A technique for the accurate measurement of cardiac ventricular pressures in chronic animals.
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Animals↗
Biomedical subjects
K G Cornish
Publications and source records attributed to K G Cornish.
Direct evidence for myogenic autoregulation of the renal microcirculation in the hamster.
We transplanted neonatal hamster renal tissue into a hamster check pouch chamber and subjected the renal tissue to increases and decreases in extravascular pressure. A decrease in extra-vascular pressure decreased, and an increase in extravascular pressure increased, the diameter of preglomerular arterioles. Thus, the change in preglomerular arteriolar diameter was directly related to alterations in extravascular pressure. Neither saralasin nor indomethacin affected these changes, whereas papaverin prevented them. The efferen arterioles responded passively to changes in extravascular pressure; i.e., the changes in their diameter were inversely related to changes in extravascular myogenic autoregulation of preglomerular vessels.
Afferent Pathways↗
Reflex cardiovascular and respiratory effects of serotonin in conscious and anesthetized dogs.
Cardiovascular and respiratory effects of intra-left atrial or intra-left ventricular injection of serotonin were studied in conscious dogs (n = 8), anesthetized closed-chest dogs (n = 13) and anesthetized open-chest dogs (n = 9). Serotonin (50-200 microgram), injected as a bolus, resulted in an initial bradycardia and hypotension followed by a delayed tachycardia and hypertension in the conscious dogs. The hypertension was seen as an increase of 21.5 +/- 2.7 (mean +/ SE) mm Hg from a control pressure of 102.5 +/- 1.9 mm Hg, whereas the initial decrease in pressure was 22.6 +/- 1.9 mm Hg. The tachycardia was 23.3 +/- 3.9 beats/min above a control heart rate of 104.9 +/- 3.9 beats/min whereas the bradycardia was 58.5 +/- 3.7 beats/min below control. There was a significant attenuation of the hypotension in both groups of anesthetized dogs. In fact, no hypotension was elicited in the open-chest anesthetized dogs. Open-chest anesthetized dogs showed only a hypertensive response (mean increase 67.2 +/- 5.5 mm Hg). Stimulation of respiration was seen in all groups of dogs. In conscious dogs there was a 214.8 +/- 15.4% increase in respiratory depth and a 20.8 +/- 3.1 breaths/min increase in respiratory rate. Atropine significantly reduced the bradycardia and abolished the hypotension in conscious dogs. Bilateral cervical vagotomy did not abolish the response in open-chest anesthetized dogs. We conclude that the so-called "hypertensive coronary chemoreflex" is altered dramatically by the state of the preparation and by anesthesia.
Anesthesia↗
Heart rate changes caused by chemical stimulation of the amygdaloid body.
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Acetylcholine↗
A modification of the dialytrode for simultaneous CNS recording and chemical stimulation.
Currently, chemical stimulation of the brain is done either with a single cannula that is inserted at the time the drug is delivered or with two cannulae that permit perfusion of the area of interest. The dialytrode is a push-pull cannula consisting of two concentric tubes, a porous membrane covering the tip of the tubing and a platinum wire loop that extends around the membrane and is used for EEG recordings. Studies with the dialytrode indicate that while the membrane is relatively impermeable to bacteria, molecules the size of neurotransmitters pass easily through the membrane. Therefore, the dailytrode is well suited for chronic chemical stimulation studies.
Amygdala↗
Evidence for the conversion of angiotensin I to angiotensin II by the coronary microcirculation.
Cardiac tissue from hamster neonates was transplanted into the hamster cheek pouch. After vascularization of the transplanted tissue the vessels were tested for their ability to convert angiotensin I (AI) to angiotensin II (AII). AI caused vasoconstriction of the coronary vessels which was reduced significantly by converting enzyme inhibitor and the AII antagonist (Sar1-Ala8) angiotensin II. It was concluded that the vessels of transplanted cardiac allografts convert AI to AII in a manner similar to that observed in the whole heart indicating that this procedure provides a good model for studying the microcirculation of the heart.
Angiotensin I↗
Direct evidence for the presence of a different converting enzyme in the hamster cheek pouch.
Kininase II (angiotensin I-converting enzyme) is generally accepted to be the enzyme responsible for the conversion of angiotensin I (A I) to angiotensin II (A II). This study examined the response of the microvasculature of the hamster cheek pouch to the local application of A I, A II, and the renin substrate, tetradecapeptide (TDP). A I and TDP caused a localized vasoconstriction that was not blocked by converting enzyme inhibitors (CEI: BPF5a for A I and BPF5a and the nonapeptide inhibitor for TDP). However, both the A II antagonist [Sar1, Ala8]angiotensin II and the antiserum to A II blocked completely the A I- and TDP-induced vasoconstriction. Sixty-eight percent of the applied A I was converted to A II in the presence of CEI as well as in its absence. It is concluded that the vasculature of the hamster cheek pouch converts significant amounts of A I to A II by a route that does not involve kininase II.
Angiotensin I↗
The interaction of the Bainbridge and Bezold-Jarisch reflexes in the conscious dog.
Experiments were undertaken to determine the efferent path of the Bainbridge reflex and to investigate the interaction of the Bainbridge reflex with the Bezold-Jarisch reflex in conscious, chronically instrumented dogs. The Bainbridge reflex was elicited by distending the left atrium by inflating a chronically implanted balloon catheter. The Bezold-Jarisch reflex was elicited using chemical stimulation of left ventricular receptors with infusions of veratridine (0.1-0.8 micrograms/kg/min) into the left circumflex coronary artery. Heart-rate responses to left atrial balloon inflation were compared before and after either beta-1 antagonism with metoprolol or cholinergic antagonism with atropine, and before and during left ventricular receptor stimulation with intracoronary veratridine. Left atrial balloon inflation alone caused a significant increase in heart rate (70.1 +/- 5 bpm), left atrial pressure (14 +/- 3 mmHg) and mean arterial blood pressure (10 +/- mmHg). Heart-rate responses to left atrial distension were inhibited, but not abolished by either cholinergic or beta-1 antagonism. Left atrial distension after both cholinergic and beta-1 antagonism abolished the heart-rate response to balloon inflation. These results indicate that the efferent component of the Bainbridge reflex has both a vagal and a sympathetic component in conscious dogs. Left atrial distension during simultaneous left ventricular receptor stimulation resulted in a significantly decreased tachycardia than did left atrial distension alone (26 +/- 3 bpm compared to 68 +/- 8 bpm in the control experiments). In addition, the slope of the heart rate vs left atrial pressure relationship was significantly inhibited by left ventricular receptor stimulation (1.8 +/- 0.2 bpm/mmHg compared to 5.7 +/- 0.3 bpm/mm Hg in the control experiments). There were no significant differences in either the left atrial pressure or arterial blood pressure changes between the two groups. These data suggest an interaction between these two reflexes that may be occurring in the central nervous system.
Animals↗