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Biomedical subjects

M Petty

Publications and source records attributed to M Petty.

18 recordsLinked to original sources
PubMed1996

Damage control.

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Chemical Industry↗
PubMed1991

Hypothalamic blood flow autoregulation remains unaltered following surgical and pharmacological blockade of central vasopressin.

Experiments were carried out in urethane anaesthetized, ventilated rats to determine if brain arginine-vasopressin (AVP) plays a physiological role in cerebral blood flow autoregulation. Autoregulation was tested by determining local hypothalamic blood flow in the mediobasal hypothalamic area (HBF; H2-gas clearance technique) during consecutive stepwise lowering of systemic mean arterial pressure to 80, 60 and 40 mm Hg, by hemorrhage. Endogenous AVP was blocked by transecting the rostral, lateral and dorsal neuronal connections of the hypothalamus (including the median eminence) from all major brain areas, by bilateral transection of the vasopressin-containing fibres in the hypothalamo-hypophyseal tract to the median eminence at the level of the lateral retrochiasmatic area (RCAL), and finally by intracerebroventricular (i.c.v.) administration of an AVP antagonist, d(CH2)5Tyr(Me)AVP (AAVP). Significant increases of daily water intake indicated impaired vasopressin release following both types of surgical transection. Resting HBF was significantly elevated both after surgical isolation of the hypothalamus and after 10 ng AAVP administration compared to controls. Blood flow autoregulation in the hypothalamic region was seriously impaired following surgical isolation of the hypothalamus. However, HBF autoregulation remained just as effective as that of the control rats following either selective bilateral transection of the vasopressin pathways or following AAVP treatment. The present data indicate that AVP may play a role in the control of resting hypothalamic blood flow, but does not support a role of AVP in HBF autoregulatory mechanisms.

Animals↗
PubMed1991

Clinical validation of a second-generation fructosamine assay.

The serum fructosamine assay, used to monitor short-term clinical glycemic control, reportedly has several technical drawbacks. However, technical improvements have resulted in a new second-generation assay of fructosamine. We evaluated this second-generation assay (from Roche Diagnostics) in 529 nondiabetic and diabetic patients and found a highly significant correlation with results of the first-generation assay (r = 0.91, P less than 0.001). Use of the second-generation assay with samples from patients classified on the basis of glycemic control according to their glycohemoglobin (GHb) values, enabled us to discriminate between the nondiabetics, diabetics with "good/moderate" control (i.e., GHb less than 10%), and diabetics with "poor" control (GHb greater than or equal to 10%). We evaluated the validity of the second-generation assay to assess short-term glycemic control in 23 non-insulin-dependent diabetic patients who participated for 10 weeks in an intensive intervention program designed to rapidly normalize the clinical glycemic profile. Results correlated significantly with the one-week average capillary blood glucose concentration (CBG) and with the three-week average CBG in all 23 patients. In addition, the second-generation fructosamine assay results demonstrated a significant decrease at each week of study, as did the average CBG. Results of the first- and second-generation assays correlated significantly at each week of study. GHb correlated significantly with both the second- (r = 0.78, P less than 0.001) and first-generation fructosamine assay results (r = 0.77, P less than 0.001) for the baseline blood samples of the intervention study, but this correlation decreased (to r = 0.35, P = 0.09 and r = 0.34, P = 0.09, respectively) by the conclusion of the study.

Adult↗
PubMed1985

Differential effects of central angiotensin II and substance P on sympathetic nerve activity in conscious rats. Implications for cardiovascular adaptation to behavioral responses.

The centrally induced effects of angiotensin II and substance P on the cardiovascular system and on neuronal efferent activity of the splanchnic, renal, and adrenal nerves were investigated in chronically instrumented conscious rats. The pressor responses to substance P injected into the lateral brain ventricle were accompanied by marked and short latency increases in heart rate, cardiac output, splanchnic, renal, and adrenal nerve activity, and a rise in plasma noradrenaline and adrenaline. Behaviorally, an arousal-type reaction was observed. In contrast, the pressor responses to intracerebroventricular angiotensin II were associated with initial decreases in heart rate, cardiac output, splanchnic, renal, and adrenal nerve activity, and a fall in plasma noradrenaline at the time of the maximal blood pressure increase. In some but not all animals, a second blood pressure peak associated with increases in heart rate and splanchnic nerve activity was observed after several minutes. Incomplete chronic sinoaortic baroreceptor deafferentiation prevented the angiotensin II-induced fall in heart rate but not the initial fall in splanchnic nerve activity. The decreases in splanchnic nerve activity also occurred in diabetes insipidus rats and persisted in Long Evans rats after vascular vasopressin receptor blockade with d(CH2)5AVP, despite marked reductions of the pressor responses in both groups. Peripheral alpha-adrenoceptor blockade with prazosin or ganglion blockade with hexamethonium inhibited the central angiotensin II pressor responses only in combination with vasopressin receptor blockade. On the other hand, either sympatholytic drug, alone, abolished the pressor responses in the diabetes insipidus rats. This indicates that in intact conscious rats the central pressor effects of angiotensin II are initiated by vasopressin release but become dependent on the sympathetic nervous system when vasopressin is absent or not effective. When rats were allowed to drink in response to angiotensin II, a further sharp rise in blood pressure occurred, together with increases in heart rate and splanchnic nerve activity. The results demonstrate fundamental differences in the mechanisms by which central pressor peptides can influence cardiovascular and autonomic function. It is conceivable that the distinct sympathetic response patterns to central angiotensin II and substance P receptor stimulation form part of a specific cardiovascular adjustment to the individual behavioral reactions, such as drinking, as in the case of angiotensin II, or arousal within the central processing of pain, as in the case of substance P.

Action Potentials↗
PubMed1984

Sympathetic activation following central vasopressin receptor stimulation in conscious rats.

Vasopressin (AVP)-containing pathways from hypothalamic neurons have been shown to project to blood pressure controlling brain centres. This suggests that AVP neurons may be involved in central blood pressure regulation. The effects of central AVP receptor stimulation on blood pressure, heart rate and directly recorded efferent sympathetic nerve activity in the splanchnic nerve (SNA) were investigated in conscious chronically instrumented rats. Intracerebroventricular (i.c.v.) injections of AVP (1-100 ng) caused dose-dependent blood pressure increases (maximum 26.9 +/- 3.5 mmHg) together with marked rises in heart rate and SNA. More pre-treatment with the AVP receptor antagonist d(CH2)5AVP (3/micrograms i.c.v.) completely prevented the central responses to AVP. Intracarotid injection of the same AVP doses produced rises in blood pressure accompanied by drastic falls in heart rate and SNA, similar to those seen after i.v. AVP injection. Thus, stimulation of specific neuronal AVP receptors produces a characteristic haemodynamic and sympathetic response pattern with marked sympathetic nerve activation, which is clearly distinct from the responses to vascular AVP receptor stimulation. It is concluded that AVP pathways in the brain can contribute to central blood pressure control via regulation of sympathetic outflow to the periphery.

Animals↗
PubMed1982

The cardiovascular effects of centrally administered substance P in the anaesthetised rabbit.

The cardiovascular effects of Substance P (SP) administered into the cisterna magna (i.c.) of the pentobarbitone anaesthetised rabbit have been investigated. SP given i.c. in low doses (0.2-10 ng/kg) caused a dose related rise in blood pressure and bradycardia. Both responses were attenuated by pretreatment with intravenous (i.v.) pentolinium. SP given i.v. (1 ng/kg-1 microgram/kg) caused a dose related fall in pressure and tachycardia. The pressor response observed after i.c. administration was reduced by pretreatment with morphine and enhanced by naloxone. Bilateral sinoaortic denervation also enhanced the pressor effect of SP, but after deafferentation naloxone had no further effect. Pretreatment with clonidine abolished this rise in pressure. It is concluded that the central administration of SP has a direct pressor effect whereas the bradycardia appears to result from both direct and indirect effects, leading to a decrease in cardiac sympathetic activity. Both actions are mediated by the autonomic nervous system. SP may be involved in the central regulation of blood pressure and modulation of baroreceptor reflex activity.

Anesthesia↗
PubMed1982

Chemical stimulation of the nucleus of the solitary tract and the resulting blood pressure response.

The cardiovascular effects of catecholamines and related substances after local application into the nucleus tractus solitarii (NTS) of the medulla oblongata of urethane anesthetized rats are summarized. The catecholamines in the nanomolar dose range appear to activate stereospecifically receptor sites in the NTS, resulting in a decrease in blood pressure. Bradycardia occurs after bilateral administration of higher doses. The type of catecholaminergic receptors involved is discussed on the basis of the effects of different catecholamine receptor stimulating agents and pharmacological blockade. Both alpha-methylnoradrenaline and alpha-methyladrenaline are active and it is concluded that they both may contribute to the antihypertensive action of alpha-methyldopa. It is probable that an alpha-type of receptor mediates these hypotensive effects in the NTS. The nature of this receptor needs further characterization.

Animals↗
PubMed1977

Mechanism of cardiovascular effects of clonidine in conscious and anesthetized rabbits.

The actions of intravenous clonidine [2-(2,6 dichlorophenylamino)-2-imidazoline hydrochloride] on blood pressure and heart rate were examined in conscious rabbits. Complete transection of thecervical spinal cord increased the intensity and duration of the hypertensive effect of 30 microgram/kg of clonidine and completely abolished the fall in blood pressure. Heart rate slowing by clonidine was reduced. Result were similar 1 hour, 24 hours and 7 days after cord transection. Bilateral aortic sinus nerve section (baroreceptor deafferentation) increased both the hypertensive and hypotensive action of clonidine but reduced the bradycardia. When cervical cord transection was combined with batensive action, were abolished. We conclude that whereas the hypertensive action results from a direct effect on peripheral adrenoceptors, the fall in blood pressure is related to a reduction in sympathetic tone mediated at the level of the brain stem or more rostrally. The heart rate slowing results from both a reduction in sympathetic tone and also an enhanced vagal outflow. The increase in vagal tone seems to be dependent on the intergrity of baroreceptor afferent pathways.

Animals↗
PubMedDate not supplied

Terminally ill patients' expectations of nurses.

This exploratory study was undertaken to discover what nursing behaviours terminally ill patients desire. To rank patients' attitudes and judgements a Q-sort consisting of 70 cards was used. The statements covered three categories: physical and psycho-emotional care of patients and psycho-emotional care of significant other/s. "I would like the nurse to help me remain at home for as long as possible" was the most favoured statement and the least favoured was: "I would like the nurse to talk to me about death and dying." The overall theme was that responsive rather than directive nursing behaviours were desired. Analysis identified five Factors from which a model of responsive nursing care was developed. Interpretation of the Factors indicated patients desired responsive nursing care that enabled them and their families to bring their own resources to the dying process, rather than having imposed upon them care which nurses deemed appropriate.

Humans↗