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Biomedical subjects

J H Rankin

Publications and source records attributed to J H Rankin.

At least 73 records · Page 4Linked to original sources
PubMed1978

Effect of x-irradiation of tumour bed on tumour blood flow and vascular response to drugs.

The blood flow of tumours growing in rat mammary glands previously exposed to 1500 R X-rays was 52% that of same-sized tumours in unirradiated host tissue. About 2 months after irradiation, the blood flow of the mammary gland was raised and that of the skin was unchanged, compared with the corresponding unirradiated tissue. Tumours growing in preirradiated and unirradiated mammary glands responded similarly to bolus injections of noradrenaline, angiotensin II, and isoprenaline. The responses of the irradiated tissues to these drugs were, however, not always the same as those of the corresponding unirradiated tissues. Exposure of the lungs to approximately 1500 R X-rays made the animals uniquely sensitive to bolus injections of noradrenaline and angiotensin II.

Angiotensin II↗
PubMed1978

Measurement of mammary tumor blood flow in unanesthetized rats.

Blood flow to mammary tumor MT-W9B in minimally disturbed, unanesthetized inbred WF rats was measured with radioactively labeled 25-mu (diameter) microspheres. The distribution of the blood flow estimates was not described by a normal probability density function but could be normalized with a natural log transformation of the data. The relative blood flow to the tumor tissue was always greater than that to the surrounding normal tissue and was dependent on the tumor size, transplantation site (axillary vs. inguinal), and physiologic state of the animal. The growth of this tumor did not alter the blood flow to the adjacent normal tissues. However, the cardiac output and coronary blood flow increased with increasing tumor size. Two blood flow estimates could be performed on the same animal within a time-span of 15 minutes.

Anesthesia↗
PubMed1978

Myocardial perfusion and function during acute right ventricular systolic hypertension.

Hemodynamics, myocardial function, and regional myocardial blood flow (MBF) were measured in 6 closed-chest ponies anesthetized with ketamine hydrochloride before (control) and after creation of acute right ventricular systolic hypertension (RVSH) during normoxia and isocapnic hypoxia. The right ventricular (RV) systolic pressure during each RVSH approached 90 mmHg. There were significant alterations in the pattern of total ventricular MBG distribution in favor of the RV. Because RV myocardium received proportionate increments to its endocardium as well as epicardium, it is concluded that autoregulation in the RV coronary vascular bed had not been abolished even during hypoxia + RVSH. Marked increase in MBF to the right side of the septum during each RVSH with little change in perfusion to other regions suggests that RV contraction is supported by the right side of the septum. Because these increments occurred with decreased RV coronary driving pressure they were the consequence of compensatory coronary vasodilatation. The slow heart rate of the pony in the presence of a large coronary vasodilatory reserve may have been the major factor in allowing large increments in MBF to the stressed regions despite decreased coronary driving pressure.

Acid-Base Equilibrium↗
PubMed1978

Effects of several vasoactive drugs on the vascular resistance of MT-W9B tumors in W/Fu rats.

These experiments were designed to study the effects of vasoactive drugs on normal and malignant tissue in W/Fu rats. The increase in resistance to tumor blood flow elicited by a bolus injection of 10 microgram of norepinephrine was greater than that elicited in the surrounding mammary gland tissue. A 10-fold increase in the resistance to tumor blood flow was sustained for 30 min by the infusion of norepinephrine at the rate of 1.39 microgram/min, whereas a smaller initial increase in mammary gland vascular resistance decreased with time. In contrast, the increase in resistance to tumor blood flow caused by a bolus injection of angiotensin II was less than that observed in the mammary gland tissue. A 20-fold increase in mammary gland vascular resistance could be maintained for at least 5 min by infusion of angiotensin II at the rate of 1.39 microgram/min. In comparison, such treatment caused only a 3-fold increase in the resistance to tumor blood flow. A bolus injection of 1 microgram of isoproterenol decreased the vascular resistance in all normal tissues studied, but the resistance to blood flow in the tumor remained unchanged. The results of these experiments indicate that there may be methods whereby the tumor blood flow can be manipulated for therapeutic purposes and to assist radiographic visualization of tumors.

Angiotensin II↗
PubMed1977

The effect of uterine vascular insufficiency on fetal arterial pressure and heart rate in the near-term sheep.

Fetal hypoxia secondary to uterine vascular insufficiency was induced by injecting norepinephrine or PGE2 into the maternal circulation of near-term sheep. With these drugs the uterine blood flow fell to 41 and 40% of its control value, respectively. The fetal responses to the PGE2-induced uterine contraction were a bradycardia which was apparent within 10 seconds (P less than 0.05), and a hypertension which was also apparent within 10 seconds (P less than 0.03). After the norepinephrine-induced uterine vasoconstriction, there was no observable change in the fetal arterial pressure. The fetal heart rate started to fall after 30 to 60 seconds and started to return to the control value within 90 seconds. The fetal response to uterine vascular insufficiency induced by a contraction may not have been caused by hypoxia alone as these responses were more rapid in onset than the fetal responses observed subsequent to uterine vascular insufficiency produced by vasoconstriction.

Animals↗
PubMed1976

Effect of prostaglandin E2 on ovine maternal placental blood flow.

The effect of PGE2 on regional blood flows in the chronically catheterized near-term pregnant sheep was investigated using radioactive microspheres. The injection of 20 mug PGE2 per kilogram into the left ventricle of eight sheep resulted in no change in maternal brain and noncotyledonary uterine flow. The renal blood flow increased from 692 to 892 ml/min (P less than 0.004). The uterine blood flow decreased from 673 to 317 ml/min (P less than 0.001). The trium was bypassed by injecting 7 mug PGE2 per kilogram of sheep into a fetal venous catheter and permitting it to reach the placental vasculature after placental transfer. Eleven sets of observations were made in eight animals. We observed no change in the intrauterine pressure, maternal brain flow, and noncotyledonary uterine blood flow secondary to this procedure. The maternal renal blood flow changed from 592 to 669 ml/min (P less than 0.007). The uterine blood flow increased from 762 to 853 ml/min (P less than 0.02). The uterine vascular resistance decreased from 0.124 to 0.115 mmHg x min/ml (P less than 0.04). It was concluded that 1) PGE3 crosses the placenta quite readily, and 2) PGE3 causes dilatation of the maternal placental vascular bed.

Animals↗
PubMed1976

Circulatory responses of the near-term sheep fetus to prostaglandin E2.

The effect of prostaglandin E2 (PGE2) on the fetal circulation was measured in chronically catheterized ewes using radioactive microspheres. The injection of 10 mug/kg PGE2 into six fetuses resulted in a biphasic pressor response with a hypotensive period followed by a prolonged period of hypertension. The fetal arterial pressure rose from 45 to 63 mmHg (P less than 0.002). The placental membrane flow changed from 36 to 16 ml/min (P less than 0.004), the fetal renal blood flow changed from 8.6 to 7.1 ml/min per kg of fetus (P less than 0.001). It was postulated that the hypotensive response was due to a direct effect of PGE2 on the heart and the hypertensive response was due to PGE2 releasing a vasoconstricting agent into the fetal circulation. In nine experiments the PGE2 was administered to the maternal lcirculation. This caused a fetal hypertension and a vasoconstriction of the fetal renal, placental membrane, and umbilical circulations. These changes were similar in time course and magnitude to those described above. It is postulated that PGE2 crosses the placenta and that the fetal responses seen in this series are similar to those seen when PGE2 is administered to the fetal circulation.

Animals↗