive response was elicited by two Taenia solium metacestode antigens. In addition, 8 of 10 patients had a detectable humoral response to the antigenic glycoproteins of the cestode. Considering both the cellular and humoral response, all of the patients with NCC presented an active peripheral immunity.

Adult↗

PubMed2003

Failure of activation of spinal motoneurones after muscle fatigue in healthy subjects studied by transcranial magnetic stimulation.

During a sustained maximal effort a progressive decline in the ability to drive motoneurones (MNs) develops. We used the recently developed triple stimulation technique (TST) to study corticospinal conduction after fatiguing exercise in healthy subjects. This method employs a collision technique to estimate the proportion of motor units activated by a transcranial magnetic stimulus. Following a sustained contraction of the abductor digiti minimi muscle at 50 % maximal force maintained to exhaustion there was an immediate reduction of the TST response from > 95 % to about 60 %. This effect recovered to control levels within 1 min and implies that a decreased number of spinal MNs were excited. Additional TST experiments after maximal and submaximal efforts showed that the decrease in size of the TST response was related to duration and strength of exercise. Motor evoked potentials (MEPs) after conventional transcranial magnetic stimulation (TMS) and responses to peripheral nerve stimulation were recorded following the same fatigue protocol. The size of both the MEPs and the peripheral responses increased after the contraction and were in direct contrast to the decrease in size of the TST response. This points to increased probability of repetitive spinal MN activation during fatigue even if some MNs in the pool failed to discharge. Silent period duration following cortical stimulation lengthened by an average of 55 ms after the contraction and recovered within a time course similar to that of the TST response depression. Overall, the results suggest that the outflow from the motor cortex could become insufficient to drive all spinal MNs to discharge when the muscle is fatigued and that complex interactions between failure of activation and compensatory mechanisms to maintain motor unit activation occur during sustained voluntary activity. When inability to maintain force occurs during submaximal effort, failure of activation of motor units is predominant.

Adult↗

PubMed1982

Human alveolar macrophages suppress the proliferative response of peripheral blood lymphocytes.

Human alveolar cells were isolated from bronchopulmonary lavage fluids obtained from patients undergoing clinically indicated bronchoscopy. Alveolar cells strongly suppressed the proliferation of peripheral blood lymphocytes in response to mitogens and antigens. Separation of the alveolar cells into adherent and nonadherent fractions indicated that the suppression was mediated by the adherent cells, or alveolar macrophages. Indomethacin at least partially relieved suppression, suggesting the involvement of prostaglandin synthesis. The suppression could be duplicated by supernatants obtained from unstimulated cultures of alveolar cells. Some specificity of suppression was apparent, in that not all proliferating cells were suppressed. T lymphocytes may be more readily suppressed than B lymphocytes, and the most susceptible cells may be a subpopulation of T lymphocytes.

Cell Adhesion↗

PubMed2003

An early and sustained peripheral inflammatory response in acute ischaemic stroke: relationships with infection and atherosclerosis.

Central nervous system and peripheral inflammation is important in the responses to ischaemic stroke, and may also predispose to its development. We aimed to identify (1) the extent to which a peripheral inflammatory response is activated in patients following acute stroke, and (2) whether there was evidence for preexisting peripheral inflammation. Thirty-six patients with ischaemic stroke within 12 h of onset of symptoms had serial blood samples taken up to 12 months for analysis of markers of inflammation. Thirty-six control subjects, individually matched for age, sex and degree of atherosclerosis, were also studied. Median C-reactive protein (CRP) was elevated, relative to controls (2.08 mg/l), from admission (4.31 mg/l) (p</=0.001) until 3 months (2.90 mg/l) (p</=0.01), the greatest elevation occurring at 5-7 days (17.67 mg/l) (p</=0.001). Elevations were also seen in erythrocyte sedimentation rate (ESR) and white blood cell (WBC) count until 3 months. Median plasma IL-6 was also elevated, relative to controls (9 pg/ml), by 24 h after onset of symptoms (22 pg/ml) (p</=0.01), and remained elevated at 5-7 days (23 pg/ml) (p</=0.01), but not at 3 months. Less marked elevations in these markers were seen in patients without evidence of infection except for IL-6, which was not increased in the absence of infection. These data provide evidence of an early and sustained peripheral inflammatory response to acute ischaemic stroke in patients with or without evidence of infection. The very early increase in concentrations of inflammatory markers after stroke may either be induced by stroke itself, or may indicate a preexisting inflammatory condition in stroke patients which may contribute to the development of stroke.

Acute Disease↗

PubMed1993

Reduced responses of peripheral blood lymphocytes to heat-denatured food antigens in food-sensitive atopic dermatitis.

Although some patients with food-sensitive atopic dermatitis exhibit allergic symptoms to certain raw foods, they do not exhibit or scarcely exhibit allergic symptoms to boiled or cooked foods. In this study, although peripheral blood mononuclear cells responded to raw food antigens (ovalbumin or bovine serum albumin), the proliferative responses of peripheral blood mononuclear cells were reduced in heat-denatured food antigen-stimulation, in the hen egg- or cow milk-sensitive patients with atopic dermatitis who did not exhibit or scarcely exhibited allergic symptoms to the boiled or cooked foods although the patients exhibited allergic symptoms to the raw foods. Our results show that proliferative responses of peripheral blood mononuclear cells to heat-denatured food antigens are good parameters for diet counseling in food hypersensitivity.

Antigens↗

PubMed1988

Cardiac and peripheral circulatory responses to angiotension and vasopressin in dogs.

To determine the cardiac and peripheral circulatory responses to changes in afterload with angiotension and vasopressin, we increased mean aortic pressure 25% and 50% above control in splenectomized and ganglion-blocked dogs. We compared these responses to similar mechanical increases in aortic pressure produced by partial balloon occlusion of the descending aorta. With 25% or 50% increases in aortic pressure, angiotensin, vasopressin, and balloon inflation produced no changes in heart rate, right atrial, and mean pulmonary artery pressures. At 25% increase in aortic pressure, cardiac output was maintained with angiotensin and balloon occlusion but decreased with vasopressin. At 50% increase in aortic pressure, cardiac output was maintained with only balloon occlusion and decreased with both angiotensin and vasopressin. Whenever cardiac output fell, central blood volume did not increase as after-load increased. These changes in preload can be explained by alterations in the venous circulation. Vasopressin did not alter venous compliance or unstressed vascular volume but increased resistance to venous return. Angiotensin also increased resistance to venous return but decreased venous compliance and did not change unstressed vascular volume. Balloon occlusion had no effects on these parameters. We conclude that: (a) angiotensin caused significant venoconstriction resulting in maintenance of cardiac output at 25% but not 50% increase in aortic pressure; (b) vasopressin increased the resistance to venous return without venoconstriction; this resulted in a fall in cardiac output even with a 25% increase in aortic pressure; and (c) the effects of the agents on the venous circulation were independent of the mechanical effects of a pressure increase in the arterial circulation.

Angiotensin II↗