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Biomedical subjects

D W Clark

Publications and source records attributed to D W Clark.

At least 55 records · Page 3Linked to original sources
PubMed1978

Blood pressure and vascular resistance in genetically hypertensive rats treated at birth with 6-hydroxydopamine.

Genetically hypertensive (GH) rats of the New Zealand strain and normotensive (N) rats were sympathectomized from birth with 6-hydroxydopamine (100 mg/kg,s.c, on alternate days, seven treatments). In adult treated rats from each strain (GHTr and NTr), blood pressure was lower than normal. Functional tests and electron microscopy showed that denervation was virtually complete in mesenteric and hindlimb arteries; the innervation of the renal artery was little affected. Ganglionic blockade still caused a large fall in blood pressure in treated rats. Vascular resistance was higher in blood-perfused hindlimbs and tails of GH rats than in those of N rats; in contrast, resistance was similar in limbs and tails of GHTr and NTr rats and was greater than that found in untreated N rats. Saline-perfused limb vessels had neither neurogenic nor myogenic tone and resistance was higher in GH limbs (whether these were from treated rats or not) than in untreated N limbs. In saline-perfused NTr limbs, there was a paradoxical structural adaptation (probably luminal narrowing) of the hindlimb blood vessels and resistance was higher than in untreated N rats. The resistance of saline-perfused GH and GHTr limbs was similar. A high peripheral resistance appears to be the main mechanism sustaining genetic hypertension, and the integrity of the vasomotor sympathetic nerves is necessary for the development of this form of experimental hypertension.

Animals↗
PubMed1977

Changes in rat hind limb vascular resistance following intracerebroventricular drug administration.

The right hind limbs of rats (which had previously implanted intraventricular guide cannulae) were isolated from the systemic circulation, but with the nerves to the limb remaining intact, and perfused using a constant output blood pump. Using this preparation, changes in vascular resistance, blood pressure and heart rate were monitored following injection of noradrenaline, phentolamine and propranolol into the lateral cerebral ventricles (i.c.v.) of rats anaesthetised with alpha-chloralose. All three drugs lowered blood pressure. Noradrenaline administered i.c.v. induced a nervously mediated vasocilatation and an insignificant fall in heart rate whereas i.c.v. phentolamine administration was followed by a nervously mediated vasoconstriction in the isolated hind limb and a gradual rise in heart rate. After i.c.v. administration of propranolol there was no evidence of an immediate nervously mediated vasodilatation but heart rate fell significantly. Following i.c.v. phentolamine or propranolol vasodilatation did not occur in the hind limb until after the time taken for circulating blood ro reach the isolated vascular bed. The vasodilatatory and hypotensive responses to i.c.v. noradrenaline were not evident following prior i.c.v. injection of phentolamine. These results indicate the suitability of this preparation for investigations of central actions of other drugs.

Animals↗
PubMed1975

A technique for unknotting an intracardiac flow-directed balloon catheter.

Described is an unusual complication occurring during right-sided cardiac catheterization using a 7F flow-directed balloon catheter. During an attempt to direct the catheter from the main pulmonary artery into the pulmonary wedge position, the tip became entangled in a loop of catheter and knotted. Initially, all attempts to unknot or remove the catheter failed. A movable core guide wire was passed through the major lumen of the catheter, resulting in the immediate unknotting of the catheter, thus allowing its withdrawal.

Cardiac Catheterization↗
PubMed1975

Effects of oestrogens and pregnancy on the distribution of sheep erythrocytes and the antibody response in mice.

Mice pre-treated with three oestrogenic preparations showed increased hepatic and reduced splenic uptake of 51Cr-labelled sheep erythrocytes (SRBC). The anitbody response to SRBC wahe number of antibody-forming cells in the spleen parallels the amount of SRBC localizing in this organ and that both can be depressed or enhanced by appropriate pre-treatments with oestrogens or colloidal carbon. The effects of these agents are mediated through stimulation or 'blockade' of the phagocytic activity of liver macrophages. Changes in localization of SRBC in pregnant mice were similar to those found after treatment with oestrogens. These changes were, however, rather small and the antibody response of pregnant animals was not affected.

Animals↗
PubMed1975

Vasodilator responses to K+ in genetic hypertensive and in renal hypertensive rats.

Vascular responses to K+ were studied in 37 genetically hypertensive (GH) rats of the New Zealand strain, 12 weight-matched and 11 age-matched normotensive control rats, 21 renal hypertensive (RH) rats with one renal artery clipped and the other kidney untouched, and 18 sham-clipped normotensive control (N) rats, under intravenous chloralose and pentobarbitol anesthesia. KCI in an isosmolar solution, delivering 1.84 X 10(-3), 3.07 X 10(-3), or 4.60 X 10(-3) mEq. K+ per minute was infused intra-arterially into the isolated pump-perfused (blood, 1 ml. per minute) hindlimb vascular beds, increasing measured limb arterial plasma [K+] up to 12 mEq. per liter without changing arterial pressure. The K+ infusions at all three rates reduced limb resistance (P less than 0.01). There was a linear correlation (P less than 0.01) between initial limb resistance and magnitude of response. Analysis of covariance indicated that there were no significant differences between responses in GH and normotensive control rats (P less than 0.1). In contrast, responses in RH rats were decreased (P less than 0.01) when compared to responses in N and GH rats. Thus, the vascular response to K+ is attenuated in renal hypertensive rats, as we have previously found in renal hypertensive dogs and essential hypertensive men, suggesting an underlying defect in vascular K+ metabolism. This abnormality is apparently not shared by genetically hypertensive rats of the New Zealand strain.

Animals↗
PubMed1972

Long-lasting peripheral and central effects of 6-hydroxydopamine in rats.

1. In newborn rats treated with 6-hydroxydopamine hydrobromide (6-OHDA) (50-150 mg/kg on 5-7 days) a widespread and long-lasting dose related sympathectomy was demonstrated.2. When rats given 6-hydroxydopamine (100 mg/kg, seven treatments) in the neonatal period were killed at 10 weeks the concentration of noradrenaline (NA) in the heart, mesentery and vas deferens was significantly reduced. There was no alteration in the catecholamine content of the adrenal glands.3. The amplitude of the responses of perfused mesenteric arteries from 6-hydroxydopamine treated rats to intra-arterial noradrenaline was not increased, compared with controls, but the duration of responses was increased.4. 6-Hydroxydopamine given to newborn rats caused a long-lasting depletion of noradrenaline in three of the five regions of the central nervous system (cortex, cerebellum and spinal cord) studied. The concentration of noradrenaline in the pons-medulla was increased, but in the thalamic region was unchanged. The treated rats showed significantly lower exploratory activity.5. Treatment of newborn rats with 6-hydroxydopamine thus has striking and long-lasting effects on peripheral and central adrenergic systems.

Adrenal Glands↗