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Biomedical subjects

T Bennett

Publications and source records attributed to T Bennett.

At least 325 records · Page 18Linked to original sources
PubMed1982

Comparison of the effects of chronic chloroquine treatment and denervation on noradrenergic mechanisms.

Nine or 52 day old chicks were treated with daily intraperitoneal of 75 mg/kg chloroquine diphosphate for 14 days. The response of the sympathetically innervated expansor secundariorum muscle to electrical stimulation or to noradrenaline were then measured in vitro. Noradrenergic nerves were examined by fluorescence histochemistry. The main effect observed 30-90 min after the last dose of chloroquine was supersensitivity to exogenous noradrenaline. This was no longer detectable from expansor muscles taken 18-24 h after the last dose of chloroquine. However, noradrenergic nerves in tissues from chronically treated chicks taken 18-24 h after the last dose of chloroquine were less fluorescent than those from control animals. Chronic chloroquine treatment reduced the body weight of chicks. There was also a reduction in the weight of the expansor muscle, due to a reduction in both muscle mass and water content. Surgical denervation increased the weight of the expansor muscle by increasing its muscle mass and abolished the fluorescence of its noradrenergic nerves 3 days after surgery. The denervated expansor muscle responded very weakly to electrical stimulation and its supersensitivity to noradrenaline was maximal 3-5 days after surgery. The denervated expansor muscle developed a lower maximum response to noradrenaline.

Aging↗
PubMed1982

The effects of chronic chloroquine administration in growing chicks.

The effects of chronic administration of graded doses of chloroquine diphosphate, given by daily intraperitoneal injections for up to 52 days, have been examined using chicks. Some of the factors contributing to the observed effects were investigated. Chloroquine depressed the increase in body weight of growing chicks in a dose-related fashion and reduced the body weight of adult fowl, possibly as a result of reducing food and water intakes. Stunting (as assessed from femur length and circumferential growth) following chronic chloroquine administration was found to be dose-dependent. Chloroquine reduced the dry mass and water content of most muscle types and organs examined especially skeletal muscle, smooth muscle and the spleen. However, there was an increase in the wet and dry mass of the adrenal glands, but only with the lowest dose regimen (30 mg/kg daily for 52 days). Chronic chloroquine treatment reduced the size and the number of smooth muscle cells per bundle in the expansor secundariorum. It also caused bleaching of black feathers and reddening of white feathers.

Animals↗
PubMed1982

Comparison of the effects of chloroquine quinacrine and quinidine on autonomic neuroeffector mechanisms.

The in vitro effects of 3 antimalarial compounds (chloroquine, quinacrine and quinidine) on 3 components of the autonomic nervous system have been investigated. The expansor secundariorum muscle was used for studying noradrenergic mechanisms, the chick oesophagus for cholinergic mechanisms, the rat bladder for "purinergic" mechanisms, and the mouse ileum for prostaglandin-mediated responses. Chloroquine reduced responses to noradrenergic and "purinergic" nerve stimulation to similar extents, possibly due to a non-specific effect; it induced supersensitivity to exogenous noradrenaline. Both chloroquine and quinacrine had atropine-like actions in concentrations up to 1 X 10(-4)M; larger concentrations had a direct depressant action on smooth muscle. Quinacrine blocked noradrenergic nerves in a similar fashion to guanethidine but failed to induce supersensitivity to exogenous noradrenaline; it was a potent antagonist of the responses to "purinergic" nerve stimulation. Quinidine blocked responses to "purinergic" nerve stimulation, caused moderate antagonism of alpha-adrenoceptor-mediated effects, but was a weak muscarinic receptor antagonist. The antimalarial compounds were more potent antagonists of prostaglandin-mediated responses than of "purinergic" responses. However, not all their actions could be attributed to prostaglandin antagonism.

Animals↗
PubMed1981

Hypoglycaemia, hypothermia and shivering in man.

1. The present experiments were designed to elucidate the reasons for the fall in central body temperature during hypoglycaemia. 2. The first experiment was carried out at a room temperature of 25 degrees C on 11 male subjects. Hypoglycaemia was induced by infusion of insulin. Heat production (calculated from respiratory gas exchange) rose from a baseline of 5.10 +/- 0.13 kJ/min (mean +/- SEM) to a peak of 6.25 +/- 0.21 kJ/min (P less than 0.001), but core temperature fell concurrently by 0.51 +/- 0.08 degrees C and skin temperature fell by 1.1 +/- 0.2 degrees C. The net heat loss was due to peripheral vasodilatation and sweating. 3. To determine the effect of insulin-induced hypoglycaemia on thermoregulation in a cool environment, the experiment was repeated at a room temperature of 18-19 degrees C on five of the subjects who had air blown over them until shivering was sustained. During this time heat production rose to 10.13 +/- 1.67 kJ/min, but core temperature remained constant. Shivering stopped as plasma glucose fell below 2.5 mmol/l during insulin infusion and the subjects said they no longer felt cold. 4. During hypoglycaemia in the cold peripheral vasodilatation and sweating occurred, skin temperature fell by up to 0.8 degrees C and core temperature fell below 35 degrees C, so subjects had to be rewarmed. 5. Recovery of plasma glucose after hypoglycaemia in the cold was impaired at low body temperatures, but shivering was restored within seconds when glucose was given intravenously.

Adult↗
PubMed1981

Effect of adrenalectomy on the development of isolation-induced hypertension in rats.

1. Male Wistar rats develop systolic arterial hypertension when housed in glass metabolism cages. The present experiments were designed to investigate the involvement of the adrenal glands in this form of hypertension. 2. Rats were bilaterally adrenalectomized and maintained by either salt supplementation (1% sodium chloride solution instead of tap water to drink) or steroid replacement (corticosterone solution in the drinking water). 3. Adrenalectomized rats treated as above did not develop hypertension in response to isolation, whereas sham-operated rats (drinking either 1% saline or tap water) did. 4. Hypertension in the sham-operated rats was not accompanied by a renal retention of sodium and water. 5. It is concluded that increased adrenal activity is involved in the development of isolation-induced hypertension, but not by causing a fluid retention and hence volume expansion. The relative contributions of adrenal medullary and cortical activity remain to be determined.

Adrenal Glands↗
PubMed1981

Trend in vasectomy acceptance: 1974-1981.

It is often heard in Thai population seminars and workshops that Thai men are resistent to vasectomy. There are claims that due to traditional fears of vasectomy or an unwillingness to play a role in family planning most Thai men will not accept vasectomy services even if they are offered nearby. This assumption may be wrong. The Research and Evaluation Unit of the Family Health Division has graphed a new acceptance of vasectomy by month service January, 1974-June, 1981. The graph also plots important events that should be related to vasectomy acceptance. Indeed it appears that when extra effort is made, such as a demonstration mobile team, private sector reimbursement, short-term campaigns and the deployment of mobile teams, willing and waiting acceptors are there. The fact that "extra effort" is required with vasectomy is probably more the result of a general reluctance to undergo the procedure than rather fear or hard-core resistance.

Asia↗
PubMed1980

Cardiovascular responses to graded reductions of central blood volume in normal subjects and in patients with diabetes mellitus.

1. Cardiovascular responses to graded increments of lower body negative pressure were studied in non-diabetic subjects and in patients with diabetes mellitus. 2. in all subjects, low levels of negative pressure (which did not affect significantly systemic arterial pressure) induced forearm vasoconstriction, suggesting normal function of the 'low pressure' cardiopulmonary baroreflex. However, in some diabetic patients the response to higher levels of negative pressure was abnormal, and it seems likely that although afferent mechanisms were intact there was impairment of efferent vasoconstrictor function. 3. Changes in R--R interval were linearly related to changes in systolic blood pressure induced by higher levels of negative pressure. The slope of the relationship was taken as the sensitivity of the 'high pressure' arterial baroreflex; diabetic patients showed a reduced sensitivity compared with normal subjects. Furthermore, in diabetic patients, abnormalities of R--R interval control were more common than abnormalities of vasoconstrictor function, suggesting that heart-rate control is impaired earlier than vasomotor function in diabetic autonomic neuropathy.

Adult↗
PubMed1980

Cardiovascular reflexes in patients after myocardial infarction. Effect of long-term treatment with beta-adrenoceptor antagonists.

A double-blind study was made of men who had had a myocardial infarction at least one year previously, and who were being treated with propranolol, atenolol, or placebo. They were compared with age- and sex-matched control subjects. Under resting conditions, there were no differences between the systemic arterial blood pressures, forearm blood flows, or heart rates of the control subjects and the post-infarction patients treated with placebo. The patients, however, showed signs of reduced sympathetic effects on the cardiovascular system when their reflex responses to the Valsalva manoeuvre, lower body negative pressure, and performance of a mental task were assessed. Long-term treatment with propranolol or artenolol had little effect on resting systemic arterial blood pressure or forearm blood flow, but caused a significant reduction in resting heart rate. Differences in the reflex responses of these patients and those on placebo were attributable to the effects of the beta-adrenoceptor antagonists on resting heart rate. These results indicate that post-infarction patients do not have signs of overactivity of autonomic nervous control of the cardiovascular system. Furthermore, long-term treatment of such patients with beta-adrenoceptor antagonists does not impair cardiovascular reflexes.

Adrenergic beta-Antagonists↗
PubMed1980

Systemic arterial hypertension in rats exposed to short-term isolation; intra-arterial systolic and diastolic blood pressure and baroreflex sensitivity.

A system is described for accurately recording systolic and diastolic blood pressure in conscious, unrestrained rats. The system consists of a portion of flexible intra-arterial catheter joined to a length of rigid plastic tubing which is connected to a transducer via a stainless steel needle and tap. The whole system is filled with degassed saline. Traces obtained on a recording oscilloscope indicate that this system gives a flat response to 35 Hz. With this system we have shown that systolic and diastolic blood pressures are significantly greater in rats which have been isolated for 15--20 days than in group-housed animals, both in the anaesthetized and conscious state. Measurements were made of the pulse-interval response to an increase in systolic blood pressure induced by either a bolus injection or a slow infusion of a vasoconstrictor drug as a means of assessing baroreflex sensitivity. There was a significant reduction of the baroreflex sensitivity of isolated rats compared to grouphoused animals. The present findings indicate that the elevation in blood pressure seen in isolated rats is not a transient response to the stress of the indirect measurement techniques used in previous studies.

Animals↗
PubMed1979

Cardiovascular responses to lower body negative pressure in normal subjects and in patients with diabetes mellitus.

The cardiovascular responses of non-diabetic and diabetic subjects to lower body negative pressure at 1.3, 2.7, and 5.3 kPa (10, 20, and 40 mmHg) were measured. The diabetics fell into two groups--those showing little change in systolic blood pressure with lower body negative pressure at 5.3 kPa (40 mmHg) and those showing falls greater than 2.7 kPa (20 mmHg). The patterns of response in the former group of diabetics and in the non-diabetics were similar. The diabetics who showed a fall in systolic blood pressure with lower body negative pressure nonetheless responded with a forearm vasoconstriction indicating that the vasomotor dysfunction was localised to some other vascular bed. In one subject forearm vasodilatation occurred with lower body negative pressure at 5.3 kPa (40 mmHg) although his response to milder levels of lower body negative pressure appeared normal. It is suggested that the integrity of vasomotor reflexes is most reliably tested by exposure to stepped increases in lower body negative pressure.

Adolescent↗
PubMed1979

Prevention and reversal of isolation-induced systolic arterial hypertension in rats by treatment with beta-adrenoceptor antagonists.

1. Rats were made hypertensive by 5 days of continuous isolation in glass metabolic cages; in the text "hypertensive" means having a systolic blood pressure greater than 145 mmHg. 2. Daily intraperitoneal injections of either propranolol (5 mg/kg) or atenolol (5 mg/kg) reduced systolic blood pressure within 3 days and the systolic blood pressure remained low provided that the treatment was continued. 3. Treatment with metoprolol also lowered the systolic blood pressure of isolated rats but only when a larger dose (10 mg/kg) was given. 4. Systolic blood pressure returned to hypertensive levels following withdrawal of treatment after 15 days of isolation. However, following cessation of treatment after 27 days of isolation, the systolic blood pressure did not rise. 5. Rats given propranolol in the drinking water (intake equivalent to a daily dose of 5 mg/kg) before and during isolation did not develop hypertension. 6. The possibility that suppression of sympathetic function by the beta-adrenoceptor antagonists was responsible for these changes is discussed.

Adrenergic beta-Antagonists↗
PubMed1979

Vasomotor responses to the Valsalva manoeuvre in normal subjects and in patients with diabetes mellitus.

Cardiovascular responses to the Valsalva manoeuvre were examined in 19 non-diabetic subjects and 32 diabetic patients, some with signs of autonomic dysfunction. All the non-diabetic subjects showed an overshoot in systemic arterial pressure and a bradycardia after the manoeuvre, and in 11 of them only forearm vasoconstriction occurred. However, in eight non-diabetic subjects a forearm vasodilatation was observed at some stage after the Valsalva manoeuvre. Similar patterns of vasomotor responses were seen in some of the diabetic patients. However, those diabetics with postural hypotension showed a systemic arterial hypotension after the Valsalva manoeuvre with no significant change in forearm vascular resistance. Such a response is abnormal but forearm vasodilatation alone may not be.

Adolescent↗
PubMed1979

Fluorescence histochemical and ultrastructural observations on preterminal noradrenergic axons following ligation or treatment with 6-hydroxydopamine.

This study was designed to compare the effects of 6-hydroxydopamine (6-OHDA) treatment with those of mechanical constriction of noradrenergic preterminal fibres in the rat. Constriction produced a progressive accumulation of glyoxylic acid induced fluorescence, attributable to noradrenaline, in nerve trunks proximal to applied ligatures. The electron microscope showed that this accumulation comprised large numbers of granular vesicles in swollen axons. Degenerative changes were also present and the axonal microtubules were distorted or absent. Preterminal fibres also contained accumulated noradrenaline histofluorescence after 6-ODHA (100 mg/kg) treatment, though this accumulation was not as focal as it was after constriction. The ultrastructural appearance of preterminals from 6-OHDA-treated rats closesely resembled that seen proximal to constrictions. Swollen axons were present. These contained many granular vesicles and exhibited degenerative changes. The microtubules were disrupted or absent. It is suggested that 6-OHDA produces accumulation of noradrenaline storage vesicles and other organelles in preterminal fibres because the primary lesion of the terminals presents a barrier to intra-axonal transport of these organelles.

Adrenergic Fibers↗